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  1. Feb 2018
    1. On 2014 Jan 07, Brett Snodgrass commented:

      Dear Author,

      Thank you for the excellent article. Although the fistula closed without a specific ligation procedure, the three procedures probably altered the hemodynamics of the right ventricle and permitted the vessel of Wearn to become less prominent and/or close. The closure may be physiologic or anatomic, and I do not think we have sufficient information to make a definitive determination. The closure would probably be considered anatomic if the vessel lumen became fibrosed.

      Please consider viewing the following post related to this article.

      https://twitter.com/BrettSnodgrass1/status/415904348074287105

      Comments and feedback are welcome.

      Thank you kindly.


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    1. On 2014 Feb 27, George W Hinkal commented:

      The National Cancer Institute has been investing in the development of an online webportal of curated cancer nanotechnology data called caNanoLab. The numerical data, nanomaterial characterizations and composition information for the ten nanoparticles related to this publication have been added to the database and can be found at:

      https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=33161216&page=0&tab=ALL

      https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=33161218&page=0&tab=ALL

      https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=33161217&page=0&tab=ALL

      https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=33161226&page=0&tab=ALL

      https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=33161221&page=0&tab=ALL

      https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=33161222&page=0&tab=ALL

      https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=33685522&page=0&tab=ALL

      https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=33161224&page=0&tab=ALL

      https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=33161225&page=0&tab=ALL

      https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=34766848&page=0&tab=ALL

      The left navigation links on these pages provide information about each sample (under Navigation Tree).

      For general information on how to use caNanoLab, please visit https://cananolab.nci.nih.gov/caNanoLab/home.jsp


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    1. On 2014 Mar 05, Gwinyai Masukume commented:

      In the introduction of this article, the authors state: “We report the largest case series of advanced abdominal pregnancies from sub-Saharan Africa from 1976 to 2006.” This case series has 20 patients.

      In 1989, in the article below originating from Africa, South of the Sahara, 23 cases were described. This would thus be the ‘largest case series of advanced abdominal pregnancy from sub-Saharan Africa between 1976 and 2006’.

      White RG. Advanced abdominal pregnancy--a review of 23 cases. Ir J Med Sci. 1989; 158(4):77-8. White RG, 1989


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    1. On 2016 Aug 23, Ben Goldacre commented:

      This trial has the wrong trial registry ID associated with it on PubMed: both in the XML on PubMed, and in the originating journal article. The ID given is NCT002289835. We believe the correct ID, which we have found by hand searching, is NCT00289835.

      This comment is being posted as part of the OpenTrials.net project<sup>[1]</sup> , an open database threading together all publicly accessible documents and data on each trial, globally. In the course of creating the database, and matching documents and data sources about trials from different locations, we have identified various anomalies in datasets such as PubMed, and in published papers. Alongside documenting the prevalence of problems, we are also attempting to correct these errors and anomalies wherever possible, by feeding back to the originators. We have corrected this data in the OpenTrials.net database; we hope that this trial’s text and metadata can also be corrected at source, in PubMed and in the accompanying paper.

      Many thanks,

      Jessica Fleminger, Ben Goldacre*

      [1] Goldacre, B., Gray, J., 2016. OpenTrials: towards a collaborative open database of all available information on all clinical trials. Trials 17. doi:10.1186/s13063-016-1290-8 PMID: 27056367

      * Dr Ben Goldacre BA MA MSc MBBS MRCPsych<br> Senior Clinical Research Fellow<br> ben.goldacre@phc.ox.ac.uk<br> www.ebmDataLab.net<br> Centre for Evidence Based Medicine<br> Department of Primary Care Health Sciences<br> University of Oxford<br> Radcliffe Observatory Quarter<br> Woodstock Road<br> Oxford OX2 6GG


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    1. On 2016 Jan 12, Peter Gøtzsche commented:

      The odds ratio for death was 1.95 (95% confidence interval 1.21 to 3.14), when psychotic patients received 3 or more antipsychotics simultaneously instead of one, thus doubling the mortality. However, the authors adjusted for somatic comedication and the adjusted odds ratio was 1.16 (0.68 to 2.00). This is a fatal error. The death rate soared, the more drugs for somatic illnesses, the patients received (27 times if they received at least 10), and the use of, for example, cardiovascular drugs were 37% and 16% among those who died and those who survived (controls), respectively. The use of diabetes drugs was 12% and 6%, respectively. Since increased doses and the use of several antipsychotics simultaneously increase the incidence of somatic illnesses, it is blatantly wrong to adjust for the use of somatic comedication, as this is part of the causal chain from psychosis to death. In this manner, the adjustment removes a relation between polypharmacy and death that actually exists.

      Better studies have shown that polypharmacy with antipsychotics increases deaths, as expected. Some of these studies are mentioned in the current study’s Discussion section.

      Peter C Gøtzsche, Professor and Director, Nordic Cochrane Centre


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    1. On 2016 Oct 03, Morten Oksvold commented:

      Please note that after an investigation at the University of Cologne, six articles where T. Wenz figures as first or senior author were found to contain questionable data due to scientific misconduct. This article is one of these six articles.

      The conclusion from the report was ready June 28, 2016, please see the link (in German):

      http://www.portal.uni-koeln.de/9015.html?&tx_news_pi1[news]=4335&tx_news_pi1[controller]=News&tx_news_pi1[action]=detail&cHash=1deb8399d7f796d65ca9f6ae4764a1ce


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    1. On 2014 Jul 04, Ferenc Zsila commented:

      In page 583, the authors claim that "We also examined anthocyanidin–DNA interactions spectrophotometrically at pH 7.5 but were unable to demonstrate significant or consistent shifts in l max or maximum absorbance that would indicate the interaction between the two at this pH as has been observed for other flavonoids (Webb and Ebeler 2004)."

      However, all details of the spectrophotometric measurements are missing from the experimental section. Name and concentration of the tested anthocyanidin(s), concentration of the DNA, temperature, solvent, optical pathlength, wavelength range, and the type of the instrument used all remain unknown. Additionally, the absorption spectra are not shown either.


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    1. On 2013 Oct 31, John Cannell commented:

      I congratulate the authors on a fine study. I wonder if they know that a recent meta-analysis found the the risk of preeclampsia is inversely related to maternal 25(OH)D levels?

      Tabesh M, 2013

      If not, it shows how little communication is occurring between autism spectrum disorder (ASD) scientists and the broader scientific realm. Each ASD scientist seems to be immersed in his or her own research interest but seemingly oblivious to the larger body of science research.

      Thus the vitamin D theory of ASD (vitamin D deficiency being the environmental risk factor for this highly heritable disorder) is consistent with the authors work. Three recent studies, using community controls, have found 25(OH)D levels are significantly lower in children with ASD. Two of the studies below (Mostafa et al and Gong et al) also found ASD severity, as rated on standard ASD rating scales, is inversely correlated with 25(OH)D levels. Mostafa et al found an R value of -.86 for the association of serum 25(OH)D with ASD severity.

      Gong ZL, Luo CM, Wang L, Shen L, Wei F, Tong RJ, Liu Y. Serum 25-hydroxyvitamin D levels in Chinese children with autism spectrum disorders. Neuroreport. 2013 Oct 1. Gong ZL, 2014

      Meguid NA, Hashish AF, Anwar M, Sidhom G. Reduced serum levels of 25-hydroxy and 1,25-dihydroxy vitamin D in Egyptian children with autism. J Altern Complement Med. 2010 Jun;16(6):641-5. Meguid NA, 2010

      Mostafa GA, Al-Ayadhi LY.Reduced serum concentrations of 25-hydroxy vitamin D in children with autism: relation to autoimmunity. J Neuroinflammation. 2012 Aug 17;9:201. Mostafa GA, 2012

      There is a plethora of basic science explaining why low gestational or early childhood 25(OH)D levels would adversely effect brain development.

      DeLuca GC, Kimball SM, Kolasinski J, Ramagopalan SV, Ebers GC. Review: the role of vitamin D in nervous system health and disease. Neuropathol Appl Neurobiol. 2013 Aug;39(5):458-84. doi: 10.1111/nan.12020. DeLuca GC, 2013

      Eyles DW, Feron F, Cui X, Kesby JP, Harms LH, Ko P, McGrath JJ, Burne TH. Developmental vitamin D deficiency causes abnormal brain development. Psychoneuroendocrinology. 2009 Dec;34 Suppl 1:S247-57. doi: 10.1016/j.psyneuen.2009.04.015. Epub . Review. Eyles DW, 2009

      Furthermore, the vitamin D theory of autism explains most of the epidemiological facts of ASD.

      Cannell JJ. On the aetiology of autism. Acta Paediatr. 2010 Aug;99(8):1128-30. Cannell JJ, 2010

      Cannell JJ. Autism and vitamin D. Med Hypotheses. 2008;70(4):750-9. Cannell JJ, 2008

      70% of American toddlers do not take the American Pediatric Association's recommended vitamin D supplement of 400 IU/day. As milk consumption has fallen, so have toddler’s vitamin D levels.

      Cannell JJ. Autism, will vitamin D treat core symptoms? Medical Hypotheses. 2013 Aug;81(2):195-8. Cannell JJ, 2013

      Some autism researchers seem cognizant of the entire body of autism research. For example, a group of well-known European autism researchers, including Professor Christopher Gillberg of the Gillberg Neuropsychiatric Institute, have recently called for the need for “urgent research” into the vitamin D deficiency theory of ASD.

      Kočovská E, Fernell E, Billstedt E, Minnis H, Gillberg C. Vitamin D and autism: clinical review. Res Dev Disabil. 2012 Sep-Oct;33(5):1541-50. doi: 10.1016/j.ridd.2012.02.015. Epub 2012 Apr 21.Kočovská E, 2012

      However, these scientists appear to be in the minority. Until all autism researchers become cognizant of the wider body of scientific research, we will continue to wonder how to prevent - and perhaps even treat - this modern day plague.

      John J Cannell, MD

      Vitamin D Council

      http://www.vitamindcouncil.org


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    1. On 2017 May 31, David Nunan commented:

      Readers may not be aware of the notice of concern raised with this paper and another paper (Paterna S, 2008) by the same group published in Clinical Science in 2008, both of which were included in a 2012 systematic review published in BMJ Open Heart which was subsequently retracted. Whilst there is a link above to the notice of concern, here I've provided the contents of that notice. This paper has not been retracted.

      Concern has been raised regarding a paper published in the Journal of Cardiac Failure: “Long-Term Effects of Dietary Sodium Intake on Cytokines and Neurohumoral Activation in Patients With Recently Compensated Heart Failure,” by Parrinello et al, J Card Fail 2009;15:864–73. The paper contains a dataset identical to that published by the same authors in Clinical Science 2008;114:221–30. The corresponding author, Dr di Pasquale of Palermo, Italy, has indicated that an error was made during a “cut and paste” process, and a table from the 2008 Clinical Science paper was mistakenly reproduced in the 2009 Journal of Cardiac Failure paper. Dr di Pasquale also coauthored an online manuscript in Heart, August 21, 2012, using a meta-analysis of 6 earlier papers, and that online report also includes the duplicated data. When questioned about the data, Dr di Pasquale reported that by unintentional error he had inserted the table from the earlier 2008 paper (Clinical Science) into the 2009 paper (Journal of Cardiac Failure). The Dean of the Medical School at the University of Palermo was notified and asked to investigate the matter. It was reported that Dr di Pasquale lost the raw data owing to a “computer crash” without having made backup files. The data are therefore not verifiable. Based on the information at hand, we have been unable to independently determine with certainty the cause of duplication of the dataset. Given the fact that there are duplicate data published, and there is no way to validate or verify the veracity of the data, readers should be cautioned in the application of the findings reported in these manuscripts to their clinical practice.

      Gary S. Francis, MD Professor of Medicine, University of Minnesota Editor-in-Chief, Journal of Cardiac Failure http://dx.doi.org/10.1016/j.cardfail.2013.05.015


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    1. On 2017 Aug 20, Daniel Weiss commented:

      This paper shows the insensitivity of two tiered testing for Lyme disease. Patients were “categorized as having Lyme disease, and met the CDC surveillance criteria for diagnosis”, i.e. positive serology or positive culture. Nonetheless, only “two-thirds of patients with acute neuroborreliosis or carditis … were seropositive by two-tier testing”. Therefore, one third were negative.

      These authors also state that “IgM testing in Lyme disease has been problematic” and the CDC requirement that “IgM criteria should only be used to support the diagnosis of early LD in persons with illness of <1 month duration” “reduces the sensitivity of serologic testing” in certain patient groups.

      This is one of many papers that argue against the reliance on serologic tests to rule out Lyme disease.


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    1. On 2014 Oct 15, Amanda Capes-Davis commented:

      More recent work has shown that hTERT-EEC is misidentified and is actually MCF-7. So hTERT-EEC cells are from breast carcinoma, not immortalized endothelium.

      It's important to test cell lines to confirm they correspond to the expected donor and are not cross-contaminated, using a consensus technique such as STR profiling. Journals are increasingly requiring testing as a prerequisite before publication and this will help to address the widespread use of misidentified cell lines in the scientific literature.

      It's also a good idea to check before using a cell line to see if others have documented a problem previously. ICLAC maintains a list of known misidentified cell lines at http://iclac.org/databases/cross-contaminations/.


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    1. On 2014 Nov 19, Kaccie Li commented:

      The authors of this study generalized the subjects from the United States to be white/Caucasian which is a serious oversight. A cursory look at US demographics would reveal that just over 75 percent of the population is white which is probably already questionable to generalize the entire group as white, but a closer look reveals even more concerning factors. Consider the populations in the studies classified under "white" in Table 2 of this article where the first two entries were studies done by Wang and colleagues (ref 13) and Porter and colleagues (ref 14). The first study was done at Baylor College of Medicine where a meager 43 percent of the student population is white. Suppose subject recruitment was done in the city Houston in general, the conclusions of Lim's study can be further put under scrutiny since only about 25 percent of Houston's population is white (non-hispanic). Similar things could be stated about individuals recruited in Porter's study (ref 14) at the University of Rochester where only about 76 percent of the student body is white. Lim and Fam does not mention the possibility of the presence of significant African and Asian Americans being an unknown factor that could have affected their results and conclusions.


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    1. On 2015 Dec 01, S A Ostroumov commented:

      DOI:10.1134/S0012496609050159; In the presence of this aquatic, submerged, free-floating higher plant (rigid hornwort) in water system, it was occured that a decrease in concentrations of the four heavy metals (cadmium; copper; lead; zinc; Cu, Zn, Cd, and Pb) in the water medium accelerated. The aquatic macrophytes served as a factor to speed up the water purification (decontamination) process in the aquatic system. The method for measuring the heavy metals was stripping voltammetry. This paper is in the database of the United States Environmental Protection Agency (U.S.EPA), titled: Health & Environmental Research Online (HERO): http://hero.epa.gov/index.cfm?action=reference.details&reference_id=362778; FULL TEXT ONLINE FREE: https://www.researchgate.net/publication/40481671; KEYWORDS: the additional keywords for this paper in the database HERO: phytoremediation; polluted water; water pollution; water quality; Ceratophyllum demersum; Ceratophyllum; Ceratophyllaceae; Nymphaeales; dicotyledons; angiosperms; Spermatophyta; plants; eukaryotes; water composition and quality; Aquatic Biology and Ecology (MM300); Water Resources (PP200); Pollution and Degradation (PP600); Industrial Wastes and Effluents. The additional keywords: decontamination, aquatic, submerged, free-floating, higher plant, phytotechnology, ecotechnology, macrophytes, environmental toxicology, environmental chemistry, hornwort, rigid hornwort, coontail, coon's tail, stripping voltammetry; **


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    1. On 2014 Aug 01, Mark Yarchoan commented:

      Overall, this study raises interest in a link between metabolic derangements and Alzheimer’s disease (AD). However, one concern I have is that in evaluating a possible association between low circulating leptin and incident dementia, the authors adjusted for current BMI, but not amount or direction of recent weight change. It is well known (and reiterated in this article) that, “Although midlife obesity is associated with an increased risk of AD, late-life weight loss is known to precede the onset of clinical AD.” Therefore, it is to be expected that the AD and normal groups might have similar overall weight and BMI, but a different direction and rate of BMI change (AD group rapidly losing weight, normal aging group keeping or gaining weight). Leptin levels are correlated with current body fat mass, but appear to be even more significantly affected by direction of weight change. For example, 14% intentional weight loss in human subjects results in a 64.5% reduction in leptin levels (Sumithran et al. NEJM 2014/ PMID: 22029981). Therefore, I am concerned that the observed differences in leptin levels in this study may simply be a consequence of the significant and early weight loss seen in AD.


