410 Matching Annotations
  1. Jan 2024
    1. when you actually have chronic anything usually it's not a good result

      for - chronic disease - usually chronic is not a good sign - too much of a good thing turns out to be bad - it means too much of something, like inflammation will cause harm - when inflammation knob is stuck on high, it becomes a problem

      metaphor - inflammation and forest fire - If you are camping in the forest, a small fire keeps you warm and you can cook - Inflammation is like that small fire going out of control and burning the whole forest down

    2. cancer without disease

      for - cancer without disease - microscopic cancer

      definition - cancer without disease

      • biologically we are actually all forming cancers in our body all the time
      • because all it takes for our 40 trillion cells to do is
      • to make those little mistakes
      • I told you 10 000 mistakes are fixed every day
      • A few of those sneaking through
      • will turn into a microscopic tumor microscopic cancer
      • and this is called cancer without disease
      • because as tiny little mutant cancer can grow up to the size of the tip of a ballpoint pen
      • and then it's frozen like a pimple can't go any bigger
      • because it doesn't have
        • a blood supply
        • no oxygen
        • no food
        • nothing to feed it and so
      • those little microscopic cancers sit there
      • until another one of our defense systems our immune system wings by like a cop on a beat and sees this abnormal cell sitting on that street corner in a good neighborhood and then says
        • "get in the car we're taking you away"
      • and so our immune system destroys these microscopic cancers
      • but some microscopic cancers are able to hijack our body's regular angiogenesis defense system
      • and selfishly grow blood vessels to feed themselves.
  2. Nov 2023
    1. Xylitol appears to be favored over all kinds of carbohydrates except fructose.47

      Avoid fructose so that bacteria consume xylitol.

    1. sumption of decreasing virulence with time is a double-edged sword in NativeAmerican disease history. Recent Native Americans have extreme susceptibility to oftenacute infections such as influenza and tuberculosis (Indian Health Service 1999; Koenig1921; Matthews 1886). Although, as detailed later in this paper, many factors, includingsocio-economic conditions, diet, and other concurrent infections, could be contributing tothis incidence, these factors seem to pale by comparison with disease history. Essentially,current incidence rates account for the absence of crowd infections prior to Columbus andabsence explains the present incidence rate

      .

    2. se diseases, once introduced, severelywinnowed Native American populations.

      .

    3. Since the mid-twentieth century it has been widely accepted that Old World populationsintroduced infectious diseases to Native Americans beginning with the Columbianvoyages of AD 149

      .

  3. Jun 2023
    1. Dr Sokhna Thiam, from the African Population and Health Research Center in Nairobi, Kenya, added that water-borne enteric diseases are among the “primary expected health impacts” of climate change.

      Basically climate changes makes the leading cause of child deaths much worse

  4. May 2023
    1. Figure 1Optical genome mapping reveals 173 Mb pericentric inversion on chromosome 1 with a breakpoint within the USH2A gene.

      Optical Genome mapping can detect balanced structural variant as shown in previous studies. Fadaie Z, et al; 2021 amazingly identified an intragenic inverted duplication by OGM and Long read sequencing (Pacbio).

    2. Structural variants (SVs) play an important role in inherited retinal diseases (IRD).

      Structural variants, specifically CNVs (Copy Number Variants) contribute to more than 10% of undiagnosed IRD cases

  5. Feb 2023
    1. Review coordinated by Life Science Editors.

      Reviewed by: Dr. Angela Andersen, Life Science Editors

      Potential Conflicts of Interest: Dr. Mill has worked with Life Science Editors on other manuscripts.

      Background: Retinitis pigmentosa (RP) is a group of rare eye diseases that cause vision loss. Symptoms usually start in childhood, and most people eventually lose most of their sight. There is no cure for RP. Mutations in retinitis pigmentosa GTPase regulator (RPGR) cause RP and compromise the renewal of light-sensitive “disc” membranes (specialized cilia) at the outer segment of photoreceptors, resulting in the loss of these cells over time. Evidence suggests that disc formation is similar to the release of ectosomes (small extracellular vesicles) and that both rely on the actin cytoskeleton. Knockdown of RPGR in retinal pigmented epithelium cells showed stronger actin filaments and reduced cilia suggesting that it may regulate nascent photoreceptor disc formation by regulating actin-mediated membrane extension in the retina (Gakovic et al., Human Molecular Genetics, 2011). In addition, RPGR patient iPSC-retinal models displayed phenotypes consistent with abnormal actin regulation (Megaw et al., Nature Communications, 2017; Karam et al., J Personalized Medicine, 2022).

