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  1. Last 7 days
  2. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    FAM134B-mediated ER-phagy degrades APP and suppresses Alzheimer’s disease pathology
    37
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    pmc.ncbi.nlm.nih.gov/articles/PMC13324857/
  3. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    Confined migration induces non-lethal DNA damage in developing neurons
    3
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    pmc.ncbi.nlm.nih.gov/articles/PMC13293896/
  4. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    A brain reward circuit inhibited by next-generation weight-loss drugs in mice
    22
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    pmc.ncbi.nlm.nih.gov/articles/PMC13293854/
  5. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    IL-22 promotes genesis of small intestinal secretory cells that protect against cholera in mice
    4
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    pmc.ncbi.nlm.nih.gov/articles/PMC13310123/
  6. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    Efficient in vivo pharmacological inhibition of ΔFOSB, an AP-1 transcription factor, in brain
    1
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    pmc.ncbi.nlm.nih.gov/articles/PMC13288968/
  7. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    Microtubule binding protein Togaram1 is required for proper development of mammalian forebrain and neural primary cilia
    2
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    pmc.ncbi.nlm.nih.gov/articles/PMC13309068/
  8. www.sciencedirect.com www.sciencedirect.com
    Protocol for semi-automatic quantitative bioimaging analysis of synapse loss
    10
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    sciencedirect.com/science/article/pii/S266616672600328X
  9. www.sciencedirect.com www.sciencedirect.com
    Protocol for ultrasound-guided injection into the murine portal vein to initiate liver metastasis
    2
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    sciencedirect.com/science/article/pii/S2666166726003230
  10. 54.241.53.176 54.241.53.176
    '-html.html
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    54.241.53.176/b66822b2907bb6d00b9e83a81725f62d71cd041a/'-html.html
  11. www.sciencedirect.com www.sciencedirect.com
    A cold-induced GDF15-secreting adipocyte subpopulation regulates energy homeostasis through endocrine signaling
    4
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    sciencedirect.com/science/article/pii/S2211124726006819
  12. www.sciencedirect.com www.sciencedirect.com
    An IL-15 fusion with albumin-binding domain boosts immunotherapy therapy in glioblastoma via FGF-2 competition regulating FGFR1/2
    5
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    sciencedirect.com/science/article/pii/S0304383526004581
  13. onlinelibrary.wiley.com onlinelibrary.wiley.com
    Oxygen Response Index: A Potential OE-MRI-Derived Non-Invasive Biomarker for Assessing Radiation Treatment Efficacy
    1
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    onlinelibrary.wiley.com/doi/10.1002/mrm.70480
  14. onlinelibrary.wiley.com onlinelibrary.wiley.com
    Leishmanicidal Potential of Eugenia pyriformis Cambess. (Myrtaceae) Leaf Extracts: Metabolomics and Mechanism of Action
    1
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    onlinelibrary.wiley.com/doi/10.1002/cbdv.71471
  15. onlinelibrary.wiley.com onlinelibrary.wiley.com
    LC–MS/MS-QTOF Based Phytochemical Characterization and In Vitro Pharmacological Potentials of the Endemic Variety, Humboldtia brunonis var. raktapushpa
    4
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    onlinelibrary.wiley.com/doi/10.1002/cbdv.71466
  16. onlinelibrary.wiley.com onlinelibrary.wiley.com
    Three Chromene Meroterpenoids With Potential Anti-Inflammatory Activity From Rhododendron anthopogonoides
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    onlinelibrary.wiley.com/doi/10.1002/cbdv.71465
  17. onlinelibrary.wiley.com onlinelibrary.wiley.com
    Terpenoids From Leaves of Diospyros kaki and Their Neuroprotective Effects
    1
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    onlinelibrary.wiley.com/doi/10.1002/cbdv.71443
  18. onlinelibrary.wiley.com onlinelibrary.wiley.com
    Microenvironmental Cues That Regulate Cancer Cell Dormancy in Estrogen-Receptor Positive and Triple-Negative Breast Cancer Cell Lines
    4
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    onlinelibrary.wiley.com/doi/full/10.1002/cam4.72059
  19. advanced.onlinelibrary.wiley.com advanced.onlinelibrary.wiley.com
    Modulation of Lung Adenocarcinoma by Phosphorylated FOXN3-Mediated Transcriptional Inactivation of p53
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    advanced.onlinelibrary.wiley.com/doi/10.1002/advs.76449
  20. advanced.onlinelibrary.wiley.com advanced.onlinelibrary.wiley.com
    Cerium Nanoparticle-Mediated Inhibition of the NSUN2/m5C Axis Suppresses Synovial Aggression in Rheumatoid Arthritis
    1
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    advanced.onlinelibrary.wiley.com/doi/10.1002/advs.76401
  21. advanced.onlinelibrary.wiley.com advanced.onlinelibrary.wiley.com
    WT1-Targeted Oral Bifidobacterium longum Vaccine Enhances Checkpoint Blockade Efficacy in Pancreatic Cancer
    1
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    advanced.onlinelibrary.wiley.com/doi/10.1002/advs.202524323
  22. febs.onlinelibrary.wiley.com febs.onlinelibrary.wiley.com
    FEBS Press
    1
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    febs.onlinelibrary.wiley.com/doi/10.1002/2211-5463.70294
  23. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    CortexCAM: A Camera Array Microscope for Cortex-Wide Cellular Imaging in Freely Locomoting Mice
    1
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    pmc.ncbi.nlm.nih.gov/articles/PMC13252553/
  24. tesda-course.pages.dev tesda-course.pages.dev
    Lesson 1 · Find Numbers in Workplace Documents — TESDA Foundational Skills
    3
    1. emmieorbon 08 Jul 2026
      Measuring jugReadingOil level marked at750 milliliters

      I suggest presenting this information in a diagram or illustration since the question asks for the oil level. Providing the value of 750 directly encourages students to simply copy the given information rather than locate it from the provided data.

    2. emmieorbon 08 Jul 2026
      He keeps his Daily Time Record (DTR), the sheet where he writes his time in and time out each day

      Since the question asks for the value of psi, the DTR does not provide any information needed to solve the problem and only adds unnecessary length. I suggest removing it to make the question more concise.

    3. emmieorbon 08 Jul 2026
      Date filedAugust 3

      Sick leave should be filed immediately upon returning to work and not before.

      This could be changed to Wellness Leave or change the reason of absence.