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    1. On 2015 Oct 07, Peter Good commented:

      Shaw recently presented compelling evidence that acetaminophen (Tylenol) depletes glutathione in autism, asthma, and other disorders: “The characteristic loss of Purkinje cells in the brains of people with autism is consistent with depletion of brain glutathione due to excess acetaminophen usage, which leads to premature brain Purkinje cell death.”[1] Shaw observed that Cuba vaccinates all their children, especially against measles, yet their autism incidence is only 1/300th of ours in the U.S. What’s the difference, according to Shaw? Cuba prohibits over-the-counter acetaminophen, and only rarely allows acetaminophen prescribed for vaccinations, because acetaminophen is limited by the embargo. Deth noted that acetaminophen (like mercury) readily binds selenium-containing proteins that underlie the glutathione system [2]. By depleting glutathione, acetaminophen may effectively deplete glutamine because glutamine enters cells more easily than glutamate, thus often provides glutamate to synthesize glutathione [3].

      As Shaw noted, Bauer and Kriebel reported recommendations that acetaminophen (paracetamol in the UK) be given before and after circumcision: “These guidelines include the suggestion of a first dose . . . two hours prior to the procedure, and doses every 4–6 hours for 24 hours following the procedure. Thus newborn males often receive 5–7 doses . . . during the developmentally vulnerable initial days of life.” They also cited evidence that may explain the increased number of children born autistic: “In the early 1980’s about 42% of women used paracetamol during the first trimester of pregnancy. The rate climbed to over 65% in the early 1990’s, where it has essentially remained through 2004.”[4]

      For further evidence of glutathione depletion in autism, see: Chronic neurochemical asymmetry and dysconnection in autism. Implications of a personal trial of oral citrulline + taurine – published at <http:/www.autismstudies.net>

      references 1. Shaw W. Evidence that increased acetaminophen use in genetically vulnerable children appears to be a major cause of the epidemics of autism, attention deficit with hyperactivity, and asthma. J Restorative Medicine 2013;2:1–16. 2. Deth R (PhD). Personal communication 2010. 3. Hong RW, Rounds JD, Helton SW, Robinson MK, Wilmore DW. Glutamine preserves liver glutathione after lethal hepatic injury. Ann Surg 1992;215:114–119. 4. Bauer AZ, Kriebel D. Prenatal and perinatal analgesic exposure and autism: an ecological link. Environ Health 2013;12:41.


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    1. On 2013 Nov 01, Darren L Dahly commented:

      I am currently drafting a paper following from this work that uses mixture modelling to cluster study participants based on these socio-economic indicators. A poster of the preliminary work can be found here. http://f1000.com/posters/browse/summary/1089836 It offers a different perspective from this previous paper that focused on results from linear models.


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    1. On 2014 Feb 07, Saša Branković commented:

      This theory is a (probably unintentional) plagiarism. Because, Manfred Velden (1974) had introduced the uncertainty (entropy) processing hypothesis of the orienting response and Saša Branković (2001) implemented the model into the theory of motivation, which has been called the theory of informational needs.


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    1. On 2016 Aug 08, Stuart RAY commented:

      The single line "Erratum in Correction [Hepatology. 2015]" above does not capture the complex recent history of this publication. That correction notes a 12-fold (person-years vs. person-months) calculation error that, once corrected, eliminates any statistical difference in HCC rates between those with HBsAg loss and those with HCC persistence.

      Fortunately, an alert and astute reader (Chee-Kiat Tan, Singapore General Hospital) called attention to the important implications of this error in a Letter to the Editor [which, I hope, will be linked from this Pubmed record]. The authors provided a fairly terse reply.

      In a notably rare Editorial response to Tan's letter, Michael Nathanson and Norah Terrault note that a key conclusion of the report is arguably strengthened by the correction: that HCC can occur in persons even after HBsAg loss, even in the absence of cirrhosis.

      The importance of vigilance for HCC in persons with HBV infection (even in the absence of detectable HBsAg) is amplified by this correction; careful reading of the literature is also emphasized.


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    1. On 2013 Nov 24, John Sotos commented:

      Medical educators I’ve known have often cited the case histories in the Journal‘s CPCs as model presentations of clinical information.

      Unfortunately, case 2-2010 jeopardizes this reputation by saying the patient experienced “an episode of pain in his left arm … that radiated to his heart” (1).

      Medical trainees should not emulate this statement, for three reasons:

      First, it is not believable. The complex innervation of thoracic structures prevents localization of pain to any internal organ.

      Second, it is ambiguous. Many patients believe pain near the left breast is “heart pain” (2), whereas physicians generally associate retrosternal discomfort with cardiac ischemia.

      Third, even if this statement were a direct quote from the patient, it violates the precept to “question [the patient] until sufficient details are obtained to categorize the symptom in medical terms” (3).

      No institution of medical education can rest on its laurels. I hope The Journal will re-dedicate itself to maintaining its pre-eminence in this vital field.

      (1) Isselbacher EM, Kligerman SJ, Lam KM, Hurtado RM. Case records of the Massachusetts General Hospital. Case 2-2010. A 47-year-old man with abdominal and flank pain. N Engl J Med. 2010 Jan 21;362(3):254-62. Pubmed 20089976 doi: 10.1056/NEJMcpc0905548.

      (2) Wood P. Diseases of the Heart and Circulation. 2nd ed. London: Eyre and Spottiswoode, 1956. Page 4.

      (3) DeGowin RL. DeGowin & DeGowin’s Bedside Diagnostic Examination. 5th ed. New York: Macmillan, 1987. Page 24.


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    1. On 2016 Nov 06, David Juurlink commented:

      Regarding the risk of addiction during chronic opioid therapy, readers of this review are directed to the correspondence associated with Vowles KE, 2015, in which the authors note: "Importantly, of the 26 studies reviewed by Noble et al., only 2 (7.7%) reported rates of opioid addiction and those authors imputed (page 8) an addiction rate of zero in the other 24 studies (92.3%). Although there is clear utility in their broader findings, we would urge caution in assuming absence of any particular phenomenon simply because it is not reported."


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    1. On 2014 Jan 07, Brett Snodgrass commented:

      Dear Author,

      Thank you for the excellent article.

      Please provide your kind attention to the distinction between the Thebesian veins and the vessels of Wearn.

      Please consider the following post and associated links to PubMed related to the heart's vasculature. https://twitter.com/BrettSnodgrass1/status/417049983028690944

      Comments and suggestions are welcome.

      Thank you kindly.


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    1. On 2017 Jul 07, Morten Oksvold commented:

      This article should have been retracted after an investigation by The University of Maryland found this article to contain "compromised" data (a total of 26 articles in 11 journals were affected). The journal Cancer Research was informed in August 2016, according to Retraction Watch.

      http://retractionwatch.com/2017/04/26/university-asked-numerous-retractions-eight-months-later-three-journals-done-nothing/


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    1. On 2014 Dec 11, Ibrahim Masoodi commented:

      Ulcerative colitis has remitting and relapsing course and is affecting millions around the globe.The biomarkers can predict the severity in a non invasive manner .There is a growing need to identify more useful biomarkers in order to predict an impending relapse . We found serum CRP and fecal markers MPO , Lactoferrin very useful.These correlated with endoscopic severity and disease activity


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    1. On 2014 Nov 19, Amanda Capes-Davis commented:

      Cell lines that are known to be misidentified are now also hosted in the NCBI BioSample database at http://www.ncbi.nlm.nih.gov/biosample/.

      The list of known misidentified cell lines continues to be updated by ICLAC and has a dedicated webpage at http://iclac.org/databases/cross-contaminations/.

      Many thanks to Tanya Barrett and NCBI staff for their work in making the data more widely accessible.


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    1. On 2017 Jun 27, Andy Collings commented:

      A subset of experimental results from this study were the focus of a replication attempt as part of the Reproducibility Project: Cancer Biology (https://osf.io/e81xl/wiki/home/). The experimental designs and protocols were reviewed and approved in a Registered Report (http://dx.doi.org/10.7554/eLife.12626) and the results of the experiments were published in a Replication Study (http://dx.doi.org/10.7554/eLife.26030).


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    1. On 2014 Jan 08, Tom Kindlon commented:

      Early diagnosis of CFS/ME has been shown to lead to a better prognosis

      It was interesting to see the various views expressed by GPs in this paper[1]. However I think a couple of useful points could have been added. There is much discussion in the paper about whether a label of CFS/ME is useful or not. The authors refer to NICE guidelines which "emphasise the importance of a definitive diagnosis"[2]. However, I think it would have been useful to add some direct evidence on this issue.

      For example, research published by the Centres for Disease Control and Prevention (CDC) which found that an earlier diagnosis led to a better prognosis[3]. This prompted the CDC to launch a two-pronged awareness drive aimed at both health professionals and the general public - the tag line for the latter was, "Get informed. Get diagnosed. Get help."[4].

      A UK study found that the longer the interval between a patient falling ill and getting a diagnosis, the greater the likelihood that they would become severely affected. [5]

      The authors mention the issue of CFS/ME being managed in primary care. It is important for GPs to know that GPs encouraging patients to do a graded exercise programme is associated with a higher rate of adverse reactions. For example, a survey which asked patients about their experiences of treatments over the previous three years found that 45% reported being made worse by a graded exercise therapy (GET) programme overseen by their GP, compared to 31% who reported being made worse by a GET under a NHS specialist and 29% of those who did a GET in other circumstances[6]. The NICE guidelines do not recommend that a GP oversee such an approach[2].

      References:

      [1] Chew-Graham C, Dowrick C, Wearden A, Richardson V, Peters S. Making the diagnosis of Chronic Fatigue Syndrome/Myalgic Encephalitis in primary care: a qualitative study. BMC Fam Pract. 2010 Feb 23;11:16.

      [2] NICE CG 53 Chronic fatigue syndrome/Myalgic encephalomyelitis (or encephalopathy) guideline.

      [3] Nisenbaum R, Jones JF, Unger ER, Reyes M and Reeves WC. A population-based study of the clinical course of chronic fatigue syndrome. Health and Quality of Life Outcomes 2003;1:49-58.

      [4] CDC Chronic Fatigue Syndrome Awareness Campaign. http://cdc.gov/cfs/awareness.htm [Last accessed: 31 March, 2010]

      [5] Pheby D and Saffron L. Risk factors for severe ME/CFS. Biology and Medicine (2009); 1 (4):50-74. http://biolmedonline.com/Articles/vol1_4_50-74.pdf [Last accessed: 31 March, 2010]

      [6] Action for M.E. and AYME Survey 2008 Results http://afme.wordpress.com/5-treatments-and-symptoms/ [Last accessed: 31 March, 2010]


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    1. On 2016 Jul 01, Anne Niknejad commented:

      'It has been shown that apoptotic stimuli induce nuclear accumulation of GSK3β colocalising it with p53 [15]. This study reported that there was no nuclear accumulation of GSK3β after DNA damage (induced by camptothecin treatment) but rather an exclusive activation of the nuclear pool with no activation of cytosolic pools. The authors showed that p53 coimmunoprecipitates with GSK3β from nuclear fractions after camptothecin treatment.'

      Actually the reference 15 is wrong, no 'p53' mention, no camptothecin treatment (but staurosporine treatment)

      http://www.ncbi.nlm.nih.gov/pubmed/?term=11495916

      The correct reference could be

      http://www.ncbi.nlm.nih.gov/pubmed/?term=12048243

      (not cited in References)


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    1. On 2013 Nov 24, John Sotos commented:

      In his letter describing recently-introduced Congressional legislation to establish “healthcare innovation zones” (1), Dr. Kirch of the Association of American Medical Colleges (AAMC) listed his financial disclosures as “none.” I believe this is misleading.

      Dr. Kirch did not disclose that the AAMC proposed such zones (2). As a federally registered lobbying organization that has spent $100,000-$400,000 annually on lobbying activities since 1999 (3), common sense dictates that one of the AAMC’s “products” is legislation.

      Thus, Dr. Kirch should have disclosed his organization’s role in the product his letter described, just as he would have disclosed if his organization had invented a new drug or device expected to benefit the organization or its affiliates. At the very least, such disclosure would have helped the JAMA editors realize he was hyping something his organization helped create.

      (1) Kirch DG. The Healthcare Innovation Zone: a platform for true reform. JAMA. 2010 Mar 3;303(9):874-875. Pubmed 20197534. doi: 10.1001/jama.2010.224.

      (2) “Rep. Schwartz introduces legislation to establish AAMC-proposed health care innovation zones.” Press Release, Association of American Medical Colleges, July 10, 2009. Online at: http://www.aamc.org/newsroom/pressrel/2009/090710.htm — accessed April 4, 2010.

      (3) Lobbying Disclosure Act Database: http://soprweb.senate.gov/index.cfm?event=choosefields — Searched on “registrant name” = “association of american medical colleges” on April 4, 2010.


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    1. On 2015 Mar 13, Martine Crasnier-Mednansky commented:

      Escherichia coli cells growing on excess glucose (Fig. 3, Environment G) do not consume acetate after glucose depletion (the acetate switch occurs before glucose is fully depleted). In fact, cells utilize both glucose and acetate during entry into the stationary phase of growth (see Fig. 1A in Wolfe AJ, 2005). Failure to assimilate acetate before glucose depletion was reported for a specific mutant strain and resulted in a diauxic type of growth (Nyström T, 1993).

      Acetate utilization by acetate-adapted cells is not diminished by glucose addition (Lowry OH, 1971). Furthermore glucose utilization by acetate-adapted cells is inhibited by acetate. It is therefore questionable whether acetate-adapted cells are `adapting´ to glucose when transferred to a medium containing a large excess of acetate (Fig. 3, Environment GA). In this context, the reversible phosphotransfer reaction between phosphoacetate kinase and the phosphotransferase system (PTS), originally proposed by Fox DK, 1986 but never established in vivo, should be physiologically relevant as to regulate the rate of sugar transport by the PTS and thus the cAMP level.


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    1. On 2014 Sep 01, Matthew Katz commented:

      This Phase II trial by RTOG demonstrated the ability to safely deliver ablative radiation doses to offer excellent local tumor control. It has transformed the prognosis for patients with medically inoperable non-small cell lung cancer. Whether stereotactic radiation can be an alternative to surgery is currently under study on protocol. But this trials clearly supports a role for stereotactic radiation in the body as well as its known role for treating brain tumors.

      Improvements have been made in dose calculation and more data now support the findings of RTOG 0236. Further study is needed to fine tune best dose schedules, technique and immobilization. Whether there is any role in node positive patients remains to be determined.


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    1. On 2015 Aug 27, Zhicheng Lin commented:

      The evidence for unconscious activation of the prefrontal no-go network is unwarranted because the activation is unlikely to be unconscious in the study. This study underestimated the true level of awareness as recently revealed in a phenomenon called "priming of awareness" (Lin and Murray, 2014, 2015).

      Refs: Lin, Z., Murray, S. O. (2014). Priming of awareness or how not to measure visual awareness. Journal of Vision, 14(1), 1–17. Lin, Z., Murray, S. O. (2015). Automaticity of unconscious response inhibition: Comment on Chiu and Aron (2014). Journal of Experimental Psychology: General, 144(1), 244–254.

      Direct links to the refs: http://jov.arvojournals.org/article.aspx?articleid=2295565 http://psycnet.apa.org/journals/xge/144/1/244/


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    1. On 2013 Dec 28, Tsuyoshi Miyakawa commented:

      The finding of elevated D2High receptors in the CaMKIIalpha heterozygous knockout mice is quite interesting, regarding the possiblity that these mice may serve as an animal model of schizophrenia or bipolar disorder. We pointed out the possibility in our paper before(Yamasaki N, 2008), though it was not cited in this paper. I'd like to add that the same KO mice also show decreased cellular activity in dentate gyrus, while it is increased in CA1 in hippocampus (Hattori S, 2013), which is also consistent with the hippocampus dysfunction hypothesis of schizophrenia (Tamminga CA, 2010).


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    1. On 2016 Jun 08, Jafar Kolahi commented:

      This article has been criticized at: Kolahi J, Bang H, Park JJ, Desbiens NA. CONSORT 2010 and Controversies Regarding Assessment of Blindness in RCTs. Dent Hypotheses 2010;1:99-105. doi:10.5436/j.dehy. 2010.1.00016.