      Question: What function of RPGR is compromised in photoreceptors to cause RP?

      Advance: The authors generated novel Rpgr mutant mice harboring human disease-causing mutations that recapitulate human disease phenotypes: aborted membrane shedding as ectosome-like vesicles, photoreceptor death and visual loss. RPGR is located at the site of disc formation – to test if it plays a role in disc genesis, they engineered a novel reporter mouse to track outer segment turnover. Rhodopsin was tagged with the self-labelling peptide SNAP- Rhodopsin is the major protein component of outer segment discs, and so incubating RhodSNAP retinal slice cultures with SNAP fluorophores results in outer segment labelling. Perturbation of RPGR resulted in a slowed rate of disc formation, leading to shortened outer segments and increased vesicle shedding. To me, the breakthrough is in the last figure: the actin depolymerizing drug Cytochalasin D in PBS was injected intravitreally, and fixed retinas were analyzed 6 hours later by electron microscopy. Cytochalasin D treatment significantly reduced the number of shed vesicles from the base of the outer segment in Rpgr-mutant mice (they now look like wild-type).

      Significance: Nails down the disease-relevant function of RPGR and a molecular mechanism of RP in photoreceptor cells, in vivo, in mice. Pharmacological rescue not only demonstrates the importance of the mechanism to disease but also sheds light on a potential therapeutic avenue for RP.

  6. Jan 2023
    1. the numbers are 00:14:09 something like that you drop it down to you've got 88 percent less chance or actually it's it's 12 percent chance for most diseases so most diseases are protected by these diets

      !- vegan and pescatarian diets : disease impacts - reduce by 88%

  7. Dec 2022
    1. The polio-vaccine conspiracy theory has had direct consequences: Sixteen countries where polio had been eradicated have in recent months reported outbreaks of the disease – twelve in Africa (Benin, Botswana, Burkina Faso, Cameroon, Central African Republic, Chad, Ethiopia, Ghana, Guinea, Mali, Sudan, and Togo) and four in Asia (India, Indonesia, Saudi Arabia, and Yemen). Yemen has had the largest polio outbreak, with more than 83 cases since April. The WHO calls this "a major epidemic."
    1. I came here after recalling a critique by Bessel van der Kolk's "The Body Keeps the Score: Brain, Mind, and Body in the Healing of Trauma" regarding the disease model and it's negative impact on adequately helping people with trauma. van der Kolk's critique was similar to Marc Lewis' critique of the disease model as it applies to addiction from "The Biology of Desire: Why Addiction Is Not a Disease". This made me wonder what the term "disease" actually means and whether or not some general consensus existed within the medical community. This article suggests there is no such consensus.

      This article is by Jackie Leach Scully who holds a "PhD in cellular pathology, University of Cambridge; BA (Hons) in biochemistry, University of Oxford; MA in psychoanalytic studies, Sheffield University".

      Scully does several insightful things in this paper the following are the ones that were most salient to me upon the first read: - distinguishes "disease" from "disability" - contrasts the "social model" and "medical model" perspectives on "disability" - The "medical model" referred to here is probably what Lewis & van der Kolk are critiquing as the "disease model".<br /> - Are the "medical" and "disease" model different? - the social model seems to have arisen as a response to the inadequacy of the medical model

          - "The social model's fundamental criticism of the medical model is that it wrongly locates 'the problem' of disability in biological constraints, considering it only from the point of view of the individual and neglecting the social and systemic frameworks that contribute to it. The social model distinguishes between impairment (the biological substrate, such as impaired hearing) and the disabled experience. In this view the presence of impaired hearing is one thing, while the absence of subtitling on TV is quite another, and it is the refusal of society to make the necessary accommodations that is the real site of disability. A social model does not ignore biology, but contends that societal, economic and environmental factors are at least as important in producing disability."
      