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    tesda-course.pages.dev/build/num-2a-l1
  25. accessphysiotherapy.mhmedical.com accessphysiotherapy.mhmedical.com
    The Shoulder
    1
    1. federico.canosa 08 Jul 2026
      The G-H joint is a true synovial joint connecting the upper extremity to the trunk as part of the upper kinetic chain. The G-H joint is a ball-and-socket joint—the humeral head forms roughly half a ball or sphere (Fig. 16-1), whereas the glenoid fossa forms the socket. The orientation of the articular surface of the glenoid is posterior (retroverted) relative to the transverse plane of the scapular axis. The degree of retroversion varies but on average is less than 7 degrees.2 An increase in the retroversion angle predisposes the shoulder to posterior G-H joint instability and posterior labral tears, whereas a decrease in the retroversion angle (anteversion) predisposes the shoulder to anterior instability.3

      Estudiar bien este concepto

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    accessphysiotherapy.mhmedical.com/content.aspx
  26. reviewmyemails.com reviewmyemails.com
    Contact Review My Emails
    1
    1. YT_reviewmyemails 08 Jul 2026
      Security · account · everything else The team Security

      Let's ensure we use other people's team faces on this page because when I was just mine three times so take it from the above page you could take Bruno and Vy for example

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    reviewmyemails.com/website/contact
  27. reviewmyemails.com reviewmyemails.com
    Done-for-You List Cleaning
    1
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    reviewmyemails.com/website/done-for-you/
  28. www.propublica.org www.propublica.org
    How BP Execs Influenced a Climate Study That Shaped a Generation of Global Policy
    8
    2. HeinzWittenbrink 08 Jul 2026
      Exxon started giving money for climate research to Columbia University’s Lamont-Doherty Earth Observatory in the late 1970s. Then in 1991, the company funded the launch of the Joint Program on the Science and Policy of Global Change at Massachusetts Institute of Technology, according to the program’s former co-director, Henry Jacoby. Chevron, Shell and BP also later supported the program, which developed influential climate-related models.
      company: ExxonMobil Institution: Lamont-Doherty Earth Observatory Institution: Joint Programm in the Science and Policy of Global Change expert: Henry Jacoby company: Chevron company: Shell
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    propublica.org/article/wedges-climate-research-bp-fossil-fuel-princeton
  29. reviewmyemails.com reviewmyemails.com
    Review My Emails
    3
    1. YT_reviewmyemails 08 Jul 2026
      Drop your list here. CSV, XLSX, up to 100MB. First

      Can we add a small simple animation here that won't slow down the page as if something was being dragged dropped into it or the color changing or something

    3. YT_reviewmyemails 08 Jul 2026
      Your newsletterJuly issue: the numbers are inSPAM Your newsletterJune issue

      Can we add more lines that shows like a email report so the open rate so it would be the 808 out of 58098 but as a percentage and then a small click rate click to open rate a bounce one and a spam rate in an unsubscribe one so spam complaint rate would be 0% bounce rate will be 0% the unsubscribe would be like 0.1% and then for the open so you can do the calculation and then take a click rate that would make sense based on the amount of emails over actually opened

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    reviewmyemails.com/website
  30. learn.microsoft.com learn.microsoft.com
    はじめに - Training
    1
    1. nz98 08 Jul 2026
      このモジュールでは、開発者が GitHub Copilot を使用するさまざまな方法について説明します。 生産性の向上、開発者の好みに適合し、ソフトウェア開発ライフサイクル (SDLC) への影響について説明します。

      SDLC

      ss/psy/cp/agent/code/sdlc
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    learn.microsoft.com/ja-jp/training/modules/developer-use-cases-for-ai-with-github-copilot/1-introduction
  31. learn.microsoft.com learn.microsoft.com
    GitHub Copilot でのコード補完 - Training
    1
    1. nz98 08 Jul 2026
      コメントドリブン コード生成

      Comment-Driven Development (CDD) is a software development approach where you write the code's documentation and logical steps in plain English comments before writing any actual executable code

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    learn.microsoft.com/ja-jp/training/modules/github-copilot-across-environments/1-introduction
  32. www.medrxiv.org www.medrxiv.org
    Single-cell transcriptome-wide Mendelian randomization and colocalization analyses reveal immune-cell-specific mechanisms and actionable drug targets in prostate cancer
    3
    1. Public_Reviews 08 Jul 2026

      eLife Assessment

      This study presents a useful compendium of triangulated single-cell eQTLs, Mendelian randomisation and colocalization of genetic signals in prostate cancer datasets. Biological interpretation in the context of the aging prostate gland, the tumour microenvironment and immune cell specificity is incomplete, so this study is a starting point for further study, and would require validation of the resulting putative causal genes.

      Summary
    2. Public_Reviews 08 Jul 2026

      Reviewer #1 (Public review):

      Summary:

      Using Mendelian randomisation on available GWAS data, the investigators identified eGenes associated with prostate cancer and applied the data to define relevant immune cell types involved. Additional analysis was performed to explore potential candidate targets and agents from licensed medicines.

      This is an interesting approach as the investigators have expertise in other research fields, applied here to prostate cancers. The use of three different datasets is significant, and the approach to further analyse implicated eGenes in drug target analysis is relevant and timely.

      A particular strength is taking putative genes from Mendelian randomisation analysis to target and potential drug agents.

      Some aspects of the study would need to be clarified to enable interpretation of the findings in the context of the prostate gland and prostate cancers: expanding the descriptions of the supporting Supplementary Data and Tables, explanations of the analysis for the general reader, and clarification of the selection of eGenes (Figure 5).

      Review 1
    3. Public_Reviews 08 Jul 2026

      Reviewer #2 (Public review):

      Summary:

      This study integrates bulk and single-cell transcriptomic-derived eQTLs from two separate consortia (PRACTICAL and Finngen) to identify immune-cell-specific therapeutic targets in prostate cancer. Mendelian randomization and Bayesian colocalization have been used to produce druggable eGene modules through STRING and DrugBank.

      This is an interesting study that is attempting to address risk-associated, immune-specific transcriptomic repertoires in prostate cancer. It is knitting together concepts of drug repurposing and prostate cancer immunogenicity. This is an entirely computational study, which would benefit from some wet lab experimental validation.

      It is very tricky to attribute cell-type-specific responses, especially when the majority of genes involved represent cytoskeletal or stress responses, which are ubiquitous throughout the prostate microenvironment. This point is relevant for the drug repurposing section: if these drugs are targeting immune cell-specific repertoires, what would the response be of the entire environment? It would be useful to contextualize the validity of each proposed therapy in a specific prostate cancer context and the involvement of AR antagonism or radiotherapy.