      Full text is available via: https://www.researchgate.net/profile/Jafar_Kolahi/publication/49583226_CONSORT_2010_and_Controversies_Regarding_Assessment_of_Blindness_in_RCTs/links/0f2cd8bca299367d1640cfd0.pdf


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    1. On 2014 Sep 03, Matthew Katz commented:

      This phase III trial is a classic example of how combined modality therapy (radiation combined with medical therapy) can provide effective cure for laryngeal cancer with an organ-preserving approach that can mean a major difference in quality of life. Surgery still may be needed, but for patients with a good response chemoradiation can be an effective nonsurgical treatment. More recent studies have suggested that doing the two treatments together (concurrent therapy) is superior though the toxicity may also be higher Forastiere AA, 2003


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    1. On 2014 May 09, Madhusudana Girija Sanal commented:

      It is all about numbers! It is statistics which defines what cancer is! One reason is that all definitions are a matter convenience for humans to classify, work or learn. Definitions quite often cannot be ‘black and white’ and hence statistical approaches are wise. The author note that the sixth hall mark of six hallmarks defined by Hannan and Weinberg, that is “the ability to invade and metastasis” is the only ‘real’ hallmark of cancer. However it is known that everything moves around, invade and proliferate need not be a cancer- example is endometriosis. Giant-cell tumor of the bone is considered benign but can spread to other parts including the lungs. Moreover during embryonic development different cell lineages compete and invade each other. Winners proliferate secrete autocrine factors, attracts blood vessels, force defeated cells to apoptosis or even ‘eat’ them up. This is not cancer! So what can be the hallmark or defining features of cancer? What I am proposing is a preliminary outline which may be further modified by “Wiki” efforts to make it more accurate. The following conditions needs to be satisfied to define a cancer: 1) Non physiological rate of cell division. Non physiological rate is defined as a growth rate which is a statistical outlier spatially and temporally for a given type of cell and organism. 2) A change, genetic or epigenetic with reference to the healthy genome which is a statistical outlier spatially and temporally for a given cell type and organism. Healthy reference genome and epigenome may be defined as the genome of individuals which satisfy two conditions a) falling within the statistically defined normal range of anatomical and physiological parameters for a population b) demonstrated longevity above 99.9 percentile of the population of a given organism.

      Cancer is a dynamic process-continuous evolution and selection. It is often,but not mandatory (at least theoretically) to be started by or seeded by a mutation and 'nurtured' or maintained by epigenetics. This is because epigenetic modification are faster as well as reversible. The effect of environment is mediated often (through cytokines, microRNA or even by physical factors) through epigenetic adaptations.Sooner or later more mutations and epigenetic changes accumulate during evolution and selection. This process is accelerated by chemotherapy (especially when using alkylating agents) radiation. Very specific and interesting mutations can evolve during targeted therapy (example-nilotinib).


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    1. On 2014 Feb 13, David Keller commented:

      The April 2010 Resident's Clinic discussed a 38-year-old woman with a history of gastric bypass who presented with profound anemia due to severe copper deficiency. She was noted to have an abnormally high zinc level. Her copper deficiency was attributed mainly to malabsorption due to her bowel surgery, and it was also noted that high zinc levels may induce copper deficiency. The question then arises as to why her zinc level was so high. The only clue is that the patient "had a history of frequent upper respiratory infections". Unfortunately, she was not asked whether she had used any of the over-the-counter zinc lozenge products which are sold as alternative sore throat remedies (for example "Cold-Eze"). Clinicians should not neglect to inquire about such non-prescription remedies or supplements when taking a patient's medication history, as important information may be learned.


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    1. On 2014 Sep 06, Ryan Radecki commented:

      Post-publication commentary: "The Most Dangerous Holiday!"

      Here in the United States, it is Labor Day – a Federal holiday established in 1886 by U.S. President Grover Cleveland. We, apparently, have Canada to thank for this innovation.

      But, what was actually news to me – Labor Day is actually the highest-volume holiday for pediatric trauma, outpacing all other holidays. I’d have thought 4th of July – with it’s various explosive devices – would be the most popular pediatric trauma holiday, but, between 1997 and 2006, Labor Day takes the lead, followed by Memorial Day, and 4th of July as a close third. Halloween, Easter, Thanksgiving, New Year’s and Christmas round out the list, in that order.

      http://www.emlitofnote.com/2014/09/the-most-dangerous-holiday.html


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    1. On 2017 Aug 05, Fernando Castro-Chavez commented:

      Dear Reader, Here is where I did the discovery for the first time that by using the rotating circular classic representation of the genetic code, a series of resonances were able to be found, such as that every 90 degrees we had the hydrophobic amino acids per each quadrant, and the same applies when studying the rest of the properties of the amino acids, there is resonance for the basic, and for the hydrophobic amino acids, as well as for the phosphorilatable ones. This lead me to discover the rules of variation, that equivalent amino acids, produced by equivalent codons allow for the equally functional diversity of proteins and enzymes making all the wonderful array of varieties within each group of compatible organisms, which are the ones capable to interbreed producing a fertile offspring. Sincerely, Fernando Castro-Chavez.


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    1. On 2017 Jan 20, Andy Collings commented:

      A subset of experimental results from this study were the focus of a replication attempt as part of the Reproducibility Project: Cancer Biology (https://osf.io/e81xl/wiki/home/). The experimental designs and protocols were reviewed and approved in a Registered Report (http://dx.doi.org/10.7554/eLife.06959) and the results of the experiments were published in a Replication Study (http://dx.doi.org/10.7554/eLife.17584).


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    1. On 2016 Nov 18, Morten Oksvold commented:

      An investigation committee at Wayne State University (WSU) recommends that 42 articles from Fazlul Sarkar to be retracted (report finished August 31, 2015). This article represents one of them.

      This information was published by Retraction Watch (November 17, 2016) and you can find a link to the full report here:

      http://retractionwatch.com/2016/11/17/details-of-investigative-report-into-sarkar-released-by-aclu/

      This article should therefore no longer be cited.


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    1. On 2016 Aug 24, Ben Goldacre commented:

      This trial has the wrong trial registry ID associated with it on PubMed: both in the XML on PubMed, and in the originating journal article. The ID given is NCT00018255. We believe the correct ID, which we have found by hand searching, is NCT01068210.

      This comment is being posted as part of the OpenTrials.net project<sup>[1]</sup> , an open database threading together all publicly accessible documents and data on each trial, globally. In the course of creating the database, and matching documents and data sources about trials from different locations, we have identified various anomalies in datasets such as PubMed, and in published papers. Alongside documenting the prevalence of problems, we are also attempting to correct these errors and anomalies wherever possible, by feeding back to the originators. We have corrected this data in the OpenTrials.net database; we hope that this trial’s text and metadata can also be corrected at source, in PubMed and in the accompanying paper.

      Many thanks,

      Jessica Fleminger, Ben Goldacre*

      [1] Goldacre, B., Gray, J., 2016. OpenTrials: towards a collaborative open database of all available information on all clinical trials. Trials 17. doi:10.1186/s13063-016-1290-8 PMID: 27056367

      * Dr Ben Goldacre BA MA MSc MBBS MRCPsych<br> Senior Clinical Research Fellow<br> ben.goldacre@phc.ox.ac.uk<br> www.ebmDataLab.net<br> Centre for Evidence Based Medicine<br> Department of Primary Care Health Sciences<br> University of Oxford<br> Radcliffe Observatory Quarter<br> Woodstock Road<br> Oxford OX2 6GG


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    1. On 2013 Dec 31, Tom Kindlon commented:

      I had a response published: FINE trial for CFS. Missing data

      BMJ. 2010 Jun 9;340:c2990. doi: 10.1136/bmj.c2990. FINE trial for CFS. Missing data. Kindlon T. http://www.ncbi.nlm.nih.gov/pubmed/20534661 Kindlon T, 2010

      My original e-letter from which this was drawn can be read here: http://www.bmj.com/rapid-response/2011/11/02/missing-data


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    2. On 2015 Dec 24, Tom Kindlon commented:

      Step test data were subsequently published

      "There were no between group differences in any of the step test measures at 20 or 70 weeks"(1).

      Reference:

      Wearden AJ1, Emsley R. Mediators of the effects on fatigue of pragmatic rehabilitation for chronic fatigue syndrome. J Consult Clin Psychol. 2013 Oct;81(5):831-8. doi: 10.1037/a0033561.


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    1. On 2016 Nov 20, Morten Oksvold commented:

      An investigation committee at Wayne State University (WSU) recommends that 42 articles from Fazlul Sarkar to be retracted (report finished August 31, 2015). This article represents one of them.

      This information was published by Retraction Watch (November 17, 2016) and you can find a link to the full report here:

      http://retractionwatch.com/2016/11/17/details-of-investigative-report-into-sarkar-released-by-aclu/

      This article should therefore no longer be cited.


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    1. On 2013 Oct 28, Jamie Horder commented:

      A historical note: in January 2009, shortly before this study was due to be completed, it was terminated early on the instructions of the local Research Ethics Committee. The reason for this was that rimonabant had just been withdrawn from the European market due to concerns over the high prevalence of depression in users - ironically, the very phenomenon that motivated this study.


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    1. On 2016 Sep 19, Morten Oksvold commented:

      Please note that a rather extensive correction was published 7 December 2011: "The wrong images were mistakenly presented for day 3 for the wild-type and the racX ylmE double mutant in figure S4. The original and correct images are now shown. Also, the wrong image was presented for the mixture of L-amino acids in panel B of fig. S13 and has now been removed."

      In 2013, the Losick group published results showing that D-amino acids inhibited bacterial growth and the expression of biofilm matrix genes and that the strain they originally used to study biofilm formation (B. subtilis) has a mutation in the D-tyrosyl-tRNA deacylase gene, an enzyme that prevents the misincorporation of D-amino acids into protein (Leiman et al., 2013). In a B. subtilis strain, which has a working copy of this gene, D–amino acids did not inhibit biofilm formation. The conclusion from their study was that "the susceptibility of B. subtilis to the biofilm-inhibitory effects of D-amino acids is largely, if not entirely, due to their toxic effects on protein synthesis.

      Does that mean that they no longer see D-amino acids as a specific mechanism to disassemble biofilms in B. subtilis but rather as nonspecific inhibitors of growth in some genetic backgrounds?

      Leiman et al. (2013) make no comment on the ability of D-amino acids to inhibit biofilm formation in staphylococcus aureus and Pseudomonas aeruginosa, as claimed in this article. The whole concept of biofilm dissasembly by D-amino acids therefore appears confusing.

      It was recently published an article showing that D-amino acids do not inhibit biofilm formation in Staphylococcus aureus (Sarkar S and Pires MM, 2015).


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    2. On 2016 Oct 13, Ilana Kolodkin-Gal commented:

      The supporting material for this paper was corrected, and the source data were provided to the editors of the Science journal. As for D-amino acids and biofilm formation: Non-canonical D-amino acids are small molecules interfering with cross-linking and transglycosylation of the peptidoglycan (Lam et al., 2009; Cava et al., 2011), and have been shown to trigger biofilm disassembly (Kolodkin-Gal et al., 2010), without affecting planktonic growth. This observation was later reproduced in various model organisms, such as Staphylococcus aureus (Hochbaum et al., 2011; Sanchez et al., 2013), Pseudomonas aeruginosa (Yu et al., 2012; Sanchez et al., 2014), the plant pathogen Xanthomonas citri (Li and Wang, 2014) , Escherichia coli (Xing et al., 2015) and in mixed biofilms (Si et al., 2014), as well as in other models published in numerous more recent publications. Furthermore, in our group we have generated so far two independent peer-reviewed publications clarifying the mode of action of D-aa for biofilm inhibition: http://onlinelibrary.wiley.com/doi/10.1111/1758-2229.12346/abstract http://www.jove.com/video/54612/methodologies-for-studying-b-subtilis-biofilms-as- Lastly, we established a consistent and robust experimental framework to study the effect of these small molecules biofilm inhibitors (Bucher et al., 2016).


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    1. On 2016 Aug 23, Ben Goldacre commented:

      This trial has the wrong trial registry ID associated with it on PubMed: both in the XML on PubMed, and in the originating journal article. The ID given is NCT0027813. We believe the correct ID, which we have found by hand searching, is NCT00278135.

      This comment is being posted as part of the OpenTrials.net project<sup>[1]</sup> , an open database threading together all publicly accessible documents and data on each trial, globally. In the course of creating the database, and matching documents and data sources about trials from different locations, we have identified various anomalies in datasets such as PubMed, and in published papers. Alongside documenting the prevalence of problems, we are also attempting to correct these errors and anomalies wherever possible, by feeding back to the originators. We have corrected this data in the OpenTrials.net database; we hope that this trial’s text and metadata can also be corrected at source, in PubMed and in the accompanying paper.

      Many thanks,

      Jessica Fleminger, Ben Goldacre*

      [1] Goldacre, B., Gray, J., 2016. OpenTrials: towards a collaborative open database of all available information on all clinical trials. Trials 17. doi:10.1186/s13063-016-1290-8 PMID: 27056367

      * Dr Ben Goldacre BA MA MSc MBBS MRCPsych<br> Senior Clinical Research Fellow<br> ben.goldacre@phc.ox.ac.uk<br> www.ebmDataLab.net<br> Centre for Evidence Based Medicine<br> Department of Primary Care Health Sciences<br> University of Oxford<br> Radcliffe Observatory Quarter<br> Woodstock Road<br> Oxford OX2 6GG


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    1. On 2016 Aug 23, Ben Goldacre commented:

      This trial has the wrong trial registry ID associated with it on PubMed: both in the XML on PubMed, and in the originating journal article. The ID given is NCT00122184. We believe the correct ID, which we have found by hand searching, is NCT00132184.

      This comment is being posted as part of the OpenTrials.net project<sup>[1]</sup> , an open database threading together all publicly accessible documents and data on each trial, globally. In the course of creating the database, and matching documents and data sources about trials from different locations, we have identified various anomalies in datasets such as PubMed, and in published papers. Alongside documenting the prevalence of problems, we are also attempting to correct these errors and anomalies wherever possible, by feeding back to the originators. We have corrected this data in the OpenTrials.net database; we hope that this trial’s text and metadata can also be corrected at source, in PubMed and in the accompanying paper.

      Many thanks,

      Jessica Fleminger, Ben Goldacre*

      [1] Goldacre, B., Gray, J., 2016. OpenTrials: towards a collaborative open database of all available information on all clinical trials. Trials 17. doi:10.1186/s13063-016-1290-8

      * Dr Ben Goldacre BA MA MSc MBBS MRCPsych<br> Senior Clinical Research Fellow<br> ben.goldacre@phc.ox.ac.uk<br> www.ebmDataLab.net<br> Centre for Evidence Based Medicine<br> Department of Primary Care Health Sciences<br> University of Oxford<br> Radcliffe Observatory Quarter<br> Woodstock Road<br> Oxford OX2 6GG


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    1. On 2016 Aug 23, Ben Goldacre commented:

      This trial has the wrong trial registry ID associated with it on PubMed: both in the XML on PubMed, and in the originating journal article. The ID given is NCT00527782. We believe the correct ID, which we have found by hand searching, is NCT00527787.

      This comment is being posted as part of the OpenTrials.net project<sup>[1]</sup> , an open database threading together all publicly accessible documents and data on each trial, globally. In the course of creating the database, and matching documents and data sources about trials from different locations, we have identified various anomalies in datasets such as PubMed, and in published papers. Alongside documenting the prevalence of problems, we are also attempting to correct these errors and anomalies wherever possible, by feeding back to the originators. We have corrected this data in the OpenTrials.net database; we hope that this trial’s text and metadata can also be corrected at source, in PubMed and in the accompanying paper.

      Many thanks,

      Jessica Fleminger, Ben Goldacre*

      [1] Goldacre, B., Gray, J., 2016. OpenTrials: towards a collaborative open database of all available information on all clinical trials. Trials 17. doi:10.1186/s13063-016-1290-8 PMID: 27056367

      * Dr Ben Goldacre BA MA MSc MBBS MRCPsych<br> Senior Clinical Research Fellow<br> ben.goldacre@phc.ox.ac.uk<br> www.ebmDataLab.net<br> Centre for Evidence Based Medicine<br> Department of Primary Care Health Sciences<br> University of Oxford<br> Radcliffe Observatory Quarter<br> Woodstock Road<br> Oxford OX2 6GG


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    1. On 2013 Oct 28, John Cannell commented:

      The control group in this study was flawed. The authors used children undergoing outpatient tonsillectomies as controls. Such children are likely to have low 25(OH)D levels.