      • brings up a subtle point that there are two jumps "from gene to phenotype, and from phenotype to experience" and that some of the arguments mentioned "suggest that the 'harm' of the impairment is not straightforwardly related to phenotype. What ought to concern us about disease and disability is the disadvantage, pain or suffering involved, and in a sense the impairment is always a kind of surrogate marker for this experience."
    1. OMIM 612718

      Case#: pt I, 21 y/o male

      DiseaseAssertion: GAMT deficiency

      FamilyInfo:non-consangeous parents of Yemenite Jewish descent

      CasePresentingHPOs: expressive speech was delayed, reduced strength and stamina, delayed general cognitive function

      CaseHPOFreeText: N/A

      CaseNotHPOs:N/A

      CaseNotHPOFreeText: N/A

      Biochemical analyte testing: abnormal CK and EMG results

      Brain Magnetic Resonance Spectroscopy (MRS): appeared normal

      GAMT activity assay: N/A

      Zygosity: autosomal recessive

      Variant 1: OMIM 612718

      ClinVarID: N/A

      CAID: N/A

      gnomAD: N/A

    1. OMIM 300352)

      Case#: N/A

      DiseaseAssertion: AGAT mutation

      FamilyInfo: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      Biochemical analyte testing: N/A

      Brain Magnetic Resonance Spectroscopy (MRS): N/A

      GAMT activity assay: N/A

      Zygosity: homozygous

      Variant 1: OMIM 602360

      ClinVarID: 8303

      CAID: CA340769

      gnomAD: N/A

    2. OMIM 601240

      Case#: N/A

      DiseaseAssertion: AGAT mutation

      FamilyInfo: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      Biochemical analyte testing: N/A

      Brain Magnetic Resonance Spectroscopy (MRS): N/A

      GAMT activity assay: N/A

      Zygosity: homozygous

      Variant 1: OMIM 602360

      ClinVarID: 8303

      CAID: CA340769

      gnomAD: N/A

    3. OMIM 602360

      Case#: N/A

      DiseaseAssertion: AGAT mutation

      FamilyInfo: N/A

      CasePresentingHPOs: N/A

      CaseHPOFreeText: N/A

      CaseNotHPOs: N/A

      CaseNotHPOFreeText: N/A

      Biochemical analyte testing: N/A

      Brain Magnetic Resonance Spectroscopy (MRS): N/A

      GAMT activity assay: N/A

      Zygosity: homozygous

      Variant 1: OMIM 602360

      ClinVarID: 8303

      CAID: CA340769

      gnomAD: N/A

  8. Nov 2022
    1. Use of predictive algorithms in-homemonitoring of chronic obstructivepulmonary disease and asthma:A systematic review

      Use of predictive algorithms in-home monitoring of chronic obstructive pulmonary disease and asthma: A systematic review

    Tags

    Annotators

  9. Oct 2022
  10. Sep 2022
    1. The underlying theme tyingthese myths together is that poverty is often perceived to be an issue of“them” rather than an issue of “us”—that those who experience povertyare viewed as strangers to mainstream America, falling outside accept-able behavior, and as such, are to be scorned and stigmatized.

      One of the underlying commonalities about the various myths of poverty is that we tend to "other" those that it effects. The "them" we stigmatize with the ills of poverty really look more like "us", and in fact, they are.

      Rather than victim shame and blame those in poverty, we ought to spend more of our time fixing the underlying disease instead of spending the time, effort, energy, and money on attempting to remedy the symptoms (eg. excessive policing, et al.) Not only is it more beneficial, but cheaper in the long run.