      Strengths and limitations of this study:

      Strengths:

      This is a scientifically interesting and potentially impactful study, particularly in its attempt to integrate immune-cell-specific transcriptomics, causal inference, and drug repurposing in prostate cancer. The methodology is well described, and the data (albeit limited) are well analyzed.

      Limitations:

      The central weakness is the overstatement of the conclusions regarding immune-cell-specific causality, without sufficiently contextualizing the biological meaning of the findings.

      Highlighted genes, such as LMNA, XBP1, histone-related genes, and stress-response markers, are ubiquitous regulators involved in fundamental cellular processes, including ageing, unfolded protein response (UPR), integrated stress response (ISR), chromatin remodeling, proliferation, and metabolism. It is unclear whether these signatures truly represent immune mechanisms, or instead reflect broader inflammatory and age-associated biology expected within an ageing glandular organ such as the prostate.

      Immune cell identity alone may not be sufficient to infer biological relevance because immune state characterization (e.g., exhausted versus functional T cells, or distinct macrophage/myeloid phenotypes) is largely absent from the current analysis. The assertion that specific immune populations are correlated with prostate cancer susceptibility is probably an overstatement unless the nature of these cells can also be characterized.

      The interpretation of "causal variants" is not always specified, i.e., what phenotype is being associated: prostate cancer susceptibility, recurrence, progression, or treatment response (e.g. is there direct causality from immune-cell variants to prostate cancer?).

      Overall, there is a need for stronger biological and translational contextualization: how do the identified pathways relate to ageing-associated inflammation, PIN, microbiome-driven inflammatory changes, and stress-response biology in the prostate gland? While the manuscript identifies network hubs and enriched pathways, it often stops short of explaining what these modules biologically represent or how they may influence prostate cancer development, progression, treatment resistance, or immune evasion.

      There are additional publicly available spatial transcriptomic or single-cell datasets which could be used to validate whether the purported immune-cell-specific genes are genuinely enriched in immune populations adjacent to tumour cells. In the drug repurposing analyses, the current study does not explicitly handle prostate cancer subtypes such as HSPC, CRPC, NEPC, or DNPC and co-treatment with androgen receptor antagonism or radiotherapy.

      Review 2
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    medrxiv.org/content/10.64898/2026.03.10.26348013v1
  33. www.biorxiv.org www.biorxiv.org
    Cell cycle-dependent variation in endocytosis drives phenotypic diversity in M. tuberculosis
    3
    1. Public_Reviews 08 Jul 2026

      eLife Assessment

      This useful study explores how macrophage cell-cycle state may influence endocytosis, Mycobacterium tuberculosis uptake, and the intracellular stress experienced by bacteria. While the question is interesting and the experimental approach has promise, the evidence for the central claim that endocytic capacity is specifically regulated by cell-cycle stage is incomplete. The main concern is that fluorescence-based sorting and total-fluorescence measurements likely covary with cell size, so the reported phenotypes could reflect biomass accumulation or other cell-cycle-associated changes rather than endocytic capacity as the causal determinant. As a result, whilst the study raises a hypothesis that is of importance, additional controls are required before the proposed mechanism can be considered well supported.

      Summary
    2. Public_Reviews 08 Jul 2026

      Reviewer #1 (Public review):

      Summary:

      The manuscript- "Cell cycle-dependent variation in endocytosis drives phenotypic diversity in M. tuberculosis" by Subhash et al. demonstrates how host cell heterogeneity shapes intracellular pathogen phenotypes. The central and novel finding of this study (G2-phase cells have higher endocytic capacity and harbour more oxidised Mtb) highlights that a host cell cycle (interphase-driven) changes in endocytic capacity regulate bacterial redox states.

      Strengths:

      Overall, the study is well-executed and conceptually rich, establishing a causal link between host cell cycle progression, endocytic heterogeneity, and M. tuberculosis phenotypic diversity.

      The combination of multiple modalities, including live-cell imaging, flow cytometry, scRNA-seq, and redox-sensitive bacterial reporters, supports these findings and substantially strengthens the biological relevance of the work.

      The writing is generally clear, and the figures are well-organised.

      This work will be of interest to readers across cell biology, microbiology, and infection biology

      Weaknesses:

      However, several central claims are only partially supported, the mechanistic depth is limited, and several experimental and analytical concerns need to be addressed.

      Major Comments:

      (1) The authors demonstrate a correlation between the G2 phase and elevated endocytic capacity. However, the mechanistic link (upstream molecular mechanism) between the cell cycle and endocytic upregulation remains largely unaddressed. The authors speculate that membrane biogenesis during volumetric expansion may drive increased endocytosis and note that lipid biosynthesis genes are upregulated in high-endocytic cells. It would substantially strengthen the paper to test this directly, by examining whether inhibition of lipid biosynthesis (e.g., with fatostatin or cerulenin) selectively reduces the G2-associated increase in endocytic capacity. Alternatively, cyclin-CDK axis perturbations (e.g., CDK1 inhibition with RO-3306 to specifically block G2/M entry) could be used to ask whether cells arrested in G2 maintain elevated endocytosis, helping distinguish cell-cycle-position-dependent from cell-cycle-progression-dependent effects.

      (2) The current data show a clear association between high endocytic capacity and more oxidised Mtb, and the authors (consistent with their prior work) hint at lysosomal delivery as the likely mechanism. However, direct evidence for this in the current paper is limited. An experiment examining phagosomal pH or lysosomal fusion (e.g., using a pH-sensitive reporter or lysotracker) specifically in high- and low-endocytic-capacity cells after infection would help confirm this.

      (3) Temporal resolution of Mtb redox dynamics. The plasticity experiment (Figure 6C-D) is elegant and shows that Mtb redox states revert as host cells divide and daughters enter G1. However, the experiment compares day 0 and day 3 post-sorting, which spans multiple cell divisions. While a finer time resolution (spanning 24h) would establish the causal relationship, the authors could discuss the possibility and consequences of multiple cell divisions between day 0 and day 3 used in the present study.

      (4) Relevance of G2 percentages in differentiated macrophages. In Figure 7 and Supplementary Figure S7, only 4.4-5.7% of THP-1-derived macrophages and 5.7% of BMDMs are in G2. While the authors demonstrate statistically significant differences in Mtb redox states between G1 and G2 macrophages, the biological significance of such a small G2 fraction in a non-dividing population deserves discussion specifically with respect to: a) Are these cells re-entering the cycle? b) Is the G2 designation capturing a distinct functional state rather than active cycling? The authors should include additional markers (e.g., phospho-histone H3 for mitotic cells or BrdU incorporation to test for active S-phase) to characterise this population and clarify its identity and origin in differentiated macrophages, thereby meaningfully informing interpretation.