      Seventy-eight percent of Auckland children undergoing tonsillectomy had vitamin D insufficiency.

      Reid D, Morton R, Salkeld L, Bartley J.Vitamin D and tonsil disease--preliminary observations. Int J Pediatr Otorhinolaryngol. 2011 Feb;75(2):261-4.

      Also, 25(OH)D levels of children with ear infections were about one-half that of community controls.

      Cayir A, Turan MI, Ozkan O, Cayir Y, Kaya A, Davutoglu S, Ozkan B.Serum vitamin D levels in children with recurrent otitis media. Eur Arch Otorhinolaryngol. 2013 Mar 30.

      In addition, in a prospective study, lower serum 25(OH)D levels were associated with increased risk of laboratory-confirmed respiratory tract infections RTI in children.

      Science M, Maguire JL, Russell ML, Smieja M, Walter SD, Loeb M. Low serum 25-hydroxyvitamin D level and risk of upper respiratory tract infection in children and adolescents. Clin Infect Dis. 2013 Aug;57(3):392-7.

      As Molloy et al did not use community controls, they did not find lower 25(OH)D levels in children with ASD compared to controls but 3 studies of ASD and 25(OH)D using community controls have found significant differences.

      Gong ZL, Luo CM, Wang L, Shen L, Wei F, Tong RJ, Liu Y.Serum 25-hydroxyvitamin D levels in Chinese children with autism spectrum disorders. Neuroreport. 2013 Oct 1.

      Meguid NA, Hashish AF, Anwar M, Sidhom G.Reduced serum levels of 25-hydroxy and 1,25-dihydroxy vitamin D in Egyptian children with autism. J Altern Complement Med. 2010 Jun;16(6):641-5.

      Mostafa GA, Al-Ayadhi LY.Reduced serum concentrations of 25-hydroxy vitamin D in children with autism: relation to autoimmunity. J Neuroinflammation. 2012 Aug 17;9:201.


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    1. On 2016 Aug 30, Ben Goldacre commented:

      This trial has the wrong trial registry ID associated with it on PubMed. The ID given is NCT00350855 - the correct ID is NCT00350389. This has been corrected in a subsequent correction published in the originating journal, but not in the PubMed metadata.

      This comment is being posted as part of the OpenTrials.net project<sup>[1]</sup> , an open database threading together all publicly accessible documents and data on each trial, globally. In the course of creating the database, and matching documents and data sources about trials from different locations, we have identified various anomalies in datasets such as PubMed, and in published papers. Alongside documenting the prevalence of problems, we are also attempting to correct these errors and anomalies wherever possible, by feeding back to the originators. We have corrected this data in the OpenTrials.net database and this ID has been corrected within the journal itself; we hope that this trial’s text and metadata can also be corrected in PubMed.

      Many thanks,

      Jessica Fleminger, Ben Goldacre*

      [1] Goldacre, B., Gray, J., 2016. OpenTrials: towards a collaborative open database of all available information on all clinical trials. Trials 17. doi:10.1186/s13063-016-1290-8 PMID: 27056367

      * Dr Ben Goldacre BA MA MSc MBBS MRCPsych<br> Senior Clinical Research Fellow<br> ben.goldacre@phc.ox.ac.uk<br> www.ebmDataLab.net<br> Centre for Evidence Based Medicine<br> Department of Primary Care Health Sciences<br> University of Oxford<br> Radcliffe Observatory Quarter<br> Woodstock Road<br> Oxford OX2 6GG


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    1. On 2018 Jan 03, Denise N Slenter commented:

      The information captured in Figure 1 and 2 of this article, is available as a machine readable pathway at the WikiPathways database (https://www.wikipathways.org/index.php/Pathway:WP3933). Figure 3 is available at WikiPathways as well (https://www.wikipathways.org/index.php/Pathway:WP4195). These pathways can be used for data analysis in e.g. Pathvisio (https://doi.org/10.1371/journal.pcbi.1004085) and Cytoscape (https://doi.org/10.1101/gr.1239303).


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    1. On 2015 Nov 30, S A Ostroumov commented:

      In the paper, it was discovered that the aquatic higher plant (macrophyte) hornwort (other English names: rigid hornwort, coontail, coon's tail; the Latin name: Ceratophyllum demersum) immobilized gold (Au) nanoparticles after their addition to water. This is the first time it was shown that the nanoparticles of gold (Au) in substantial amount bind to the living biomass of the aquatic macrophyte (namely, Ceratophyllum demersum). The concentrations of Au were measured in the samples of the phytomass using neutron activation analysis (NAA). As a result of the binding and/or immobilization of the nanoparticles, the amount of Au in the samples of the phytomass increased manifold (by a factor of 430) above the background level of gold in the plant tissues. The increase was by two orders of magnitude. The new data added some new information to the modern vision of the multifunctional role of the biota in the migration of elements in aquatic ecosystems, and water self-purification. Also, the result added new information to the studies of interactions of Au with organisms that may contribute to new biotechnologies (namely, phytotechnologies to remove heavy metals from water). DOI: 10.1134/S0012496610020158. https://www.researchgate.net/publication/44634488_The_aquatic_macrophyte_Ceratophyllum_demersum_immobilizes_Au_nanoparticles_after_their_addition_to_water;

      Some additional key words: nanomaterials, sorption, biosorption, immobilization, environmental chemistry, biogeochemistry, water quality,


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    1. On 2014 Jan 31, George W Hinkal commented:

      The National Cancer Institute has been investing in the development of an online webportal of curated cancer nanotechnology data called caNanoLab. The numerical data and additional nanomaterial characterizations related to this publication have been added to the database and can be found at:

      https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=41418753&page=0&tab=ALL

      https://cananolab.nci.nih.gov/caNanoLab/characterization.do?dispatch=summaryView&sampleId=41418752&page=0&tab=ALL

      The left navigation links on these pages provide information about each sample (under Navigation Tree).

      For general information on how to use caNanoLab, please visit https://cananolab.nci.nih.gov/caNanoLab/home.jsp


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    1. On 2014 Sep 06, David Keller commented:

      Are melanoma patients with pre-existing autoimmune disease at increased risk of severe immune reaction to ipilimumab?

      Patients with pre-existing autoimmune disease were excluded from this clinical trial. Even so, Grade 3 or 4 immune-related adverse events occurred in 10 to 15% of patients treated with ipilimumab. Is the rate of immune-related adverse events (IRAE) even higher in patients with pre-existing autoimmune disease who are treated with ipilimumab for melanoma? Clinical trials of immune checkpoint inhibitors all exclude such patients, but post-approval data on adverse events could supply an estimate of their relative risk ratio (RRR) with the following equation:

      RRR = ( IRAEp / IRAEt ) / (prevalence of AIDM)

      where RRR is the relative risk ratio for a severe adverse event in a melanoma patient with preexisting autoimmune disease who is treated with ipilimumab, and IRAEp is the number of immune related adverse events in patients with prior autoimmune disease, IRAEt is the total number of reported immune related adverse events, and the denominator is the prevalence of autoimmune diseases in melanoma patients.

      If patients with preexisting autoimmune disease are found to have a significantly elevated relative risk ratio for severe autoimmune reactions to ipilimumab compared with other melanoma patients, they should have access to that information in order to help them make difficult treatment decisions. Each melanoma patient will have their own cut-off of acceptable values for RRR.

      Recently, an anti-PD1 immune checkpoint inhibitor, pembrolizumab, was approved by the FDA for advanced melanoma patients who have failed on ipilimumab. It has been suggested that the anti-PD1 agents have a milder autoimmune adverse event profile than anti-CTLA-4 agents like ipilimumab (1,2). If this is true, it may be a reason for patients with active autoimmune diseases to be treated with the former, skipping the latter. If the RRR for a patient with preexisting autoimmune disease is found to be 5, 10 or even 20 times higher than for average patients, then this data could be used to justify treating them with pembrolizumab first-line and off-label.

      This question cannot be answered using data from the controlled clinical trials, because patients with active autoimmune diseases were excluded from these studies.

      When the FDA approved Yervoy (ipilimumab) in 2011, they mandated a risk mitigation program, including a database of all reported post-approval adverse reactions to Yervoy. In order to obtain full access to the information in that database, one must file a separate request with the FDA, under the Freedom of Information Act (FOIA), for each reported adverse reaction. The number of reports of serious adverse events associated with Yervoy filed from March 2011 through September 2014 totals nearly 4000. Since the cost of filing an FOIA request for each report is over $50, the cost to perform a detailed analysis of the entire database of adverse events is over $20,000. This fee is prohibitive, and defeats the purpose of the risk mitigation program. FDA should provide free access to this data, in order to stimulate and facilitate research into the effects of Yervoy on patient populations which were excluded from the controlled clinical trials.

      References

      1: Weber J. Review: anti-CTLA-4 antibody ipilimumab: case studies of clinical response and immune-related adverse events. Oncologist. 2007 Jul;12(7):864-72. Review. PubMed PMID: 17673617.

      2: Fecher LA, Agarwala SS, Hodi FS, Weber JS. Ipilimumab and its toxicities: a multidisciplinary approach. Oncologist. 2013 Jun;18(6):733-43. doi: 10.1634/theoncologist.2012-0483. Epub 2013 Jun 17. Review. PubMed PMID: 23774827; PubMed Central PMCID: PMC4063401.


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    1. On 2015 May 22, thomas samaras commented:

      Many conflicting studies exist that show shorter people have low coronary heart disease (CHD). Two review papers summarizing findings showing shorter people have less CHD than taller populations are cited below. For example, populations of short people (less than 5'5")that have virtually no CHD include the Solomon Islands, Papua New Guinea, Kalahari Bushmen, Congo Pygmies, and Kitavans. However, with Westernization, some are growing taller and heavier and seeing increases in CHD. Over the last few decades, the Japanese have held the top or third from top ranking for having the lowest CHD in the world.

      Women are shorter than men and have lower life-long mortality from CHD. The argument that smaller blood vessels contribute to CHD doesn't seem to apply to women.

      The World Cancer Research Fund (2007) has attributed our increased height, weight and chronic disease (including CHD)to our Western diet. They reported that today's chronic diseases are a relatively new occurrence. Trowell also reported that pre-Western people are generally free of Western chronic diseases, including CHD. Burkitt evaluated the medical records from almost 1000 hospitals in the non-developed world and found Western diseases (including CHD) were rare.

      The Laron dwarfs in Ecuador have been studied for over 20 years and were found to have no deaths from cancer and diabetes. They also have normal atherosclerosis in spite of being overweight and obese. About 70% of their deaths are from non-age related causes: alcoholism, infections, accidents and neurological disorders.

      It is hard to believe that shorter height per se is related to CHD since many studies show that shorter people live longer. These studies include populations in San Diego, Hawaii, Ohio, Spain, Sardinia, and Okinawa. See longevity studies cited below.

      Sources

      Samaras TT, Elrick H, Storms LH. Is short height really a risk factor for coronary heart disease and stroke mortality? A review. Medical Science Monitor 2004;10:RA63-76.

      Samaras TT. Shorter height is related to lower cardiovascular disease risk--a Narrative Review. Indian Heart Journal. 2013; 65: 66-71.

      He Q, Morris BJ, Grove JS, et al. Shorter men live longer: Association of height with longevity and FOXO3 genotype in American men of Japanese ancestry. PLOS ONE; 2014:9: 1-8.

      Samaras TT. Evidence from eight different types of studies showing that smaller body size is related to greater longevity. Journal of Scientific Research & Reports. 2014;3(16):2150-2160

      Salaris L, Poulain, Samaras. Height and survival at older ages among males born in an in-land village in Sardinia. Biodemography and Social Biology. 2012: 58(1): 1-13.

      Bartke A. Healthy aging: Is smaller better?--A mini-review. Gerontology.2012; 58:337-43.


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    1. On 2017 Aug 04, Luis Mauricio T. R. Lima commented:

      This is an interesting article showing human amylin and zinc interaction, and the role of His18 in zinc interaction.

      We have recently reported that murine amylin can also interact with zinc, and this peptide has no His18, and interaction is mediated by several other contacts, and can result in modulation of the amyloid aggregation process. https://www.ncbi.nlm.nih.gov/pubmed/27693831 http://dx.doi.org/10.1016/j.bpc.2016.09.008

      Collectively, these data suggest an universal amyloid behavior of amylin analogues and interaction with zinc, regardless of the presence of proline or His18.


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    1. On 2015 Jul 21, Richard Jenner commented:

      Figure S3C of Davidovich C, 2015 shows that the apparent repressive effect of the Xist-RepA stem loop used as a control in Figure 6D of our paper Kanhere A, 2010 is actually due to a mutation of the construct promoter, which we had overlooked. As shown by Davidovich et al, correction of this mutation abolished the apparent repressive activity. Mutations were also found in the short RNA stem loop construct, however, although reduced, the repressive activity of this stem loop remained after these were corrected (Figure S3D of Davidovich C, 2015).


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    1. On 2014 Jan 08, Tom Kindlon commented:

      There is evidence that CFS patients don't engage in “boom and bust” activity patterns

      As Maes and Twisk highlight[1], one part of the Harvey and Wessely model is the contention that CFS patients engage in “boom and bust” activity patterns. This claim has been repeated so often by various individuals that it has been seen as fact by some. But is there actual evidence for it?

      What many people may not be aware of is we do have data on the issue. A Dutch study tested a relatively large cohort of CFS patients (n=277) along with 47 healthy controls [2]. The research used actometers to provide an objective measure of activity over 12 days. It found: "Compared to healthy controls, no indication was found that the CFS patients as a group were characterised by a high number of large day-to-day fluctuations in activity."

      References:

      [1] Maes M, Twisk FN. Chronic fatigue syndrome: Harvey and Wessely's (bio)psychosocial model versus a bio(psychosocial) model based on inflammatory and oxidative and nitrosative stress pathways. BMC Med. 2010 Jun 15;8:35.

      [2] van der Werf SP, Prins JB, Vercoulen JH, van der Meer JW, Bleijenberg G. Identifying physical activity patterns in chronic fatigue syndrome using actigraphic assessment. J Psychosom Res. 2000 Nov;49(5):373-9.


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    1. On 2016 Aug 23, Ben Goldacre commented:

      This trial has the wrong trial registry ID associated with it on PubMed: both in the XML on PubMed, and in the body of the text of the article. The ID given is NCT00028572. We believe the correct ID, which we have found by hand searching, is NCT00028574.

      This comment is being posted as part of the OpenTrials.net project<sup>[1]</sup> , an open database threading together all publicly accessible documents and data on each trial, globally. In the course of creating the database, and matching documents and data sources about trials from different locations, we have identified various anomalies in datasets such as PubMed, and in published papers. Alongside documenting the prevalence of problems, we are also attempting to correct these errors and anomalies wherever possible, by feeding back to the originators. We have corrected this data in the OpenTrials.net database; we hope that this trial’s text and metadata can also be corrected at source, in PubMed and in the accompanying paper.

      Many thanks,

      Jessica Fleminger, Ben Goldacre*

      [1] Goldacre, B., Gray, J., 2016. OpenTrials: towards a collaborative open database of all available information on all clinical trials. Trials 17. doi:10.1186/s13063-016-1290-8

      * Dr Ben Goldacre BA MA MSc MBBS MRCPsych<br> Senior Clinical Research Fellow<br> ben.goldacre@phc.ox.ac.uk<br> www.ebmDataLab.net<br> Centre for Evidence Based Medicine<br> Department of Primary Care Health Sciences<br> University of Oxford<br> Radcliffe Observatory Quarter<br> Woodstock Road<br> Oxford OX2 6GG


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    1. On 2017 Dec 06, University of Kansas School of Nursing Journal Club commented:

      Team Members: Samantha Gibbs, Alyssa Cruz, Annastasia Elliot, Sam Fankhauser, Kelli Fast & Dilnoza Hamraeva [Class of 2018]

      The article was selected because it demonstrates how nurse compassion satisfaction, job satisfaction, stress, burnout, and compassion fatigue are related to nurse caring. This relates to our class discussion about factors that are essential to creating a motivational work environment, specifically intrinsic motivators. As future leader, it is important to recognize what motivates others in order to help them grow as a professional nurse. This article explores the relationship between intrinsic motivation and nurse caring which has not been explored in our course.