      Related:<br /> Gladwell, Malcolm. “Million-Dollar Murray.” The New Yorker, February 5, 2006. https://www.newyorker.com/magazine/2006/02/13/million-dollar-murray (.pdf copy available at https://housingmatterssc.org/million-dollar-murray/)

  11. Aug 2022
  12. May 2022
    1. Pathogenic germline variants in DICER1 underlie an autosomal dominant, pleiotropic tumor-predisposition disorder.

      gene name: DICER 1 PMID (PubMed ID): 33570641 HGNCID: n/a Inheritance Pattern: autosomal dominant Disease Entity: benign and malignant tumor mutation Mutation: somatic Zygosity: heterozygous Variant: n/a Family Information: n/a Case: people of all sexes, ages, ethnicities and races participated CasePresentingHPOs: individuals with DICER1-associated tumors or pathogenic germline DICER1 variants were recruited to participate CasePreviousTesting: n/a gnomAD: n/a

    1. DICER1 syndrome is an autosomal-dominant,pleiotropic, tumor-predisposition disorder arisingfrom pathogenic germline variants in DICER1, whichencodes an endoribonuclease integral to processingmicroRNAs

      DICER1 is the gene name. PubMed ID, HGCNCID, and Variant: I can't find Inheritance Pattern: autosomal-dominant The disease entity: DICER1 syndrome The type of mutation: germline. Zygosity: not known. Family Information: a family was used, DICER1 carriers, and non DICER1 variant used, some of the family members had tumors from DICER1 Case Information: mean age is 34, the range of age is 18.6 to 43 years, male, and female used, ethnicity can't find Case Presenting HPO: cancer testing, chemotherapy, radiotherapy gnomeAD: 9.2,8.3.2 Mutation type: Pleiotropic, loss of function, missense

  13. Apr 2022
    1. DICER1 syndrome is an autosomal-dominant, pleiotropic tumor-predisposition disorder

      Gene Name:DICER1 PMID: 30715996 HGNCID: Not on document Inheritance Pattern: Autosomal Dominant Disease Entity: Pleiotropic Tumor-Predisposition Disorder Mutation: Pathogenic Germline Variants Zygosity: Not in document Variant: Not in document Family Information: An individual was found who had family members who were also affected by this mutation. Because of this, those family members were also chosen to participate in this study. Mutation Type: Missense Case: The study was done on more than one individual. Roughly more than half of the individuals were female

    1. Mathew, D., Giles, J. R., Baxter, A. E., Oldridge, D. A., Greenplate, A. R., Wu, J. E., Alanio, C., Kuri-Cervantes, L., Pampena, M. B., D’Andrea, K., Manne, S., Chen, Z., Huang, Y. J., Reilly, J. P., Weisman, A. R., Ittner, C. A. G., Kuthuru, O., Dougherty, J., Nzingha, K., … Wherry, E. J. (2020). Deep immune profiling of COVID-19 patients reveals distinct immunotypes with therapeutic implications. Science, 369(6508), eabc8511. https://doi.org/10.1126/science.abc8511

    1. The DICER1 syndrome is an autosomal dominant tumor‐predisposi-tion disorder associated with pleuropulmonary blastoma, a rare pediatric lung cancer

      GeneName:DICER1 PMID (PubMed ID): PMCID: PMC6418698 PMID: 30672147 HGNCID: NOT LISTED<br /> Inheritance Pattern: Autosomal Dominant Disease Entity: Cancer; benign and malignant tumors including pleuropulmonary blastoma, cystic nephroma, Sertoli-Leydig cell tumors, multinodular goiter, Thryoid cancer, rhabdomyosarcoma, and pineoblastoma. Mutation: Somatic missense variation Mutation type: missense Zygosity: None stated Variant: unregistered…. Family Information: Characterize germline variants in familial early-onset clorectal cancer patients; The observation of germline DICER1 variation with uterine corpus endometrial carcinoma merits additional investigation. CasePresentingHPOs: uterine and rectal cancers in germline mutation

    1. Prof Francois Balloux [@BallouxFrancois]. (2021, December 9). This may have sounded somewhat naïve in early 2020, but by now, I would have expected that anyone with an interest in covid-19 might have acquired some basic notions in infectious disease epidemiology. 1/ [Tweet]. Twitter. https://twitter.com/BallouxFrancois/status/1469063480334561285