      In conclusion, this is an important mechanism-driven study that highlights an important link in host-driven bacterial phenotypic heterogeneity. The experiments are thorough, the model is well-supported, and the study has implications for infection biology.

      Review 1
    3. Public_Reviews 08 Jul 2026

      Reviewer #2 (Public review):

      In this manuscript, the authors utilize a combination of techniques to show that macrophage endocytic capacity is partially dictated by cell-cycle stage, that Mycobacterium tuberculosis (Mtb) more readily infects macrophages that are in G2/M -phases, and that bacteria that are internalized by macrophages at different stages of the cell-cycle experience different levels of intracellular stress (as reported by the redox state of the bacteria). Furthermore, the authors provide evidence that terminally differentiated macrophages retain memory of the cell-cycle stage that they were in prior to differentiation, at least in the context of endocytic capacity.

      This work provides evidence for the growing idea that fundamental heterogeneity in both host and bacterial organisms can alter the host-pathogen relationship in important ways. However, based on the current data, I am not convinced that the manuscript establishes endocytic capacity as the causal link between macrophage cell-cycle stage and bacterial state. The main issue is that fluorescence-based sorting for cell-cycle stage is likely to covary with cell size. Larger cells, including those later in the cell cycle, may be more likely to fall into the "high" fluorescence gate, while smaller cells may be enriched in the "low" population. Therefore, the observed phenotypes may still be cell-cycle-associated, but the causal determinant could be a correlated feature of cell-cycle progression rather than endocytic capacity itself. This is a significant caveat because nearly all the data, including the live-cell imaging following individual cells, rely on 'total' fluorescence, which will scale strongly with cell size.

      If the authors' conclusion that endocytic capacity is cell-cycle regulated holds true after appropriate controls, this would significantly advance our understanding of the causal interplay between host cell-cycle state, endocytosis, and Mtb physiology. However, an alternative interpretation is that the observed differences in Mtb uptake and bacterial redox state are associated with cell-cycle stage but are not caused directly by differences in endocytic capacity. For example, they could instead reflect other cell-cycle-linked changes in macrophage physiology, such as cell size, intracellular volume, metabolic state, or some other mechanism important for Mtb pathogenesis. If the authors find that their data are best explained by cell-cycle stage independent of endocytic capacity, this would still represent an important advance. However, in that case, the manuscript should clearly distinguish the association with cell-cycle state from the downstream effector mechanisms, which would remain to be determined.

      Strengths:

      The authors utilize various macrophage models for their studies, which is important considering the variability in macrophage behavior, as well as the growing evidence that differences between mouse and human macrophages are relevant for Mtb infection.

      Weaknesses:

      The most important caveat is the covariance between fluorescence-based reporters and cell size. This concern applies to both the sorting experiments, which directly measure total fluorescence, and the time-lapse microscopy experiments, in which the authors show total fluorescence rather than mean, area-normalized fluorescence in Figure 3C. This could be explained by biomass accumulation alone, rather than by a specific cell-cycle-dependent increase in endocytic capacity. Without distinguishing total signal from concentration or activity per unit cell area/volume, it is difficult to conclude that endocytosis itself is regulated by cell-cycle stage rather than simply scaling with cell size.

      Although the authors provide some evidence that the mean GFP intensity, which more closely reflects concentration, differs between the sorted populations in Figure 3B, they do not report statistics for this comparison. Moreover, this control is not carried through the rest of the manuscript, including in key experiments such as Figure 2B. As a result, it remains difficult to determine whether the observed differences between "high" and "low" populations reflect cell-cycle state specifically or instead reflect differences in total reporter fluorescence driven entirely by cell size.

      The evidence for cell-cycle-dependent effects would be more convincing if the authors included additional controls. For example, they could:

      (1) Plot both mean GFP intensity and total GFP intensity in Figure 3B, ideally alongside an unrelated fluorescent reporter that does not vary across the cell cycle. This would help distinguish changes in reporter concentration from changes driven by cell size or total fluorescence.

      (2) Sort cells based on an unrelated fluorescent marker and test whether the same phenotypes - infectivity, dextran uptake, bacterial redox state, etc. - differ between high- and low-fluorescence populations. If these phenotypes are specific to the cell-cycle reporter and not observed with an unrelated marker, this would strengthen the conclusion that the effects are linked to cell-cycle state rather than to fluorescence intensity, cell size, or sorting artifacts.

      Review 2
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    biorxiv.org/content/10.1101/2025.09.09.673684v1
  34. tesda-course.pages.dev tesda-course.pages.dev
    Lesson 1 · Recognize common workplace words and signs — TESDA Foundational Skills
    6
    3. bvluna 08 Jul 2026
      Q1. A sign shows a red circle with a red line across a lit cigarette. What does it tell you?

      Provide different sets of examples for the content and quick practice activities to reinforce understanding. Same comment applies to other quick practice

    4. bvluna 08 Jul 2026
      A common trap is to read a "do not" sign as a "you may" sign. If your reading is rusty, that mix-up is normal — check the red line first. A red line across a picture always means the action is not allowed.

      The phrase “if your reading is rusty” may sound judgmental or demeaning because it suggests that the learner’s reading ability has deteriorated. It may also embarrass learners with literacy difficulties.

    5. bvluna 08 Jul 2026
      Rosario cooks at a carinderia (a small eatery) in Pagadian City. Her time card records her shift. Table 2 shows the card after she fills it in. Table 2. Rosario's time card FieldEntryNameRosario BelarminoDateJune 5Time in8:00 AMTime out5:00 PMHours worked8 Here is how Rosario fills it in: She starts cooking at 8:00 in the morning. "Time in" means the start time, so 8:00 AM goes there.She leaves at 5:00 in the afternoon. "Time out" means the leaving time, so 5:00 PM goes there."Hours worked" asks for a count of hours, not a clock time. From 8:00 AM to 5:00 PM is 9 hours. She takes a 1-hour meal break, so she writes 8.

      The scenarios we use should reflect actual or closely comparable workplace practices. “Time in” is typically recorded when the worker arrives and logs in through the attendance system or logbook, not when the worker begins cooking or performing assigned tasks. Improve the sample scenarios to avoid inaccurate or misleading representations of workplace procedures.

    6. bvluna 08 Jul 2026
      Signs and labels that warn you Many signs and labels warn you about danger. Each one carries one clear message. Table 2 shows three warnings you will see often. Table 2. Common warning signs and labels Sign or labelWhat it meansWET FLOORThe floor is slippery. Walk with care.NO ENTRYDo not go in.FLAMMABLEThis can catch fire. Keep it away from fire and heat.