      Intrinsic motivation is an essential aspect to caring for patients. If nurses are to fully advocate for and empower patients, they must be intrinsically motivated and have support from nurse leaders on their unit. This article was selected because the research findings confirm that motivational variables in the work environment are positively correlated with nurse caring and compassion. This increased caring results in overall improved patient care and increased patient satisfaction. The nursing leadership in a work environment is essential to cultivating motivation among staff nurses and must not be overlooked. While extrinsic motivation can be a good starting point, it is the goal that all nurses will eventually operate under conditions of intrinsic motivation, meaning that the nurses are coming to work and caring for patient because they find joy in it. The findings of this study illustrate that fostering a nurse’s intrinsic motivation can result in increased nurse caring behaviors, which will therefore increase patient satisfaction (Burston & Stichler, 2010). Burtson and Stichler state that it is the job of nurse managers to, “reawaken the source of satisfaction that nurses derive from caring, while improving their sense of social belonging” (2010, p. 1829).

      As student nurses on the brink of graduation, it is imperative to our professional identity that we understand the systems set in place that motivate workers before accepting a position as an RN. This will allow us as new graduate nurses to feel motivated and empowered in the microsystem and will lead to optimal patient care and increased patient and job satisfaction. Our job satisfaction and intrinsic motivation impacts us personally as well, as we aspire to enjoy work and care for patients in a holistic manner. Even if one is not in a leadership position, future nurses can contribute to the motivational environment by acknowledging coworkers’ achievements and challenging peers to promote growth and life-long learning. If staff nurses and nurse managers promote motivational work environments, the future of nursing practice will naturally begin to foster motivational techniques that will increase both nursing and patient satisfaction as results of improved patient care.

      Burston, P. & Stichler, J. (2010). Nursing work environment and nurse caring: Relationship among motivational factors. Journal of Advanced Nursing, 66(8), 1819-1831. doi: 10.1111/j.1365-2648.2010.05336.x


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    1. On 2014 Feb 28, William Gunn commented:

      This study has been chosen for replication by the Cancer Biology Reproducibility Project.

      The Cancer Biology Reproducibility Project is a collaboration between the Center for Open Science, Science Exchange, and Mendeley to replicate key experiments from 50 impactful cancer biology studies published between 2010-2012.

      To track the progress of this replication, please visit: https://osf.io/yyqas/

      To learn more about Cancer Biology Reproducibility Project, including the full list of 50 studies, how the studies were chosen, and details about the people who are managing the project, please visit: https://osf.io/e81xl/wiki/home/


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    1. On 2016 Aug 23, Ben Goldacre commented:

      This trial has the wrong trial registry ID associated with it on PubMed: both in the XML on PubMed, and in the originating journal article. The ID given is NCT00801358. We believe the correct ID, which we have found by hand searching, is NCT01334658.

      This comment is being posted as part of the OpenTrials.net project<sup>[1]</sup> , an open database threading together all publicly accessible documents and data on each trial, globally. In the course of creating the database, and matching documents and data sources about trials from different locations, we have identified various anomalies in datasets such as PubMed, and in published papers. Alongside documenting the prevalence of problems, we are also attempting to correct these errors and anomalies wherever possible, by feeding back to the originators. We have corrected this data in the OpenTrials.net database; we hope that this trial’s text and metadata can also be corrected at source, in PubMed and in the accompanying paper.

      Many thanks,

      Jessica Fleminger, Ben Goldacre*

      [1] Goldacre, B., Gray, J., 2016. OpenTrials: towards a collaborative open database of all available information on all clinical trials. Trials 17. doi:10.1186/s13063-016-1290-8 PMID: 27056367

      * Dr Ben Goldacre BA MA MSc MBBS MRCPsych<br> Senior Clinical Research Fellow<br> ben.goldacre@phc.ox.ac.uk<br> www.ebmDataLab.net<br> Centre for Evidence Based Medicine<br> Department of Primary Care Health Sciences<br> University of Oxford<br> Radcliffe Observatory Quarter<br> Woodstock Road<br> Oxford OX2 6GG


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    1. On 2014 Jan 31, David Simpson commented:

      A minor question, but I noticed that a different composition was given for the 4-plex iTRAQ 115 label here in Figure 3 than was given in the classic iTRAQ paper: Ross et al., Mol. Cell. Proteomics 2004, 3, 1154–1169. Has the 4-plex iTRAQ 115 label composition been changed by the manufacturer since the first report was published?

      EDIT: To be clear, I'm not doubting the composition given here (it's supported elsewhere: Phanstiel et al., J. Am. Soc. Mass Spectrom. 2008, 19, 1255–1262). I'm just curious about the change from the earliest report.


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    1. On 2014 Sep 22, Thomas Perls, MD, MPH commented:

      The corrected version of this work is at: http://www.ncbi.nlm.nih.gov/pubmed/22279548

      PLoS One. 2012;7(1):e29848. doi: 10.1371/journal.pone.0029848. Epub 2012 Jan 18. Genetic signatures of exceptional longevity in humans. Sebastiani P1, Solovieff N, Dewan AT, Walsh KM, Puca A, Hartley SW, Melista E, Andersen S, Dworkis DA, Wilk JB, Myers RH, Steinberg MH, Montano M, Baldwin CT, Hoh J, Perls TT.


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    1. On 2013 Dec 20, Raphael Stricker commented:

      Fatal Clostridium Difficile Colitis Following Treatment for Lyme Disease: The Wrong Message.

      Raphael B. Stricker, MD* and Lorraine Johnson, JD, MBA*

      *International Lyme and Associated Diseases Society, P.O. Box 341461, Bethesda, MD 20827-1461. www.ILADS.org

      Holzbauer and colleagues (1) describe a case of fatal Clostridium difficile colitis in a patient treated with ten weeks of oral antibiotics for chronic Lyme disease. Rather than focusing on patient-specific risk factors and prevention of antibiotic-related complications, the authors preach about the dangers of treating Lyme disease outside the controversial guidelines of the Infectious Diseases Society of America (IDSA), which were the subject of an antitrust investigation by the Connecticut Attorney General (2,3). In doing so, the authors exaggerate the risks of treating Lyme disease and ignore the risks of failing to treat an ongoing spirochetal infection that may cause disability equivalent to congestive heart failure, and even death (4,5). Consequently the emphasis of the case report is misguided and ultimately detrimental to patient care.

      In the single case described here, no information is given about cellular or humoral immune dysfunction that may have contributed to the rapid demise of the 52-year-old patient. This rapid demise is unusual in patients less than 80 years old with C. difficile colitis (6) and suggests the presence of a hypervirulent C. difficile ribotype that might explain the clinical course. Furthermore, the authors fail to mention whether the patient received probiotic therapy during the extended oral antibiotic treatment. Probiotic therapy appears to be effective in avoiding antibiotic-induced complications, and evidence suggests that certain probiotics may neutralize C. difficile toxin (7,8). The lack of probiotic therapy may have been a significant factor in this patient’s demise.

      As for the appropriateness of antibiotic therapy in a patient with clinical and laboratory evidence of chronic Lyme disease, two points should be considered. First, two approaches to treatment of this tickborne illness have been described in the medical literature. The approach promulgated by IDSA proscribes extended antibiotic therapy for persistent symptoms related to infection with Borrelia burgdorferi, the spirochetal agent of Lyme disease (2). In contrast, the competing approach of the International Lyme and Associated Diseases Society (ILADS) considers this therapy to be appropriate based on evidence of persistent spirochetal infection (4,9,10). Second, the patient described in the report received a course of oral antibiotics that is shorter than the antibiotic courses endorsed or accepted by IDSA for chronic conditions such as tuberculosis, leprosy, complicated actinomycosis, Whipple’s disease, Q fever endocarditis, alveolar echinococcosis, osteomyelitis and asplenia prophylaxis; the risks of prolonged antibiotic therapy are considered acceptable for these conditions (11-18). While several clinical studies have demonstrated the safety of extended oral and intravenous antibiotic therapy for patients diagnosed with Lyme disease (19-22), caution should always be exercised in administering extended antibiotic therapy to any patient with a chronic infectious disease.

      References

      1. Holzbauer SM, Kemperman MM, Lynfield R. Death due to community-associated Clostridium difficile in a woman receiving prolonged antibiotic therapy for suspected Lyme disease. Clin Infect Dis 2010;51:369-70.

      2. Johnson L, Stricker RB. The Infectious Diseases Society of America Lyme guidelines: a cautionary tale about development of clinical practice guidelines. Philos Ethics Humanit Med 2010;5:9.

      3. Johnson L, Stricker RB. Final report of the Lyme Disease Review Panel of the Infectious Diseases Society of America: A Pyrrhic victory? Clin Infect Dis 2010;51:1108-9.

      4. Cameron DJ. Proof that chronic Lyme disease exists. Interdiscip Perspect Infect Dis 2010;2010:876450.

      5. Centers for Disease Control and Prevention (CDC). Three sudden cardiac deaths associated with Lyme carditis - United States, November 2012-July 2013. MMWR Morb Mortal Wkly Rep. 2013;62:993-6.

      6. Kotila SM, Virolainen A, Snellman M, Ibrahem S, Jalava J, Lyytikäinen O. Incidence, case fatality and genotypes causing Clostridium difficile infections, Finland, 2008. Clin Microbiol Infect 2011;17:888-93.

      7. McFarland LV. Meta-analysis of probiotics for the prevention of antibiotic associated diarrhea and the treatment of Clostridium difficile disease. Am J Gastroenterol 2006;101:812-22.

      8. Castagliuolo I, Riegler MF, Valenick L, LaMont JT, Pothoulakis C. Saccharomyces boulardii protease inhibits the effects of Clostridium difficile toxins A and B in human colonic mucosa. Infect Immun 1999;67:302-7.

      9. Stricker RB. Counterpoint: Long-term antibiotic therapy improves persistent symptoms associated with Lyme disease. Clin Infect Dis 2007;45:149-57.

      10. Stricker RB, Johnson L. Lyme disease: The next decade. Infect Drug Resist 2011;4:1–9.

      11. Small PM, Fujiwara PI. Management of tuberculosis in the United States. N Engl J Med 2001;345:189-200.

      12. Cox H, Kebede Y, Allamuratova S, Ismailov G, Davletmuratova Z, Byrnes G, Stone C, Niemann S, Rüsch-Gerdes S, Blok L, Doshetov D. Tuberculosis recurrence and mortality after successful treatment: impact of drug resistance. PLoS Med 2006;3:e384.

      13. Garner JP, Macdonald M, Kumar PK. Abdominal actinomycosis. Int J Surg 2007;5:441-8.

      14. Freeman HJ. Tropheryma whipplei infection. World J Gastroenterol 2009;15:2078-80.

      15. Liu YH, Wang XG, Gao JS, Qingyao Y, Horton J. Continuous albendazole therapy in alveolar echinococcosis: long-term follow-up observation of 20 cases. Trans R Soc Trop Med Hyg 2009;103:768-78.

      16. Lazzarini L, Lipsky BA, Mader JT. Antibiotic treatment of osteomyelitis: what have we learned from 30 years of clinical trials? Int J Infect Dis 2005;9:127-38.

      17. Price VE, Blanchette VS, Ford-Jones EL.The prevention and management of infections in children with asplenia or hyposplenia. Infect Dis Clin North Am 2007;21:697-710, viii-ix.

      18. Beytout J, Tournilhac O, Laurichesse H. Antibiotic prophylaxis in splenectomized adults. Presse Med 2003;32(28 Suppl):S17-9.

      19. Donta ST. Tetracycline therapy for chronic Lyme disease. Clin Infect Dis 1997;25 Suppl 1:S52-6.

      20. Donta ST. Macrolide therapy of chronic Lyme disease. Med Sci Monit 2003;9:PI136-42.

      21. Stricker RB, Green CL, Savely VR, Chamallas SN, Johnson L. Safety of intravenous antibiotic therapy in patients referred for treatment of neurologic Lyme disease. Minerva Med 2010; 101:1–7.

      22. Stricker RB, Delong AK, Green CL, Savely VR, Chamallas SN, Johnson L. Benefit of intravenous antibiotic therapy in patients referred for treatment of neurologic Lyme disease. Int J Gen Med 2011;4:639-46.

      Disclosure: RBS is a member of the International Lyme and Associated Diseases Society (ILADS) and a director of LymeDisease.org. He has no financial or other conflicts to declare.


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    1. On 2017 Jan 18, CHRISTOPH LANGE commented:

      The VEGAS/VEGAS2 software can provide p-values for the top-percentage statistic that are anti-conservative, as the computation of the null-distribution is incorrect. In our technical report, we discuss the issue and provide code that, if included in VEGAS/VEGAS2, will provide correct p-values.

      http://biorxiv.org/content/early/2017/01/17/101014


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    1. On 2014 Mar 18, Gwinyai Masukume commented:

      In Panel 1: Differential diagnoses in severe pre-eclampsia by organ system, malaria is not mentioned.

      In some settings, malaria is an important differential diagnosis of severe pre-eclampsia as it can have a significant overlap of clinical and laboratory features with severe pre-eclampsia, for example, headache, nausea, vomiting, intra-uterine growth restriction, thrombocytopenia and raised serum creatinine (1).

      Reference: (1) McGready R, Sot M, Ashley EA, Nosten F, Rijken M, Dundorp A. The diagnosis and treatment of malaria in pregnancy. guideline number 54(B). London: Royal College of Obstetricians and Gynaecologists, 2010.


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    1. On 2016 Aug 23, Ben Goldacre commented:

      This trial has the wrong trial registry ID associated with it on PubMed: both in the XML on PubMed, and in the originating journal article. The ID given is NCT00116932. We believe the correct ID, which we have found by hand searching, is NCT00116922.

      This comment is being posted as part of the OpenTrials.net project<sup>[1]</sup> , an open database threading together all publicly accessible documents and data on each trial, globally. In the course of creating the database, and matching documents and data sources about trials from different locations, we have identified various anomalies in datasets such as PubMed, and in published papers. Alongside documenting the prevalence of problems, we are also attempting to correct these errors and anomalies wherever possible, by feeding back to the originators. We have corrected this data in the OpenTrials.net database; we hope that this trial’s text and metadata can also be corrected at source, in PubMed and in the accompanying paper.

      Many thanks,

      Jessica Fleminger, Ben Goldacre*

      [1] Goldacre, B., Gray, J., 2016. OpenTrials: towards a collaborative open database of all available information on all clinical trials. Trials 17. doi:10.1186/s13063-016-1290-8

      * Dr Ben Goldacre BA MA MSc MBBS MRCPsych<br> Senior Clinical Research Fellow<br> ben.goldacre@phc.ox.ac.uk<br> www.ebmDataLab.net<br> Centre for Evidence Based Medicine<br> Department of Primary Care Health Sciences<br> University of Oxford<br> Radcliffe Observatory Quarter<br> Woodstock Road<br> Oxford OX2 6GG


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    1. On 2014 Aug 18, Raha Pazoki commented:

      Meta-analysis for rs2824292

      For those interested, Meta-analysis of the discovery and replication set for the effect of rs2824292 on risk of ventricular fibrillation in this paper can be easily done using meta package in R. The result of the Meta-analysis shows a pooled odds ratio (O.R.) of 1.68 for rs2824292 in the fixed effect model (95% confidence interval [C.I.] = 1.43, 1.97; P value = 2.2×10<sup>-10</sup> ). The random effect model shows similar values (O.R. = 1.67; 95% C.I. = 1.42, 1.98 ; P value = 1.2×10<sup>-9</sup> ).


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    1. On 2016 Jan 08, Tom Kindlon commented:

      This study uses the (so-called) empiric CFS criteria (Reeves et al., 2005)

      Although they don't make it very clear, this study used the Reeves et al. (2005) criteria(1) for defining Chronic Fatigue Syndrome (CFS) (sometimes described by the CDC as an operationalization of the Fukuda et al. (1994) criteria (2)). This can be seen by examining the Reeves et al. (2007) paper on the Georgia cohort (2).

      These (Reeves) criteria greatly increased the prevalence of CFS. The "empirical" definition gives a prevalence rate of 2.54% of the adult population(3) compared to 0.235% (95% confidence interval, 0.142%-0.327%) and 0.422% (95% confidence interval, 0.29%-0.56%) when the Fukuda definition (3) was used in previous population studies in the US(4,5).

      The definition lacks specificity. For example, one research study(6) found that 38% of those with a diagnosis of a Major Depressive Disorder were misclassified as having CFS using the empirical/Reeves definition. A letter of mine discussed my concerns in more detail(7).