    1. Carl T. Bergstrom. (2021, August 18). 1. There has been lots of talk about recent data from Israel that seem to suggest a decline in vaccine efficacy against severe disease due to Delta, waning protection, or both. This may have even been a motivation for Biden’s announcement that the US would be adopting boosters. [Tweet]. @CT_Bergstrom. https://twitter.com/CT_Bergstrom/status/1427767356600688646

    1. Dr Greg Kelly. (2021, July 2). As a pediatrician I’m going on record saying that allowing kids to be freely infected with a novel disease that has unknown long term consequences is the worst idea of 2021 despite being a pretty crowded field so far #COVID19 [Tweet]. @drgregkelly. https://twitter.com/drgregkelly/status/1411083905034117120

  14. Mar 2022
    1. Dr. Deepti Gurdasani. (2022, March 1). New study out yesterday suggesting that vaccine efficacy with current dose for 5-11 yr olds likely wanes quickly. Especially against infection, but also against hospitalisation, although protection against severe disease is higher. Seems to be closely linked to vaccine dose🧵 https://t.co/NojLODF1ED [Tweet]. @dgurdasani1. https://twitter.com/dgurdasani1/status/1498580243665367040

    1. Kerr, P. J., Cattadori, I. M., Liu, J., Sim, D. G., Dodds, J. W., Brooks, J. W., Kennett, M. J., Holmes, E. C., & Read, A. F. (2017). Next step in the ongoing arms race between myxoma virus and wild rabbits in Australia is a novel disease phenotype. Proceedings of the National Academy of Sciences, 114(35), 9397–9402. https://doi.org/10.1073/pnas.1710336114

    1. ReconfigBehSci on Twitter: ‘@STWorg @ProfColinDavis @rpancost @chrisdc77 @syrpis this is the most in depth treatment of the impact of equalities law on pandemic policy that I’ve been able to find- it would seem to underscore that there is a legal need for impact assessments that ask (some) of these questions https://t.co/auiApVC0TW’ / Twitter. (n.d.). Retrieved 22 March 2022, from https://twitter.com/SciBeh/status/1485927221449613314

  15. Feb 2022
    1. Tseng, H. F., Ackerson, B. K., Luo, Y., Sy, L. S., Talarico, C. A., Tian, Y., Bruxvoort, K. J., Tubert, J. E., Florea, A., Ku, J. H., Lee, G. S., Choi, S. K., Takhar, H. S., Aragones, M., & Qian, L. (2022). Effectiveness of mRNA-1273 against SARS-CoV-2 Omicron and Delta variants. Nature Medicine, 1–1. https://doi.org/10.1038/s41591-022-01753-y

    1. Auger, K. A., Shah, S. S., Richardson, T., Hartley, D., Hall, M., Warniment, A., Timmons, K., Bosse, D., Ferris, S. A., Brady, P. W., Schondelmeyer, A. C., & Thomson, J. E. (2020). Association Between Statewide School Closure and COVID-19 Incidence and Mortality in the US. JAMA, 324(9), 859–870. https://doi.org/10.1001/jama.2020.14348

    1. Deepti Gurdasani. (2022, January 10). Lots of people dismissing links between COVID-19 and all-cause diabetes. An association that’s been shown in multiple studies- whether this increase is due to more diabetes or SARS2 precipitating diabetic keto-acidosis allowing these to be diagnosed is not known. A brief look👇 [Tweet]. @dgurdasani1. https://twitter.com/dgurdasani1/status/1480546865812840450

    1. ReconfigBehSci. (2022, January 20). @timcolbourn @OmicronData As I said before, it’s not the function of this account to argue/advocate covid policies, but I will comment on the shape of the argument. The use of the frame “just delay” here seems hugely prejudicial. We don’t talk that way about flu or other diseases we might get repeatedly [Tweet]. @SciBeh. https://twitter.com/SciBeh/status/1484074977964011520

  16. Jan 2022
    1. ReconfigBehSci on Twitter: “RT @AliHMokdad: Vaccine effectiveness against BA.1 and BA.2. After 2 doses it was 9% (7-10%) and 13% (-26-40%) respectively for BA.1 and BA…” / Twitter. (n.d.). Retrieved January 30, 2022, from https://twitter.com/SciBeh/status/1487123660771106821