      Present the content through images or illustrations rather than text alone. Include more than three examples, where applicable, to provide learners with a wider range of samples.

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    tesda-course.pages.dev/build/lit-2a-l1
  35. www.biorxiv.org www.biorxiv.org
    Synthetic torpor in the rat protects the heart from ischaemia-reperfusion injury
    4
    1. Public_Reviews 08 Jul 2026

      eLife Assessment

      This important submission from Ambler and colleagues brings new insights into how torpor conditions may confer resilience in cases of cardioprotection. It has novelty, which can be enhanced by additional in vivo support. The study is backed by solid evidence, and represents a unique interoceptive mechanism of interest.

      Summary
    2. Public_Reviews 08 Jul 2026

      Reviewer #1 (Public review):

      Summary:

      Torpor can be induced by chemogenetic activation of the medial preoptic area. This activation leads to protection from myocardial infarction in an isolated heart preparation despite normalization of the ambient temperature, thus, in principle, uncoupling hypothermia from torpor-induced neuroprotection. Putative pathways of protection are suggested by proteomic studies.

      Strengths:

      (1) Elegant strategy for inducing torpor in rats.

      (2) Appropriate controls for verifying the neuron transducer.

      (3) Cardiac protection is significant and appears independent of hypothermia.

      (4) Interesting omic strategy to begin to find established and novel pathways mediating organ autonomous torpor-induced protection.

      Weaknesses:

      (1) The study would benefit from using inhibitory chemogenetics of the same neurons to demonstrate that this might make cardiac response to ischemia worse.

      (2) Infecting an area of the brain not known to be involved in torpor would be a useful control.

      (3) In vivo cardio protection seems essential as the validation of the strategy requires support that is in the intact animal.

      (4) The assumption that the positive effects of torpor are mediated via a phosphoproteomic change rather than a translational or transcriptional control mechanism is not established.

      (5) A 40 percent reduction in infarct size may work for genetically identical rats with no co-morbidities, but is unlikely to be significant enough to weather the variability that emerges in humans because of these differences and more. The question is not what the mechanism is, but how do we make it more robust? Overall, this is at best a preliminary data set that requires more experiments to deliver on its immense promise.

      Review 1
    3. Public_Reviews 08 Jul 2026

      Reviewer #2 (Public review):

      Summary:

      Elley and colleagues induced a synthetic torpor-like state in rats (a non-hibernating species) by chemogenetically activating neurons in the medial preoptic area of the hypothalamus. They show that this state substantially reduced cardiac infarct size in an ex vivo ischemia-reperfusion model. They further report that protection persisted when ambient temperature was raised to prevent hypothermia, and used exploratory phosphoproteomics to identify candidate cardioprotective signaling pathways.

      Strengths:

      This is the first demonstration that a torpor-like state is cardioprotective in a species that does not naturally enter torpor, which meaningfully advances the potential clinical utility of synthetic torpor. The experimental design is logical, and the controls are generally appropriate. The characterisation of the responsible neuronal population using ISH against QPLOT markers adds mechanistic depth and supports the cross-species conservation argument. The phosphoproteomic analysis, though exploratory, generates plausible and biologically coherent hypotheses grounded in the hibernation literature.

      Weaknesses:

      The primary weakness is that the central conclusion - that hypothermia is not necessary for cardioprotection - exceeds the evidence. The thermoneutral groups were not demonstrably normothermic (36.4 vs 37.05{degree sign}C, p=0.44 with n=6), core temperature telemetry was absent in the majority of control animals contributing to the infarct endpoint, and the decisive test, i.e., a correlation between individual nadir temperature and infarct size, was never performed. Additional weaknesses include the absence of sex-stratified analysis despite known estrogenic contributions to torpor

      Review 2
    4. Public_Reviews 08 Jul 2026

      Reviewer #3 (Public review):

      Summary:

      The manuscript by Elley and colleagues describes experiments on the effects of synthetic torpor on ex vivo heart ischemia. The key aspect of the study was the use of viral-vector mediated manipulation of the hypothalamic medial preoptic area (MPA) in rats. They used AAV-CaMKIIa-hM3D(Gq). The authors report that chemogenetic activation of the MPA prior to an ex vivo heart ischemia-reperfusion insult induces cardio protection against infarct size that is independent of prior in vivo hypothermia. Phosphoproteomic analysis of cardiac tissue suggested changes in cell survival and death pathways.

      Strengths:

      This study has important strengths. The idea is novel. The experimental design is appropriately rationalized and fascinating. The manuscript is written and presented concisely.

      Weaknesses:

      The study has important weaknesses in the experimental design and validation of the model.

      (1) The study is based on the use of a DREADD-designed viral vector (AAV-CaMKIIa-hM3D(Gq) -mCherry) that is activated by 2 mg/kg IP injection of CNO. The rationale is to putatively activate the MPA. The authors show no evidence for chemogenetic activation of neurons in the MPA. This could be done using a variety of different approaches, even phosphoproteomics.

      (2) The stereotaxic injections are difficult to precisely and locally place, particularly bilaterally. Figure 2F is only a schematic. It would be better to show actual low magnification brain sections (bregma +0.12 to -0.48) from a representative rat to show the placement of the AAV.

      (3) The control rats were injected with AAV-CaMKIIa-EGFP. Why was EGFP used instead of mCherry for the control?

      (4) Ideally, a mutant non-activatable variant of AAV-CaMKIIa-hM3D(Gq) should have been used for a better control.

      (5) The authors should comment on whether there is any neurotoxicity in the MPA associated with the forced AAV expression of hM3D-Gq.

      (6) Is there any inflammatory pathology seen in the MPA with AAV transduction?

      (7) There are no experiments to show that the systemic torpor is specifically associated with the MPA region. Experiments should be done with injections of AAV-CaMKIIa-hM3D(Gq)-mCherry placed in other brain regions, for example, the nearby nucleus accumbens.

      (8) The mapping of the distribution of neurons responsible for synthetic torpor is not mechanistic enough and is not directly to the point. While excitatory and inhibitory markers are examined, a more interesting and deeper approach would have been to use glutamate receptor antagonists to manipulate the torpor response.

      (9) The ischemia and reperfusion aspects of the Lagendorff method need to be clarified. The isolated hearts are already ischemic after their removal from the rat. The reperfusion aspect is caused by reflow of blood to generate oxidative stress, but in the ex vivo model, is there really reperfusion injury?