      Due to the problems with the criteria, these criteria have not been used by researchers outside those contracted to analyse CDC data (apart from Leonard Jason's research team who studied it and showed problems with it (6)).

      References:

      1 Reeves WC, Wagner D, Nisenbaum R, Jones JF, Gurbaxani B, Solomon L, Papanicolaou DA, Unger ER, Vernon SD, Heim C. Chronic fatigue syndrome – a clinically empirical approach to its definition and study. BMC Med. 2005;3:19.

      2 Reeves WC, Jones JF, Maloney E, Heim C, Hoaglin DC, Boneva RS, Morrissey M, Devlin R. Prevalence of chronic fatigue syndrome in metropolitan, urban, and rural Georgia. Popul Health Metr. 2007 Jun 8;5:5.

      3 Fukuda K, Straus SE, Hickie I, Sharpe MC, Dobbins JG, Komaroff A. The chronic fatigue syndrome; a comprehensive approach to its definition and study. Ann Int Med 1994, 121:953-959.

      4 Reyes M, Nisenbaum R, Hoaglin DC, Unger ER, Emmons C, Randall B, Stewart JA, Abbey S, Jones JF, Gantz N, Minden S, Reeves WC: Prevalence and incidence of chronic fatigue syndrome in Wichita, Kansas. Arch Int Med 2003, 163:1530-1536.

      5 Jason LA, Richman JA, Rademaker AW, Jordan KM, Plioplys AV, Taylor RR, McCready W, Huang CF, Plioplys S. A community-based study of chronic fatigue syndrome. Arch Intern Med. 1999 Oct 11;159(18):2129-37.

      6 Jason, LA, Najar N, Porter N, Reh C. Evaluating the Centers for Disease Control's empirical chronic fatigue syndrome case definition. Journal of Disability Policy Studies 2008, doi:10.1177/1044207308325995.

      7 Kindlon T. Criteria used to define chronic fatigue syndrome questioned. Psychosom Med. 2010 Jun;72(5):506-7


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    1. On 2015 Jul 18, Jan Tunér commented:

      In the paper by Kucuk, a laser of 250 mW was used for 48 seconds. This produces energy of 12 J. This parameter is not reported, only the dose of 12 J/cm2. Since the laser aperture is reported to deliver a spot of approximately 10 mm, the dose and the energy in this case gets almost the same numeric value. So far so good. The problem is the understanding of the therapeutic window for biostimulation. The authors cite other researchers and here the complications start. For instance, Hansson used 904 nm, 0.3 mW, 3 minutes. 0.3 x 180 = 0.054 J for clinical use. Mazetto used 780 nm, 70 mW, 10 s, 89.7 J/cm2 = 0.7 J for clinical use. Venanzio used 780 nm, 30 mW, 10 s, 6.3 J/cm2 at three TMJ points. 0.3 x 3 = 0.9 J. The energies in these studies have had to be recalculated since they are not reported in the papers. The three examples above are for TMD arthritic pain. The myalgic studies discussed in the Kucuk paper have the same problem. Now, looking at the energies used in the three studies above, these have been in the range 0.5 - 0.9 J per point. For an average human (keeping in mind that TMD appears to be more common in females) of 60 kg, this would mean approximately 0.2 J per kg. The mean weight of the rabbits was about 3 kg. The 12 joules applied brings 4 joules per kg. For humans this corresponds to 4 x 60 = 180 J! The Arndt-Schultz law stipulates that “For every substance, small doses stimulate, moderate doses inhibit, large doses kill.” The exact optimum for biostimulation of inflammation in the TMJ is not known, but the World Association for Laser Therapy recommends 1-2 points and a total energy of 4 J for clinical use. The TMJ is quite superficial whereas muscles require considerable higher energies due to the poor penetration into these well vasculated tissues. The power density (mW/cm2) is also of importance and low power and longer time are reported to be more effective for tissue repair than high power and short time, even using the same total energy. It is suggested that the lack of effect in the Kucuk paper is due to gross over dosage and subsequent inhibition.


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    1. On 2016 Aug 23, Ben Goldacre commented:

      This trial has the wrong trial registry ID associated with it on PubMed: both in the XML on PubMed, and in the originating journal article. The ID given is NCT0012281. We believe the correct ID, which we have found by hand searching, is NCT00122811.

      This comment is being posted as part of the OpenTrials.net project<sup>[1]</sup> , an open database threading together all publicly accessible documents and data on each trial, globally. In the course of creating the database, and matching documents and data sources about trials from different locations, we have identified various anomalies in datasets such as PubMed, and in published papers. Alongside documenting the prevalence of problems, we are also attempting to correct these errors and anomalies wherever possible, by feeding back to the originators. We have corrected this data in the OpenTrials.net database; we hope that this trial’s text and metadata can also be corrected at source, in PubMed and in the accompanying paper.

      Many thanks,

      Jessica Fleminger, Ben Goldacre*

      [1] Goldacre, B., Gray, J., 2016. OpenTrials: towards a collaborative open database of all available information on all clinical trials. Trials 17. doi:10.1186/s13063-016-1290-8

      * Dr Ben Goldacre BA MA MSc MBBS MRCPsych<br> Senior Clinical Research Fellow<br> ben.goldacre@phc.ox.ac.uk<br> www.ebmDataLab.net<br> Centre for Evidence Based Medicine<br> Department of Primary Care Health Sciences<br> University of Oxford<br> Radcliffe Observatory Quarter<br> Woodstock Road<br> Oxford OX2 6GG


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    1. On 2014 May 23, Morgan Price commented:

      According to the supplementary tables, the mRNA concentration from FISH is poorly correlated with the concentration from RNASeq or with the protein levels. This seems inconsistent with the analyses in Figure 3. In particular, the legend of Figure 3 reports a Pearson correlation of 0.77 between each gene's mRNA FISH level and its protein level. This calculation was done "for genes that express >100 copies of proteins per cell". But when I compute the same correlation coefficient, using the data in Supplementary Table 6, I get a correlation coefficient of just 0.35. (I used the columns "Mean_RNA FISH" and "Mean_Protein", and only the rows with Mean_Protein > 100 and with a Mean_RNA FISH value.)


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    1. On 2016 Jun 02, John Tucker commented:

      The authors of this paper undertook a survey of published results for trials conducted between January 2000 and December 2006. The results of this survey were that industry-only sponsored studies were more likely to obtain positive results than those partially funded by industry, and that these were in turn more likely to report positive results than those performed without industry funding. The results of this study have been widely cited as evidence that the results of industry funded studies are unreliable and tainted by bias.

      A fundamental difficulty with this type of analysis is the underlying assumption that the trials performed by industry and those performed without industry funding are substantially comparable. While the authors do not provide sufficient detail regarding their search criteria to allow perfect recapitulation, a search of the clinicaltrials.gov database with the term "hypercholesterolemia" turns up the following trials.

      *93 funded by industry alone, including 39 trials of statins and 32 trials of ezetimibe

      *7 funded jointly by industry and some other entity, including trials of orange juice, a high fat diet, and glucosamine as interventions

      *7 funded entirely by non-industry entities, including studies of garlic (2x), flaxseed (2x), a high protein diet (2x), and plant sterol-enriched tea as interventions.

      Given the vast gulf between the types of interventions being examined and their a priori likelihood of efficacy, the results of studies such as this one should be interpreted with caution.


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    1. On 2016 Dec 10, Arnaud Chiolero MD PhD commented:

      A comprehensive and bright review of principles of cancer screening. It offers insights on why intuition and common sense mislead health professionnals and patients about the supposed benefits of screening, and why an evidence-based approach is necessary in the assessment of potential benefits and harms of cancer screening.


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    1. On 2013 Dec 27, Wichor Bramer commented:

      To be a useful addition to a search strategy, sensitive filters should not be too unspecific, and specific filters not too insensitive. Developing a sensitive filter of 100% is no problem, if specificity is not considered, very general filter will find all articles, whether they are positives or negatives, but does not add value to a search, because it does not limit the number needed to read (NNR). And a filter with 100% specificity is easy to create, by taking a very rare phrase that only occurs in one or two positives, but then the sensitivity is almost zero, and the filter is useless.

      Simon, Hausner, et al. developed sensitive filters for nurse staffing with a sensitivity of almost 100%, but with a precision of 0.3% the NNR is almost 300, and even for their precise strategy the NNR was 3, with a sensitivity of less than 50%. The authors conclude themselves that 'nurse staffing studies are difficult to identify', but that is true for almost every thematic issue. The low values their filters renders them useless in practice.

      The fact that the most precise filter contains the MeSH term Outcome and Process Assessment (Health Care) is related to the fact that this is part of the search strategy of one of the systematic reviews (Kane RL, 2007) that was used to gather the positives, a review of which the presented search strategy is very difficult to read and not repeatable. http://www.ncbi.nlm.nih.gov/books/NBK38310/


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    1. On 2015 May 04, David Mage commented:

      This 1945 paper identified the prone sleeping position as a major risk factor for these infant deaths that were "entirely unexpected," that were first called SIDS by JB Beckwith in 1969. It took some 46 years for the medical profession to rediscover the prone position as a definitive risk factor for SIDS, when SM Beal and CF Finch published "An overview of retrospective case-control studies investigating the relationship between the prone sleeping position and SIDS." J Paediatric Child Health 1991;27:334-339. PMID:1836736

      Davison wrote about 318 infants dying in Birmingham, U.K., 1938-1944, as follows: "Quite a number of the children in all groups were found prone or with the face turned into the pillow -- borne out by post-mortem hypostasis -- suggesting death by obstruction to the air passages; and in the absence of other factors one might naturally conclude that death was caused by mechanical means." But that would be wrong because many of these deaths were "found to be respiratory or due to otitis media."


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    1. On 2016 Aug 23, Ben Goldacre commented:

      This trial has the wrong trial registry ID associated with it on PubMed: both in the XML on PubMed, and in the originating journal article. The ID given is NCT007919689. We believe the correct ID, which we have found by hand searching, is NCT00791986.

      This comment is being posted as part of the OpenTrials.net project<sup>[1]</sup> , an open database threading together all publicly accessible documents and data on each trial, globally. In the course of creating the database, and matching documents and data sources about trials from different locations, we have identified various anomalies in datasets such as PubMed, and in published papers. Alongside documenting the prevalence of problems, we are also attempting to correct these errors and anomalies wherever possible, by feeding back to the originators. We have corrected this data in the OpenTrials.net database; we hope that this trial’s text and metadata can also be corrected at source, in PubMed and in the accompanying paper.

      Many thanks,

      Jessica Fleminger, Ben Goldacre*

      [1] Goldacre, B., Gray, J., 2016. OpenTrials: towards a collaborative open database of all available information on all clinical trials. Trials 17. doi:10.1186/s13063-016-1290-8 PMID: 27056367

      * Dr Ben Goldacre BA MA MSc MBBS MRCPsych<br> Senior Clinical Research Fellow<br> ben.goldacre@phc.ox.ac.uk<br> www.ebmDataLab.net<br> Centre for Evidence Based Medicine<br> Department of Primary Care Health Sciences<br> University of Oxford<br> Radcliffe Observatory Quarter<br> Woodstock Road<br> Oxford OX2 6GG


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    1. On 2014 Jan 29, Amanda Capes-Davis commented:

      It is really good to see publication of new, authenticated ATC cell lines. The STR data show clearly that these cell lines come from the expected donors. It should be noted though that the STR loci here are not widely used by laboratories worldwide. The ASN-0002 Standard, published by ANSI in 2012, now recommends a consistent set of eight STR loci for cell line authentication testing.


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    1. On 2014 Jan 11, Brett Snodgrass commented:

      Dear Authors,

      Thank you for publication of the excellent article that provides important knowledge about the incidence of VCCs in HLH and their effect on survival.

      Please consider that if the VCC results from pathologic alteration of an arterioluminal vessel, then the VCC may not be synonymous with sinusoid as there is no sinusoid involved.

      However, if the VCC results from pathologic alteration of an arteriosinusoidal vessel, then the term sinusoid would appropriately apply to only a segment of the VCC. The segment of the VCC closer to the epicardium is presumably derived from the "arterio" segment of the arterio*sinusoidal connection.

      VCCs are often used synonymously with VCACs.

      1. Ventriculocoronary connections (VCCs)

      2. Ventriculocoronary arterial connections (VCACs)

      Please provide your kind consideration to the following article published by Joseph Treolar Wearn in 1933. http://bit.ly/JTWearn

      Wearn et al. described the myocardial sinusoids and noted that they connected to the arteriosinusoidal vessels but not to the arterioluminal vessels.

      The vessels of Wearn include the arterioluminal and arteriosinusoidal vessels. Depending on consensus and further study, they may include a variable segment of the myocardial sinusoids.

      Is it possible that some of the VCCs that you describe are not sinusoids but pathologically altered arterioluminal vessels?

      My opinion is that we have probably have insufficient information to definitively conclude in every case whether an arteriosinusoidal or arterioluminal vessel is involved.

      We have discussed these VCCs (VCACs)in relationship to the hypertensive right ventricle of PAIVS. The vessels of Wearn identified in PAIVS is presumably related to the VCCs that you report in the hypertensive left ventricle of MSAA.

      http://www.ncbi.nlm.nih.gov/pubmed/23332812

      The vessels of Wearn connect to both the atria and the ventricles. The vessels of Wearn include the VCC (VCACs) and atrio-coronary-connections (atrio-arterio-cameral connections).

      If the reader is interested in additional commentary related to these connections, please see the following links:

      https://twitter.com/BrettSnodgrass1/status/418829863609331712

      https://twitter.com/BrettSnodgrass1/status/421401527035510784

      https://twitter.com/BrettSnodgrass1/status/420281076070637568

      https://twitter.com/BrettSnodgrass1/status/419599948368183296

      My aim is to help produce accurate medical nomenclature and I proposed the term “vessels of Wearn” for the previously unnamed vessels. http://www.ncbi.nlm.nih.gov/pubmed/22704295

      In summary, please consider that the term sinusoids may not always be related to the VCCs you describe, but the vessels of Wearn is probably applicable (arteriosinusoidal & arterioluminal connections).

      My opinion is that accurate anatomic terminology is a basic principle underlying good medical science, and I ask others to consider whether the aforementioned definitions are appropriate. If this comment is not helpful, please let me know how it might be improved.

      Comments and suggestions are welcome.

      Thank you kindly.


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    1. On 2017 Sep 13, Donald Forsdyke commented:

      WHAT IS THEORETICAL BIOLOGY?

      In a 2011 letter to the editor, I wrote in a somewhat too boisterous fashion questioning the Editors-in-Chiefs' statement on the nature of theoretical biology. The advent of PubMed Commons now makes it possible to reproduce my unpublished letter, which quotes from their statement:

      With 23 papers in the JTB stretching from 1969 to 2009, I am perhaps qualified to congratulate the various Editors who have built on the foundation Professor Danielli so carefully laid in 1961. Yet the letter of the present Editors-in-Chief [1], while claiming to "reflect on the history of theoretical biology," notes that in 1961 "theoretical biology was largely in its infancy."

      This will raise many eyebrows – particularly among those of us who have recently celebrated the Darwin Centenary. Apart from Charles Darwin, the many others set rotating in their graves by this remark will include Gregor Mendel, Francis Galton, George Romanes, William Bateson, Herman Muller, JBS Haldane, Theodosius Dobzhansky, McFarlane Burnet and Francis Crick. At a time when "hundreds of our reviewers are women," the disregarding of these past male contributions hints at political correctness.

      That the present Editors also consider this "a field based largely on mathematics" would also have struck many of these giants – even Mendel, Galton and Haldane – as bizarre. Thus to the question: "Whether the focus and content of JTB has changed over these fifty years?" one must suspect increasing tendencies to (1) dismiss the history of our subject, (2) follow political agendas, and (3) depart from verbal analysis to mathematical modeling.

      It will be interesting to see how many of the experts in the field who have been commissioned by the present Editors to provide reviews of its past, present and future, will note what I believe to have been an unfortunate departure from Danielli’s original goals.