    1. James 💙 Neill - 😷 🇪🇺🇮🇪🇬🇧🔶. (2022, January 23). Of 51,141 deaths due to ischaemic heart diseases 32,872 (64.3%) had pre-existing conditions.💔 Do those 33k heart disease deaths not count? Or is an absence of pre-existing conditions only required for Covid deaths...😡⁉️ Source: ONS England 2019 [Tweet]. @jneill. https://twitter.com/jneill/status/1485327886164844546

  17. Dec 2021
  18. Nov 2021
    1. Cerebrospinal fluid and plasma biomarkers, as well as amyloid imaging markers, can offer information about neuropathological symptoms of AD, when no evidence markers for hippocampal volume loss can be accurately exported from MRI scanning [49]
  19. Oct 2021
    1. Prof. Akiko Iwasaki. (2021, September 23). Thankfully, we have not seen any evidence of antibody-dependent enhancement of infection or disease by any COVID vaccines to date. Vaccine are not making infections worse, and are very effective in preventing disease. [Tweet]. @VirusesImmunity. https://twitter.com/VirusesImmunity/status/1441074260534075392

    1. Magusali, N., Graham, A. C., Piers, T. M., Panichnantakul, P., Yaman, U., Shoai, M., Reynolds, R. H., Botia, J. A., Brookes, K. J., Guetta-Baranes, T., Bellou, E., Bayram, S., Sokolova, D., Ryten, M., Sala Frigerio, C., Escott-Price, V., Morgan, K., Pocock, J. M., Hardy, J., & Salih, D. A. (2021). A genetic link between risk for Alzheimer’s disease and severe COVID-19 outcomes via the OAS1 gene. Brain, awab337. https://doi.org/10.1093/brain/awab337

  20. Sep 2021
    1. Lee, J. W., Su, Y., Baloni, P., Chen, D., Pavlovitch-Bedzyk, A. J., Yuan, D., Duvvuri, V. R., Ng, R. H., Choi, J., Xie, J., Zhang, R., Murray, K., Kornilov, S., Smith, B., Magis, A. T., Hoon, D. S. B., Hadlock, J. J., Goldman, J. D., Price, N. D., … Heath, J. R. (2021). Integrated analysis of plasma and single immune cells uncovers metabolic changes in individuals with COVID-19. Nature Biotechnology, 1–11. https://doi.org/10.1038/s41587-021-01020-4

    1. Twohig, K. A., Nyberg, T., Zaidi, A., Thelwall, S., Sinnathamby, M. A., Aliabadi, S., Seaman, S. R., Harris, R. J., Hope, R., Lopez-Bernal, J., Gallagher, E., Charlett, A., Angelis, D. D., Presanis, A. M., Dabrera, G., Koshy, C., Ash, A., Wise, E., Moore, N., … Gunson, R. (2021). Hospital admission and emergency care attendance risk for SARS-CoV-2 delta (B.1.617.2) compared with alpha (B.1.1.7) variants of concern: A cohort study. The Lancet Infectious Diseases, 0(0). https://doi.org/10.1016/S1473-3099(21)00475-8

    1. Bracher, J., Wolffram, D., Deuschel, J., Görgen, K., Ketterer, J. L., Ullrich, A., Abbott, S., Barbarossa, M. V., Bertsimas, D., Bhatia, S., Bodych, M., Bosse, N. I., Burgard, J. P., Castro, L., Fairchild, G., Fuhrmann, J., Funk, S., Gogolewski, K., Gu, Q., … Xu, F. T. (2021). A pre-registered short-term forecasting study of COVID-19 in Germany and Poland during the second wave. Nature Communications, 12(1), 5173. https://doi.org/10.1038/s41467-021-25207-0

  21. Aug 2021
  22. Jul 2021
    1. typhoid diet chart in hindi(health and disease)

      typhoid diet chart in hindi(health and disease):in this pin you can see about typhoid diet chart in hindi and food in typhoid. food should be eat and not in typhoid