      (10) The authors show that whole animal oxygen consumption is reduced in the torpor state. The measurement is crude and most likely reflects the inactivity of the animal's skeletal muscle in the torpor state. A more relevant and direct experiment would be to do oxygen consumption (or Seahorse) assays on extracts of the isolated hearts.

      (11) The authors report that the synthetic torpor induces bradycardia. There is no follow-up on this important observation. The MPA-heart connection is not analyzed. (A) Is the link through cardiovascular centers in the brainstem? (B) Is the torpor-induced bradycardia mediated through increased parasympathetic or decreased sympathetic autonomic tone? Pharmacological experiments could also be done.

      Review 3
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  36. search.brave.com search.brave.com
    Brave Search
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  37. www.biorxiv.org www.biorxiv.org
    Electroconvulsive stimulation drives cortical spreading depression dependent immediate early gene expression in mice
    4
    1. Public_Reviews 08 Jul 2026

      eLife Assessment

      This study addresses a recent discovery by others that electroconvulsive therapy (ECT) generates seizure activity and spreading depolarization (SD), reflected in large increases in calcium, which can be followed by imaging calcium fluctuations in neurons. This work is useful. However, the evidence to show that SD, rather than seizures, confers the neuroplastic and other therapeutic effects of ECT is incomplete.

      Summary
    2. Public_Reviews 08 Jul 2026

      Reviewer #1 (Public review):

      The work corroborates the idea, recently suggested by Rosenthal et al. (2025), that spreading depolarization is involved in the mechanisms of electroconvulsive therapy. Using a mouse model of electroconvulsive therapy and various sophisticated approaches to visualize cortical activity, the authors provide an extensive description of traveling calcium waves induced by electroconvulsive stimulation. The study confirms that the calcium events have properties typical of cortical spreading depolarization and seeks to show that the calcium/SD waves mediate therapeutic and neuroplastic effects of electroconvulsive therapy. The authors find that after electroconvulsive stimulation associated with calcium/SD waves, Fos expression increases widely; in the cortex, this increase is localized to the hemisphere affected by calcium waves. They show that some EEG predictors of the beneficial effects of electroconvulsive therapy correlate with the occurrence of calcium/SD waves. Despite the solid methodology and the study's interesting, its conclusions are not fully supported by the data.

      In particular:

      (1)The title of the paper claims that "electroconvulsive stimulation drives cortical spreading depolarization dependent immediate early gene expression". However, immunohistochemical staining shows that Fos expression increases not only in the cortex but also in many subcortical regions, including the hippocampus and amygdala (Figure 5A). Really, conventional electroconvulsive therapy stimulates nearly the entire brain volume and induces generalized seizure activity that can trigger SD not only in the cortex but also in other brain sites. Therefore, regions beyond the cortex can also drive the effects of electroconvulsive therapy. Next, the authors use Fos staining as a marker of neuronal plasticity. However, Fos is also a marker of preceding neuronal activation. As electroconvulsive stimulation, seizures, and SD are associated with high neural activity, it is unclear whether the observed Fos upregulation results from the prior activation or heralds the subsequent plastic changes. Other markers of neuroplasticity (e.g., BDNF) should also be examined.

      (2) Postictal EEG suppression is one of the most promising correlates of positive clinical outcomes after electroconvulsive therapy. Cortical SD is also tightly coupled with suppression of neuronal activity in affected regions. Although the authors report that postictal suppression is stronger after stimulations with cortical SDs than without SDs, the cortices affected (ipsi) and unaffected (contra) by unilateral cortical calcium/SD events exhibit identical suppression (Figure 6F). The result contradicts established knowledge in the field. If the calcium events are cortical SDs, they should induce EEG suppression only in the affected hemisphere.

      (3) The study states a beneficial role of calcium/SD waves in ECS effects. However, SD alters numerous aspects of brain function, leading to a range of effects that can underlie side effects as well. Assessment of the behavioral effects of stimulation with and without calcium/SD waves can help clarify the issue.

      The results of the work suggest that cortical SD can contribute to electroconvulsive therapy-related mechanisms and help to optimize the stimulation parameters to achieve maximal therapeutic effect.

      Review 1
    3. Public_Reviews 08 Jul 2026

      Reviewer #2 (Public review):

      Summary:

      This manuscript addresses the question of mechanisms underlying the therapeutic effects of electroconvulsive therapy (ECT). Clinical efficacy of ECT in major depression (and other disorders) is well established and has often been assumed to be a direct consequence of seizure activity generated by the current application. However, as the authors point out, this explanation is unsatisfactory. A recent study (Rosenthal et al., 2025) provided evidence that ECT generates a wave of cortical spreading depolarization (CSD) in mice, and initial evidence that similar events were generated in patients undergoing ECT. Based on their observations, Rosenthal et al. proposed that CSD, rather than seizure, may engage plasticity mechanisms that contribute to the brain's clinical response to ECT. The current study adds to that prior work by reporting other consequences of CSD, in addition to sustained Ca2+ elevations. The current study also links EEG characteristics immediately following the ECT with the likelihood of generating a CSD, which can help optimize ECT parameters.

      Strengths:

      An important research topic, linking a large set of rodent studies with a limited clinical EEG data set.

      The data acquisition and analyses appear to be of very high quality, and the main results are well illustrated.

      Association between EEG characteristics linked to good clinical outcome matched by mouse EEG data linked to CSD.

      Characterization of multiple consequences of CSD following ECT in the mouse brain.

      Weaknesses:

      The main characterization of CSD propagation comes from GCaMP Ca2+ measurements, as previously reported (Rosenthal et al., 2025). That prior study also provided key electrophysiological evidence of CSD with a DC shift after ECT in mice (supplemental data). Given the prior evidence for ECT-CSD, the additional measures shown in the current manuscript are fully expected. Thus, the 2-photon imaging of Ca2+ elevations following CSD (Figure 4) is consistent with prior 2-photon imaging studies of CSD, and the complex hemodynamic and pH changes are expected to contribute to propagation of EGFP fluorescence changes (Supplemental Figure 5). These data are well presented, but, contrary to the results section here, these results appear confirmatory rather than necessary to build a case that the key event generated by ECT is a CSD.