      [1] D. Kirschner, Denise Kirschner, Fifty years of JTB: Past, present and future a letter from the editors-in-chief, J. Theor. Biol., (2011) doi:10.1016/j.jtbi.2010.09.004 Kirschner D, 2011


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    1. On 2015 May 14, University of Kansas School of Nursing Journal Club commented:

      Team 12: Effect of a Quality Improvement Intervention on End of Life Care in the ICU Group 12: Stacy Hanson, Jen Huynh, Sami Johnson, Valerie Melin, Shannan Orpin, Chelsi Puskas, Chandler Schoen

      Background: Upon review of this article, our team found many ways that the content within relates to both previous and current discussions in our Nursing in an Evolving Health Care System course. It covers recent class concepts such as quality improvement and previous topics such as creating a healthy work environment and interprofessional collaboration. We chose this article because it relates to many interests and future careers of our fellow peers upon graduation - critical care - and discusses the effect of an intervention that will improve end of life care in the ICU setting. The gap in knowledge that we feel this article attempts to fill is that of how to provide quality end-of-life care and how it affects patient and family mentality when quality of care are both inadequate and exceptional. We are aware that in this specific area of practice, mortality rates are high and studies have shown that quality of the death and dying component of care is far from adequate.

      Methods: As a team we searched, CINAHL, PUBMED & ProQuest Nursing & Allied Health Sources. We attempted to initially find an article using keywords such as “Professional Nursing Organizations” and “Professional Nursing Organizations in the healthcare setting” but we were unable to find adequate articles that other members of our class had not already claimed. We attempted a different approach and began typing keywords into the search engine such as “Quality improvement in the nursing setting” and we stumbled upon this five star research article in ProQuest. In this quantitative study, a multifaceted, interdisciplinary, quality-improvement intervention was developed to assess the quality of the death and dying process among twelve random hospitals. This study was an unblended cluster-randomized trial (Curtis et al., 2011). Other aspects that were assessed were that of family satisfaction levels, the patients length of stay in the Intensive Care Unit, how long the patient was on mechanical ventilation and the delay before removing them from this equipment and nine chart-based palliative care elements (Curtis et al., 2011). The intervention specifically focused on clinicians and assessed how five core components were integrated within their care on a day-to-day basis: “clinician education about palliative care In the ICU using a variety of education approaches, identification and raining of ICU clinician local champions for palliative care, academic detailing of nurse and physician ICU directors to address individual ICU-specific barriers to improving end-of-life-care, feedback of individual ICU-specific quality data including family satisfaction, and implementation of system supports such as palliative care order forms” (Curtis et al., 2011, p. 349). The intervention impacts all of the healthcare staff in the ICU setting, family members/loved ones and ultimately the patient during this tough time. As stated earlier, 12 hospitals were chosen randomly. Of those hospitals, six were unsystematically chosen for the intervention to be implemented, while the other six served as the control group. Patients were eligible if they had passed away in the ICU or within thirty hours upon discharge/transfer. If the patient was in the ICU for less than six hours, they were not eligible for the study (Curtis et al., 2011). Data was collected through questionnaires distributed to both nurses and family members of the deceased patient. The questionnaire, The Quality of Dying and Death (QODD), addressed to the family was sent four to six weeks after, measuring their viewpoints on their loved one’s quality of care received during the death and dying process. It also measured their levels of satisfaction with the care they received during their overall time in the ICU setting. The nurses too received the QODD questionnaire, 72 hours after death evaluating their outlook on the care they provided (Curtis et al., 2011).

      As a team we found this study to hold high importance so that we as healthcare providers can provide care that is of the utmost respect, granting the last wishes of our patients before they pass away. As nurses, it is an honor to care for someone during the death and dying process, and being a support system that the family and patient can lean on in times of need.

      Findings: After the study was implemented and the results were measured, there was no change in the quality of care provided to patients in the ICU setting during the death and dying process. With further research, we identified barriers that may have contributed to this finding. One limitation present throughout this study was the expense and time consumption of randomizing hospitals. Due to this, there was not an adequate sample size to draw appropriate conclusions from, nor equal distribution of patient characteristics. Another constraint found within the study was the complexity of the intervention implemented, making it difficult to measure the success of delivery. This study was also limited to only the United States, making transferability difficult to other regions (Curtis et al., 2011). A few of our team members have experienced the death and dying process internationally upon a service learning experience in Gulu, Uganda, summer of 2014. After reading this article, our team held a unique discussion about quality and quantity of life and the differences in protocols when it comes to dealing with the death and dying process internationally and in the states. Valerie and Stacy discussed their findings, where life-sustaining resources are not available. As a team we talked about how, even though they do not have great technology and resources their quality of life is better because their existence is not prolonged at detrimental costs.

      Implications: This literature that our team selected is important to the nursing practice because it provides us with a new perspective on how the death and dying practice can be improved to make the end of life process more accepting. Through this article, we realize how crucial it is to be able to grant the last wishes of a patient. We realize that as future nurses, death is unavoidable and for many of our career trajectories, we will be faced with this situation often. We use this study to acknowledge how important it is to advocate for family members and patients in the most vulnerable times of their life. This research article brings to light the importance of communication among all professions, the importance of patient centered care, and the importance of how quality improvement projects advance the nursing profession. As stated previously, this concept is important on a personal level, so that we can be more aware and sensitive to how we can help family members cope with one of the most difficult situations one ever has to face.

      As we transition into the new graduate position, it will be crucial that we can identify areas in need of improvement, that we continuously challenge our practice, searching for the best available evidence and protocols out there to provide patient centered, holistic care. We all are committed to our involvement in quality improvement projects as we strive to be the best nurses we can be.

      Reference: Curtis, J. R., Nielsen, E. L., Treece, P. D., Downey, L., Dotolo, D., Shannon, S., Back, A., Rubenfeld G., Engelberg, R. A. (2011). Effect of a quality-improvement intervention on end-of-life care in the intensive care unit: A randomized trial. American Journal of Respiratory and Critical Care Medicine, 183(3), 348-55.


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    1. On 2014 Feb 12, Preben Berthelsen commented:

      This study was registered with ClinicalTrials.gov (NCT00299650). The primary outcome measure was the “Reduction of the mortality rate of ARDS patients at d90”. The result of the investigation was that there was no statistically significant difference between the mortality of patients treated with NMBA or placebo. In the paper, however, the primary outcome measure has been changed to “the adjusted 90-day survival” and this change of the primary outcome measure - from crude to adjusted mortality - results in the statistically significant different mortality rates reported in the paper. In my opinion, we need more compelling and irrefutable valid evidence before we accept that 48 hours of NMBA treatment influences the mortality rate of a complex pathophysiological entity like ARDS. P.G.Berthelsen, MD. Denmark


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    1. On 2013 Nov 24, John Sotos commented:

      The diagnostic evaluation of the post-partum woman with coronary artery dissection in case 28-2010 (1) was inadequately reported.

      I suspect the patient’s cardiac catheterization included aortography, or at least a quick aortic “root shot,” that was not disclosed. Coronary dissection mandates such an evaluation, given its association with simultaneous aortic dissection and with the aortic ectasia seen in heritable disorders of connective tissue (as noted in the case’s table 2). Finding aortic disease would likely have altered this patient’s surgical management.

      More concerning, the patient’s physical examination omitted pertinent negatives related to connective tissue disorders that cause aorto-coronary dissections, e.g. body habitus, joint hypermobility, skin laxity, visual acuity, and, remarkably, the bifid uvula of Loeys- Dietz syndrome (2).

      Aortic diseases have high mortality when untreated (3). They should always be considered when adults, of any age, have chest discomfort, and should remain in the differential diagnosis even after a coronary dissection is found.

      (1) Case records of the Massachusetts General Hospital. Case 28-2010. A 32-year-old woman, 3 weeks post partum, with substernal chest pain. Sabatine MS, Jaffer FA, Staats PN, Stone JR. N Engl J Med. 2010 Sep 16;363(12):1164-73. Pubmed 20843252 doi: 10.1056/NEJMcpc1000966

      (2) Aneurysm syndromes caused by mutations in the TGF-beta receptor. Loeys BL, Schwarze U, Holm T, Callewaert BL, Thomas GH, Pannu H, De Backer JF, Oswald GL, Symoens S, Manouvrier S, Roberts AE, Faravelli F, Greco MA, Pyeritz RE, Milewicz DM, Coucke PJ, Cameron DE, Braverman AC, Byers PH, De Paepe AM, Dietz HC. N Engl J Med. 2006 Aug 24;355(8):788-98. Pubmed 16928994

      (3) Hirst AD, Johns VJ, Kime SW. Dissecting aneurysm of the aorta: a review of 505 cases. Medicine 1958;37:217-279. Pubmed 13577293


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    1. On 2013 Oct 31, John Cannell commented:

      The authors stated that markers of oxidative stress are present in autism spectrum disorder (ASD). I wonder if the authors are aware that the genes for the antioxidants superoxide dismutase and thioredoxin reductase are directly up-regulated by the secosteroid 1,25 di-hydroxy vitamin D3 (calcitriol). I believe both genes also harbor a vitamin D response element.

      Peehl DM, Shinghal R, Nonn L, Seto E, Krishnan AV, Brooks JD, Feldman D. Molecular activity of 1,25‐dihydroxyvitamin D3 in primary cultures of human prostatic epithelial cells revealed by cDNA microarray analysis. J. Steroid Biochem Mol. Biol 2004;92:131–141. PMID:15555907>

      Calcitriol also directly up-regulates glutathione reductase and increases glutathione levels.

      Jain SK, et alo. Vitamin D upregulates glutamate cysteine ligase and glutathione reductase, and GSH formation, and decreases ROS and MCP-1 and IL-8 secretion in high-glucose exposed U937 monocytes. Biochem Biophys Res Commun. 2013 Jul 19;437(1):7-11. doi: 10.1016/j.bbrc.2013.06.004. Jain SK, 2013

      Also, supplemental vitamin D significantly reduces oxidative stress in humans.

      Nikooyeh B, et al. Daily intake of vitamin D- or calcium-vitamin D-fortified Persian yogurt drink (doogh) attenuates diabetes-induced oxidative stress: evidence for antioxidative properties of vitamin D.J Hum Nutr Diet. 2013 Jul 5. doi: 10.1111/jhn.12142. Nikooyeh B, 2014

      Asemi Z, et al. Vitamin D supplementation affects serum high-sensitivity C-reactive protein, insulin resistance, and biomarkers of oxidative stress in pregnant women. J Nutr. 2013 Sep;143(9):1432-8. doi: 10.3945/jn.113.177550. Asemi Z, 2013

      Thus the vitamin D theory of ASD (vitamin D deficiency being the environmental risk factor for this highly heritable disorder) is consistent with the authors work. Three recent studies, using community controls, have found 25(OH)D levels are significantly lower in children with ASD. Two of the studies below (Mostafa et al and Gong et al) also found ASD severity, as rated on standard ASD rating scales, is inversely correlated with 25(OH)D levels. Mostafa et al found an R value of -.86 for the association of serum 25(OH)D with ASD severity.

      Gong ZL, Luo CM, Wang L, Shen L, Wei F, Tong RJ, Liu Y. Serum 25-hydroxyvitamin D levels in Chinese children with autism spectrum disorders. Neuroreport. 2013 Oct 1. Gong ZL, 2014

      Meguid NA, Hashish AF, Anwar M, Sidhom G. Reduced serum levels of 25-hydroxy and 1,25-dihydroxy vitamin D in Egyptian children with autism. J Altern Complement Med. 2010 Jun;16(6):641-5. Meguid NA, 2010

      Mostafa GA, Al-Ayadhi LY.Reduced serum concentrations of 25-hydroxy vitamin D in children with autism: relation to autoimmunity. J Neuroinflammation. 2012 Aug 17;9:201. Mostafa GA, 2012

      There is a plethora of basic science explaining why low gestational or early childhood 25(OH)D levels would adversely effect brain development.

      Eyles DW, Feron F, Cui X, Kesby JP, Harms LH, Ko P, McGrath JJ, Burne TH. Developmental vitamin D deficiency causes abnormal brain development. Psychoneuroendocrinology. 2009 Dec;34 Suppl 1:S247-57. doi: 10.1016/j.psyneuen.2009.04.015. Epub . Review. Eyles DW, 2009

      DeLuca GC, Kimball SM, Kolasinski J, Ramagopalan SV, Ebers GC. Review: the role of vitamin D in nervous system health and disease. Neuropathol Appl Neurobiol. 2013 Aug;39(5):458-84. doi: 10.1111/nan.12020. DeLuca GC, 2013

      Eyles DW, Burne TH, McGrath JJ. Vitamin D, effects on brain development, adult brain function and the links between low levels of vitamin D and neuropsychiatric disease. Front Neuroendocrinol. 2013 Jan;34(1):47-64. doi: 10.1016/j.yfrne.2012.07.001. Epub 2012 Jul 11. Review. Eyles DW, 2013

      Furthermore, the vitamin D theory of autism explains most of the epidemiological facts of ASD.

      Cannell JJ. On the aetiology of autism. Acta Paediatr. 2010 Aug;99(8):1128-30. Cannell JJ, 2010

      Cannell JJ. Autism and vitamin D. Med Hypotheses. 2008;70(4):750-9. Cannell JJ, 2008

      70% of American toddlers do not take


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    1. On 2015 Oct 05, Lydia Maniatis commented:

      In this publication, as in both older and more recent ones by various authors, "brightness" is being described as as the perceptual correlate of luminance, and is supposed to be interchangeable with lightness when there are no visible illumination boundaries. But as I've noted in comments on Blakeslee and McCourt (2015) and Gilchrist (2015), we can't say that there is a perceptual correlate of luminance, even under (apparently) homogeneous illumination, and this can be proved as follows:

      We ask an observer to report on the lightness of a set of surfaces which don't produce the impression of shadows or transparency. Then, in a second session, we present the same set of surfaces under a different level of illumination. The lightness reports for the surfaces will stay essentially the same, even though their luminances may have changed substantially. So to say that people are making "brightness" judgments - i.e. perceiving luminance - in either the first or the second or in any case doesn't seem to fit the facts.

      In the case of non-homogeneous illumination and double-layers, the position still doesn't make sense, because it implies that we see a surface plus a shadow/transparency, plus a third thing. Is this the case? And how is the value of this third percept supposed to be determined? On the basis of absolute luminance?


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    2. On 2015 Nov 02, Lydia Maniatis commented:

      In this review, Kingdom refers to the “unrelenting controversy” supposedly raging in the study of lightness/brightness/transparency: “Divided into different camps, each with its own preferred stimuli, methodology and theory, the study of LBT is sometimes more reminiscent of the social sciences with its deep ideological divides than it is of the neurosciences.” This quote makes immediately clear that the prevailing controversies reflect, not an intellectually competitive environment, but a highly permissive one of ad hoc hypotheses, each remaining safely within the limits of the stimuli and methodology that will corroborate it, again and again. Beyond these limits, the hypotheses are typically either untestable or easily falsifiable. Yet they remain in good standing for many years, part of the pseudo-controversy, generating endlessly repetitive and poorly-rationalized editorial and experimental publications.

      Kingdom's review is characteristic of this permissive approach. Despite claiming to “critically analyze” theoretical approaches, everyone essentially gets a free pass. One example is described in the asterisked footnote (below). A second example relates to Kingdom's discussion of “edge-integration models.” We learn that Rudd et al have managed to “quantitatively model assimilation, contrast and edge-integration data.” In other words, they have constructed ad hoc accounts of some data. However, while such modeling may be possible for simple stimuli, for “complex two- dimensional images the process is computationally expensive and, one cannot help feel, physiologically implausible.” But the researchers are “keenly aware of this limitation” and anticipate improving their model to, perhaps, attain plausibility.

      Of course, there is nothing wrong with working hard to validly articulate and test a hunch. But until it is testable and tested, it cannot be considered a competitor in good standing. The prevailing standard of “partial success” is a standard of failure. Controversy among proposals that are half-baked, untestable and/or fail as soon as they leave their comfort zone is of marginal scientific interest.

      • An example that I am particularly familiar with is the “anchoring theory.” I recently published a “simple test” of fundamental claims/assumptions of this construct – and it failed. The test was easy to conceive – trivial, actually - and the outcome highly predictable. I learned after the fact that at least one other investigator had, a while back, considered publishing something to the same effect. Despite this clear falsification of fundamental (if vague) assumptions (as well as previous falsifications), the failed “anchoring theory” is continuing to chalk up “successes.”


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    1. On 2016 Aug 23, Ben Goldacre commented:

      This trial has the wrong trial registry ID associated with it on PubMed: both in the XML on PubMed, and in the originating journal article. The ID given is NCT0100468. We believe the correct ID, which we have found by hand searching, is NCT01004068.