    1. World Health Organization (WHO). (2021, May 31). Today WHO has announced a new naming system for key #COVID19 variants. The labels are based on the Greek alphabet (i.e. Alpha, Beta, Gamma, etc), making them simple, easy to say and remember. 👉 https://t.co/aYCZfspZyb https://t.co/Gxt14fwVqF [Tweet]. @WHO. https://twitter.com/WHO/status/1399432092333883393

  23. Jun 2021
    1. UK is with EU. (2021, January 18). ..The reason we are in this third lockdown is because of the anti lockdowners like Lord Sumption ..We are going in circles, countries who have done well controlled the virus and now have an economic recovery ..And every life matters #GMB @devisridhar speaking truth to power https://t.co/U3BBV0uUSb [Tweet]. @ukiswitheu. https://twitter.com/ukiswitheu/status/1351089812799950850

  24. May 2021
    1. severe patients

      Garcia-Beltran et al showed that severely ill patients had the highest levels of antibodies. Anti-RBD IgG neutralisation was reduced in severely ill patients. The authors developed an antibody neutralisation potency index to indicate patients more likely to develop severe disease.


      Garcia-Beltran WF, Lam EC, Astudillo MG, Yang D, Miller TE, Feldman J, et al. COVID-19-neutralizing antibodies predict disease severity and survival. Cell. 2021;184(2):476-88.e11.

    2. SARS-CoV-2 positive children

      Some children present with severe secondary effects in response to COVID-19, similar to Kawasaki disease, termed multisystem inflammatory disease in children (MIS-C). MIS-C patients present with higher frequencies of CD4+ and CD8+ T cells and lower levels of IL-17A, ESDN and TNF-β (1, 2, 3, 4). Additionally, children with MIS-C demonstrate an increase in IgG antibodies but low IgM antibodies (2). Data suggests that binding of autoantibodies to proteins involved in immune cell signalling and in within the vasculature might explain the autoimmune reactivity contributing to MIS-C pathology (2, 4).


      1)Verdoni L, Mazza A, Gervasoni A, Martelli L, Ruggeri M, Ciuffreda M, et al. An outbreak of severe Kawasaki-like disease at the Italian epicentre of the SARS-CoV-2 epidemic: an observational cohort study. Lancet. 2020;395(10239):1771-8.

      2)Consiglio CR, Cotugno N, Sardh F, Pou C, Amodio D, Rodriguez L, et al. The Immunology of Multisystem Inflammatory Syndrome in Children with COVID-19. Cell. 2020;183(4):968-81 e7.

      3) Vella L, Giles JR, Baxter AE, Oldridge DA, Diorio C, Kuri-Cervantes L, et al. Deep Immune Profiling of MIS-C demonstrates marked but transient immune activation compared to adult and pediatric COVID-19. medRxiv. 2020.

      4) Gruber CN, Patel RS, Trachtman R, Lepow L, Amanat F, Krammer F, et al. Mapping Systemic Inflammation and Antibody Responses in Multisystem Inflammatory Syndrome in Children (MIS-C). Cell. 2020;183(4):982-95 e14.

    1. Andre, F., Booy, R., Bock, H., Clemens, J., Datta, S., John, T., Lee, B., Lolekha, S., Peltola, H., Ruff, T., Santosham, M., & Schmitt, H. (2008). Vaccination greatly reduces disease, disability, death and inequity worldwide. Bulletin of the World Health Organization, 86(2), 140–146. https://doi.org/10.2471/BLT.07.040089

    1. Howard, J., Huang, A., Li, Z., Tufekci, Z., Zdimal, V., Westhuizen, H.-M. van der, Delft, A. von, Price, A., Fridman, L., Tang, L.-H., Tang, V., Watson, G. L., Bax, C. E., Shaikh, R., Questier, F., Hernandez, D., Chu, L. F., Ramirez, C. M., & Rimoin, A. W. (2021). An evidence review of face masks against COVID-19. Proceedings of the National Academy of Sciences, 118(4). https://doi.org/10.1073/pnas.2014564118