      The authors state that "our conclusion that CSD is the primary driver of plasticity is based on its role in driving Fos expression" (line 472). Related to the point above, there is already a very well-established literature showing that CSD leads to rapid and robust Fos expression in rodent cortex, so this is fully consistent with prior work. The prior work, CSD-fos work, should be summarized and/or cited more clearly in the manuscript. Showing that Fos increases only in the hemisphere where there is a large CSD-Ca2+ wave is a clear demonstration of this. While Fos increases can certainly be well linked to plasticity in some experimental paradigms, the implication that Fos increases underlie CSD-induced plasticity and possibly therapeutic effects of ECT is not appropriate. Fos increases after CSD are a reliable marker of the very strong neuronal activation that occurs, but Fos increases are not specific for plasticity and can be activated by challenges that do not generate synaptic plasticity. A range of other gene expression changes have been identified with CSD and may contribute to adaptive plasticity; these could be mentioned alongside speculation about Fos. To support the main conclusions of this paper about CSD driving plasticity via Fos, Fos knockout or knockdown studies are needed, as has been used in prior plasticity studies.

      Review 2
    4. Public_Reviews 08 Jul 2026

      Reviewer #3 (Public review):

      Summary:

      This manuscript combines widefield calcium imaging, electroencephalography, 2-photon imaging, and immunohistochemistry in mice to re-demonstrate that electroconvulsive stimulation (ECS) induces a seizure followed by cortical spreading depolarization, as previously shown. The putative novel finding - which is not unexpected - is that ECS is also correlated with increased expression of the immediate early gene cFOS, although this has also been shown previously. The authors speculate that CSD drives cFOS expression, which might contribute to the therapeutic effects of ECT; however, experiments performed do not provide causal evidence for this hypothesis. Instead, the authors use expression of cFOS - a nonspecific activity-dependent gene induced in various pathological and non-therapeutic contexts - as a proxy for plasticity and/or therapeutic effect. Hence, overall, the significance of the findings is limited and primarily serves to replicate prior work, with the evidence evaluated as incomplete.

      Strengths:

      The experiments are generally well executed from a technical perspective.

      Main Weaknesses to be addressed in revision:

      (1) The main findings of this paper are replication experiments of prior work, and thus, the novelty and significance of this manuscript are relatively limited.

      - It is already known that the mean frequency of ECT-induced seizures decays between peak and offset in humans (Stuiver et al. Clin Neurophysiol. 2026 Jan:181:2111439. doi: 10.1016/j.clinph.2025.2111439) and mice (Murakami et al. J Pharmacol Sci 2008 Jan;106(1):78-83. 10.1254/jphs.FP0071453), which the authors re-demonstrate in Figure 1.

      - It has already been demonstrated that ECT in mouse models induces lateralized CSD waves in a manner that depends on stimulation parameters and the initial evoked response during stimulation (Rosenthal et al. Nat Comm. 2025 May 18;16(1):4619. doi: 10.1038/s41467-025-59900-1); the authors replicate this in Figures 1, 2, 3, 6.

      - It is already widely established that EEG and calcium signals are highly concordant in mouse brain physiology, as shown in Figure 1. It is already known that CSD propagates from supragranular to granular and infragranular layers (Zakharov et al. Epilepsia. 2019 Dec;60(12):2386-2397. doi: 10.1111/epi.16390) as shown in Figure 4.

      - It is already known that CSD waves induce cFOS expression (e.g., Dell'Orco et al. Front Cell Neurosci. 2023 Dec 14:17:1292661. doi: 10.3389/fncel.2023.1292661; Hermann and Hossman. Neuroscience. 1999 Jan;88(2):599-608. doi: 10.1016/s0306-4522(98)00249-8) as the authors replicate in Figure 5.

      Minimally, the authors should revise claims regarding novelty, as the manuscript, as written, is misleading to a reader not familiar with the field. There is limited innovation in re-demonstrating that these events are seizures and that they involve spreading depolarization.

      (2) The authors frame their hypothesis that CSD could be a potential mediator of the therapeutic effects of ECT, but they do not measure therapeutic effects or directly test this hypothesis. The principal advancement of the paper is showing that ECT-induced CSD triggers hemisphere-specific cFOS expression as a proxy of plasticity. However, it is already known that CSD induces cFOS expression (as noted above). The observation that cFOS expression was induced only by CSD, not by the initial seizure, is likely a byproduct of the greater activity induced by CSD than by seizure. cFOS expression is nonspecific to plasticity or therapeutic effects and can be triggered by many non-therapeutic interventions. The cFOS data thus do not meaningfully measure therapeutic plasticity. The authors also selectively cite references suggesting that EEG metrics such as seizure duration predict positive therapeutic outcomes, but this link is controversial and not well established in the clinical literature.

      Minor Weaknesses:

      (3) For the n=3 mice used for concurrent 2P imaging with microprism implant, these animals also had ChrimsonR co-expression, but there are no optogenetic studies described in this paper, which is confusing. Yet, this co-expression introduces a significant confound, as GCaMP6 emission (525/50nm band in this study) will overlap substantially with the ChrimsonR excitation spectrum. Thus, the fluorescence emission used to image these neurons may be optogenetically activating them at the same time. Please explain.

      (4) Incision of the cortex for implantation of a prism is a significant cortical injury that likely induces CSD instantaneously and may change the propensity for CSD in subsequent recordings. Please comment on this limitation and address how much time elapsed after surgery before imaging.

      (5) Method details are missing or insufficiently described for location, titer, and injection strategy for 2-photon experiments.

      (6) Given the wide range of parameters used for ECS in mice and ECT in humans, the authors should provide tables for what stimulation parameters were used for each recording. These protocols were chosen manually rather than randomly or systematically, which introduces confounding factors into analyses that use parameters as an independent variable.

      (7) While much of the cFOS staining after unilateral CSD shows hemisphere-specific asymmetry, several regions (piriform cortex, amygdala, thalamus) do appear to have bilateral cFOS expression. Please comment on this.

      (8) The discussion states: "If CSD accounts for plasticity effects, triggering a CSD in a non-seizure context may be sufficient to elicit therapeutic effects. This is supported by the clinical success of ultra-brief stimulation treatments that do not cause seizures, such as rTMS with accelerated protocols, which achieves treatment efficacy on par with ECT for major depressive disorder". Are the authors implying that TMS induces CSD? What evidence supports this idea?

      (9) This statement - "Assuming psychosis is the result of thalamocortical coupling that is too weak in frontal areas of the cortex" (lines 583-585) - may be overly speculative.

      Review 3
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  38. www3-dev.tuhh.de www3-dev.tuhh.de
    The circle of life – Jonas Informatik Blog
    1
    1. xldrkp 08 Jul 2026
      Erster Test in Grafana, Foto: Jonas Schaber

      Moin. Ich habe mir eben in Grafana das Piepsgeschehen der letzten 12 Stunden angesehen und mir die Frage gestellt, ob eine Übersetzung der klassifizierten Vogelarten in die umgangssprachliche Bezeichung (z. B. "Amsel") sinnvoll und möglich wäre. Was meinst du?