      This comment is being posted as part of the OpenTrials.net project<sup>[1]</sup> , an open database threading together all publicly accessible documents and data on each trial, globally. In the course of creating the database, and matching documents and data sources about trials from different locations, we have identified various anomalies in datasets such as PubMed, and in published papers. Alongside documenting the prevalence of problems, we are also attempting to correct these errors and anomalies wherever possible, by feeding back to the originators. We have corrected this data in the OpenTrials.net database; we hope that this trial’s text and metadata can also be corrected at source, in PubMed and in the accompanying paper.

      Many thanks,

      Jessica Fleminger, Ben Goldacre*

      [1] Goldacre, B., Gray, J., 2016. OpenTrials: towards a collaborative open database of all available information on all clinical trials. Trials 17. doi:10.1186/s13063-016-1290-8 PMID: 27056367

      * Dr Ben Goldacre BA MA MSc MBBS MRCPsych<br> Senior Clinical Research Fellow<br> ben.goldacre@phc.ox.ac.uk<br> www.ebmDataLab.net<br> Centre for Evidence Based Medicine<br> Department of Primary Care Health Sciences<br> University of Oxford<br> Radcliffe Observatory Quarter<br> Woodstock Road<br> Oxford OX2 6GG


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    1. On 2014 Sep 29, John Friesen commented:

      This well designed study demonstrates two important things about induction doses of propofol in morbidly obese patients. First, they are best normalized to the lean body weight. Second, the dose required is affected by the rate at which it is administered.

      The authors recommend using the lean body weight to estimate the dose for morbidly obese patients. However, any clinically useful weight scalar must be equal to the total body weight for patients of normal weight. Because the lean body weight is always less than the total body weight even for non-obese patients, it cannot be used directly to calculate doses drug doses: it will result in underestimation, and must be scaled upwards(1).

      For example: a woman weighing 105 kilograms with a height of 170 centimeters and a BMI of 36.3 presents for bariatric surgery. Her induction dose of propofol is based on her calculated lean body weight5 of 55.2 kilograms. She successfully loses weight, and she returns for another operation having lost 40 kilograms. She is no longer obese, and her induction dose is based on her total body weight of 65 kilograms. Assuming that she is given 2.0 mg/kg of propofol each time, her calculated dose is 110 mg when she weighs 105 kilograms, and 130 mg (20 mg more) when she weighs only 65 kilograms. This is not correct.

      The lean-scaled weight is a weight scalar that is proportional to the lean body weight for all obese and non-obese patients(2). It is calculated by multiplying the lean body weight function(3) by a normalization factor such that it is equal to the total body weight at a BMI of 22. This factor is 1.2332 for men and 1.5262 for women: for the 105 kilogram woman in the example, the lean-scaled weight is 84.2 kilograms.

      It is interesting to ask what results might have been obtained if this study had included a morbidly obese group administered propofol at a rate proportional to the lean-scaled weight. Combining the two morbidly obese groups the mean total body weight is 131.1 kg and the lean body weight is 67.05 kg. For a BMI of 46.55, the mean lean-scaled weight (given the proportion of males to females) calculates to be 91.09 kg for this imagined group. Using these values to interpolate between the results reported for the infusion rates used in the study, the dose estimated to a linear approximation is about 2.27 mg/kg of lean-scaled weight.

      The lean-scaled weight is equal to the total body weight for non-obese patients, and therefore this result can be compared directly to the 2.57 mg/kg reported for the control group. 2.27 mg/kg is close to this value, and well within the reported error. The results of this study are consistent with using the lean-scaled weight when estimating induction doses of propofol, for both obese and non-obese patients.

      References

      1 Bouillon T, Shafer SL. Does size matter? Anesthesiology. 1998 Sep;89(3):557-60.

      2 Friesen JH. Lean-scaled weight: a proposed weight scalar to calculate drug doses for obese patients. Can J Anesth. 2013 Feb;60(2):214-5.

      3 Janmahasatian S, Duffull SB, Ash S, Ward LC, Byrne NM, Green B. Quantification of lean bodyweight. Clin Pharmacokinet. 2005;44(10):1051-65.


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    1. On 2014 Oct 15, Amanda Capes-Davis commented:

      Please be careful to view the erratum here if working with hTERT-EEC cells. As shown by Korch et al 2012 (PMID 22710073), hTERT-EEC is known to be misidentified and is actually MCF-7. So cells are from breast carcinoma, not immortalized endometrium.

      Authentic stocks are always a possibility, so labs are encouraged to test their stocks using a consensus technique such as STR profiling. For a list of known misidentified cell lines, see http://iclac.org/databases/cross-contaminations/.


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    1. On 2013 Nov 01, Hilda Bastian commented:

      Our estimation of "11 systematic reviews a day" is out of date. There has been a striking increase in systematic reviews since that original analysis (ending with data from 2007). In August 2013 Paul Glasziou and I updated the data in Figure 3 estimating the number of systematic reviews, including data up to 2012.

      The update showed that by 2012, there were around 26 systematic reviews a day. The updated figure is available here. Addressing the challenges we identified in keeping up with the evidence have thus become more critical.

      (We are grateful to Claire Allen at the Cochrane Collaboration for providing the data on the number of Cochrane reviews.)


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    2. On 2013 Nov 12, Paulo Rossetti commented:

      The way to communicate science for general clinics is a complicated issue. Meta-analysis could be a two-page article only with what is extremely necessary for clinics. Maybe, some people can design a self-explained forest plot similar to what we have now for some themes with smartphone technologies.


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    3. On 2016 Sep 16, Hilda Bastian commented:

      I have posted updated data on key charts here. The data are updated to 2013 for the charts with systematic reviews and 2014 for trials.

      If you are interested in this topic, the Page MJ, 2016 paper is a must read. We relied in large part on filters to chart trends: Page and colleagues rigorously studied a month's worth of systematic reviews from 2014.

      Disclosure: I work on projects related to systematic reviews at the NCBI (National Center for Biotechnology Information, U.S. National Library of Medicine), including some aspects that relate to the inclusion of systematic reviews in PubMed.


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    1. On 2015 Jun 08, Prof.Dr.Jogenananda Pramanik commented:

      Invited co-authors: Dr.Cao Yulin MD.PhD CEO, International Centre for Biogenetics and Stem Cell Research ( ICBSCR), Beijing; Dr.Juntang Lin, Research Group Leader, Jena University, Jena, Germany.

      Despite rigorous internal and external quality control measures and close supervision from China Academy of Sciences and related Governmental regulatory agencies, we humbly accept that certain limitations and risk factors that are existing in stem cell therapeutic procedures in China like any other developed countries. However, we are painfully conscious to observe the organized efforts to hinder the flow of patients from western world to different hospitals in China seeking stem cell therapy for different disorders. Since past few years stem cell therapy is picking up tremendous popularity among patients recovering from incurable diseases like cerebral palsy, IDDM and others. Amidst several restrictions, stem cell therapy is practised in India, Malaysia and other South East Asian countries. Governmental regulatory bodies are sincerely employing necessary regulations where ever required and therefore their efforts are commendable in view of the safety of our patients. As all of us understand that virtually no medical treatment is without risk and so is for cell-based therapy in general. However, as stem cell research progresses and legitimate medical innovation using stem call-based applications become more of a reality, all those issues will hopefully be settled step by step. We in no way wish to place any blame on individuals who are determined to pursue hope in what are often extremely difficult and discouraging circumstances (1 & 2). References: 1.Editorial:Stem-cell laws in China fall short: Nature;467,633(07 October 2010/ doi.10.1038/467633a. 2.Jogenananda Pramanik & Tanu Pramanik: Stem Cell Therapy Controversial? Re: Netherlands bans stem cell therapy:BMJ2007;334doi.http;//dx.doi.org/10.1136/bmj.39072458449.DB(Published 04 January 2007)


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    1. On 2013 Oct 29, Tom Kindlon commented:

      Was this study sufficiently powered to find oxidative phosphorylation?

      It is not desirable if a promising line of enquiry is prematurely ended by an underpowered study. Looking at Table 4 and in particular, rows 1, 2 and 4 where the figures go up for the controls from test 1 to test 2 and go down for the CFS/ME patients, I am left wondering whether a bigger study would have found a statistically significant difference. This is not a criticism of the researchers as, like all teams, I'm sure they would have preferred bigger samples but funding and other issues restrict what is possible for any one study. Also, the team in this case probably did not have advance data to do power calculations. It will be interesting to see if similar changes are evident in future studies* and whether pooled data would show differences even if individual studies don't reach the magical "statistical significance".

      *if any researchers investigate this again - the volume of study in CFS is low and there is a range of issues to look at


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    1. On 2015 Mar 25, University of Kansas School of Nursing Journal Club commented:

      Team 10: Jenny Allin, Lauren Andrus, Morgan Cross, Stephanie Gass, Joey Leoni, Jamie Lockwood, Ryan Rogers, Malorie Schuler

      Upon near completion of nursing school, our class has discussed numerous topics pertaining to leadership, change agency, and collaboration, or shared governance. Our group selected this article because it encompasses the true importance of collaboration between professions, as well as displaying the true impact that nurses can have on the overall work environment and structure. Thus far we have discovered many opportunities that we will have as future nurses to become an active member in our organization. In one instance, we may become part of committees in order to give a voice to the nursing profession during in major policy changes or decision-making processes. The selected article displays the ways in which the interwoven relationship between transformational leadership and shared governance can result in a successful and motivating work environment. Additionally, we found this article to answer the question as to whether or not nurses can both impact change and promote advancements in the overall structure, while also feeling more empowered and self-confident with such involvement.

      The information from this descriptive and exploratory study, found by means of the CINAHL database, was obtained from personal reflective practices and self-reporting. The creators of the study collected the data by speaking with nurses involved in transformational leadership and the impact shared governance has on their unit and patient care as a whole. In order to acquire relevant articles to the topic we wished to review the following keywords were used: shared governance, nursing, and leadership. Our group feels the population targeted by the authors are nurses that lack confidence and motivation that their involvement in shared governance committees and processes. The nurses identified in the study do not yet realize that their input can and will make a positive impact on their peers as well as their patients. We also feel that members from various other healthcare professions could have been targeted in this study, albeit secondarily. It would be beneficial for other team members to review this study and discover the contributions nursing can make if given the respect and opportunity to do so.

      Overall, this study reinforced the fact that shared governance when paired with transformational leadership, results in a profession that can “function effectively in a contemporary healthcare environment” (Bamford-Wade & Moss, 2010, p.819). When a unit or structure provides these opportunities for their employees, those employees are then filled with a greater sense of worth, self-esteem, autonomy, and responsibility (Bamford-Wade & Moss, 2010). Although this study was conducted and completed in New Zealand, the findings were consistent with that of research attained through studies in the United States. It is interesting to see the particular successes in healthcare translate to numerous locations and cultures around the world. While our group felt this article was reliable as well as valid, we would have liked to see more concrete data and statistics related to the impact of shared governance. Self-reporting and reflections are advantageous because they disclose information that numerical figures cannot, however, specific quantitative data may have made the study much stronger.

      Information on transformational leadership and shared governance is imperative to professionals in the nursing practice. It encourages nurses to be aware of the opportunities they have available in order to become an agent of change in his or her organization. These two topics are not absolutely understood, and therefore are often overlooked or ignored by many registered nurses that have the capacity to make an incredible difference. As new graduates, it will be easy to forget these opportunities and to believe that our voices will not be heard. Our group discussed that reviewing articles and examining research that cover these topics reminds us that our profession does not simply consist of completing tasks and charting. Rather, personal and individualized patient care, safety, and beneficial work environments are essential components to our career as well, and who better to advocate for nurses than themselves? We enjoyed this article because it coincided with the information from through several of our previous BSN courses, and made us feel empowered to become leaders and members of shared governance teams in the future. While leadership may initially begin at the unit level, RN contributions can expand through the different chains of command and result in a facility-wide change in patient care.


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    1. On 2013 Oct 31, John Cannell commented:

      The authors stated that markers of oxidative stress are present in autism spectrum disorder (ASD). I wonder if the authors are aware that the genes for the antioxidants superoxide dismutase and thioredoxin reductase are directly up-regulated by the secosteroid 1,25 di-hydroxy vitamin D3 (calcitriol). I believe both genes also harbor a vitamin D response element.

      Peehl DM, Shinghal R, Nonn L, Seto E, Krishnan AV, Brooks JD, Feldman D. Molecular activity of 1,25‐dihydroxyvitamin D3 in primary cultures of human prostatic epithelial cells revealed by cDNA microarray analysis. J. Steroid Biochem Mol. Biol 2004;92:131–141. PMID:15555907>

      Calcitriol also directly up-regulates glutathione reductase and increases glutathione levels.

      Jain SK, et alo. Vitamin D upregulates glutamate cysteine ligase and glutathione reductase, and GSH formation, and decreases ROS and MCP-1 and IL-8 secretion in high-glucose exposed U937 monocytes. Biochem Biophys Res Commun. 2013 Jul 19;437(1):7-11. doi: 10.1016/j.bbrc.2013.06.004. Jain SK, 2013

      Also, supplemental vitamin D significantly reduces oxidative stress in humans.

      Nikooyeh B, et al. Daily intake of vitamin D- or calcium-vitamin D-fortified Persian yogurt drink (doogh) attenuates diabetes-induced oxidative stress: evidence for antioxidative properties of vitamin D.J Hum Nutr Diet. 2013 Jul 5. doi: 10.1111/jhn.12142. Nikooyeh B, 2014

      Asemi Z, et al. Vitamin D supplementation affects serum high-sensitivity C-reactive protein, insulin resistance, and biomarkers of oxidative stress in pregnant women. J Nutr. 2013 Sep;143(9):1432-8. doi: 10.3945/jn.113.177550. Asemi Z, 2013

      Thus the vitamin D theory of ASD (vitamin D deficiency being the environmental risk factor for this highly heritable disorder) is consistent with the authors work. Three recent studies, using community controls, have found 25(OH)D levels are significantly lower in children with ASD. Two of the studies below (Mostafa et al and Gong et al) also found ASD severity, as rated on standard ASD rating scales, is inversely correlated with 25(OH)D levels. Mostafa et al found an R value of -.86 for the association of serum 25(OH)D with ASD severity.

      Gong ZL, Luo CM, Wang L, Shen L, Wei F, Tong RJ, Liu Y. Serum 25-hydroxyvitamin D levels in Chinese children with autism spectrum disorders. Neuroreport. 2013 Oct 1. Gong ZL, 2014

      Meguid NA, Hashish AF, Anwar M, Sidhom G. Reduced serum levels of 25-hydroxy and 1,25-dihydroxy vitamin D in Egyptian children with autism. J Altern Complement Med. 2010 Jun;16(6):641-5. Meguid NA, 2010

      Mostafa GA, Al-Ayadhi LY.Reduced serum concentrations of 25-hydroxy vitamin D in children with autism: relation to autoimmunity. J Neuroinflammation. 2012 Aug 17;9:201. Mostafa GA, 2012

      There is a plethora of basic science explaining why low gestational or early childhood 25(OH)D levels would adversely effect brain development.

      Eyles DW, Feron F, Cui X, Kesby JP, Harms LH, Ko P, McGrath JJ, Burne TH. Developmental vitamin D deficiency causes abnormal brain development. Psychoneuroendocrinology. 2009 Dec;34 Suppl 1:S247-57. doi: 10.1016/j.psyneuen.2009.04.015. Epub . Review. Eyles DW, 2009

      DeLuca GC, Kimball SM, Kolasinski J, Ramagopalan SV, Ebers GC. Review: the role of vitamin D in nervous system health and disease. Neuropathol Appl Neurobiol. 2013 Aug;39(5):458-84. doi: 10.1111/nan.12020. DeLuca GC, 2013

      Eyles DW, Burne TH, McGrath JJ. Vitamin D, effects on brain development, adult brain function and the links between low levels of vitamin D and neuropsychiatric disease. Front Neuroendocrinol. 2013 Jan;34(1):47-64. doi: 10.1016/j.yfrne.2012.07.001. Epub 2012 Jul 11. Review. Eyles DW, 2013

      Furthermore, the vitamin D theory of autism explains most of the epidemiological facts of ASD.

      Cannell JJ. On the aetiology of autism. Acta Paediatr. 2010 Aug;99(8):1128-30. Cannell JJ, 2010

      Cannell JJ. Autism and vitamin D. Med Hypotheses. 2008;70(4):750-9. Cannell JJ, 2008

      70% of American toddlers do not take


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