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  39. www.nature.com www.nature.com
    Dogs distinguish human intentional and unintentional action
    2
    1. nathan09 08 Jul 2026
      In a similar manner, the dogs that ceased to move their tail mainly did so in the unwilling-condition. Ceasing and slowing down tail movement has been interpreted as signals for attentiveness, and attempting to make sense of confusing situations

      This part of the text explains that in the unwilling condition, dogs will stop waving or reduce the frequency of moving their tails during the experiment. This action can be seen as a messege to researchers that dogs are concentrating to understand what condition is happening before starting their action.

    2. Han128 08 Jul 2026
      Nevertheless, future research needs to address these alternative explanations by systematically excluding that dogs can rely on such strategies. Such research should look at the explicit role of vocal exclamations in dogs’ reactions.

      This part of the text acknowledges these could be alternative explanations for the study's results. The dogs could possibly have been reacting to the experimenter and that could have influences the final results. This is important because every scientific research has some level of error. Additionally, a researcher or an academic reading this paper could be inspired to do their own version of this experiment.

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    nature.com/articles/s41598-021-94374-3
  40. callyzer.co callyzer.co
    How to Spot Low-Quality Leads in 10 Seconds
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  41. www.derstandard.at www.derstandard.at
    Grönlands Eisschmelze schwächt Golfstrom stärker, ohne Kipppunkt zu erreichen
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  42. united24media.com united24media.com
    Five NATO Members Sign Historic Deal to Build Patriot PAC-3 Missile Facility in Europe
    1
    1. tonz 08 Jul 2026
      Five NATO members—the United States, Poland, Germany, the Netherlands, and Sweden—signed an intergovernmental agreement to build a dedicated maintenance facility for PAC-3 interceptor missiles in Europe.

      NL is partnering w USA, D, PL, S wrt Patriot missiles (NL has had them for a long time already, and deployed them to ao Israel 1991, Turkey 2003, and supplied them to Ukraine now)

      netherlands defence patriot airdefence
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  43. arxiv.org arxiv.org
    Network Formation and Dynamics Among Multi-LLMs
    1
    1. jordan_quotient 08 Jul 2026
      Second, our work highlights the poten-tial of LLMs for synthetic dataset generation, a critical area in network science. Although the accuracy ofLLM-based predictions is not yet perfect, like all other link prediction models, this approach is particu-larly valuable in scenarios where privacy concerns limit access to real-world data. By simulating realisticdatasets that capture important network properties, LLMs can facilitate research and experimentationwithout compromising sensitive informatio

      Valuable where privacy concerns limit access to real-world data (synthetic dataset generation).

      This paper outlines simile.

      gg.

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    arxiv.org/pdf/2402.10659
  44. drive.google.com drive.google.com
    SHAREABLE doc versions - Google Drive
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  45. hypothes.is hypothes.is
    Hypothesis
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  46. saalck.pressbooks.pub saalck.pressbooks.pub
    Business Communication is Receiver-Centric
    1
    1. nmosavi 08 Jul 2026
      Content Needs

      My boss would need to know that I am not in good health condition to function successfully at my job the following day, and my need for rest in order to have a fast recovery. The impact should demonstrate my clear communication and avoiding confusion, concern, or unexpected news the morning of the meeting.

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  47. socialsci.libretexts.org socialsci.libretexts.org
    14.3: Problem Solving and Decision Making in Groups
    1
    1. BraydenSteiner 08 Jul 2026
      During this step, solutions can be critically evaluated based on their credibility, completeness, and worth.

      I had to critically evaluate several solutions recently when I was upgrading my custom gaming PC. Before choosing a new processor and my new graphics card, I spent hours analyzing benchmark tests and hardware reviews to ensure the components were worth the high price tag. If I had just bought the first parts I saw without verifying their credibility, I could have ended up with a severely bottlenecked system. Taking the time to properly assess all your options is just as important in solo projects as it is in group problem-solving.

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    socialsci.libretexts.org/Bookshelves/Communication/Introduction_to_Communication/Communication_in_the_Real_World_-_An_Introduction_to_Communication_Studies/14:_Leadership_Roles_and_Problem_Solving_in_Groups/14.03:_Problem_Solving_and_Decision_Making_in_Groups
  48. socialsci.libretexts.org socialsci.libretexts.org
    14.2: Group Member Roles
    1
    1. BraydenSteiner 08 Jul 2026
      The monopolizer is a group member who makes excessive verbal contributions, preventing equal participation by other group members.

      While working at the help desk, I occasionally encounter a monopolizer during staff meetings. Sometimes, a technician will spend twenty minutes explaining a very minor software fix, completely talking over anyone else who tries to chime in. This excessive talking prevents the rest of the team from sharing their own updates or discussing more pressing network issues. It shows how one person's lack of self-awareness can easily hijack an entire group's time.

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  49. socialsci.libretexts.org socialsci.libretexts.org
    14.1: Leadership and Small Group Communication
    2
    1. BraydenSteiner 08 Jul 2026
      Participative leaders work to include group members in the decision-making process by soliciting and considering their opinions and suggestions.

      During my time in the Navy, the most respected supervisors I worked under always used a participative leadership style. Instead of just barking orders when we had a massive equipment overhaul, they would ask the junior sailors for our suggestions on the most efficient way to tackle the maintenance. Because they actively considered our input, we felt highly valued and took much more pride in the completed job. It showed me firsthand that involving the entire team in the decision-making process usually yields far better operational results.

    2. BraydenSteiner 08 Jul 2026
      Expert power comes from knowledge, skill, or expertise that a group member possesses and other group members do not.

      During my time an ISSO with the Navy, I frequently relied on expert power. Because I had specialized knowledge regarding network vulnerabilities and security protocols, senior leaders deferred to my judgment when making critical decisions. Even though I did not always have the highest formal rank in the room, my technical expertise gave me significant influence over the group's actions. It is highly rewarding when your specific skills allow you to naturally step up and guide a team.

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  50. socialsci.libretexts.org socialsci.libretexts.org
    13.3: Small Group Dynamics
    1
    1. BraydenSteiner 08 Jul 2026
      Symbolic convergence refers to the sense of community or group consciousness that develops in a group through non-task-related communication such as stories and jokes.

      Before jumping into a serious online gaming session, my squad usually spends time in the lobby just joking around and sharing stories about previous gaming disasters. None of this chatter helps us win the upcoming fight, but it significantly boosts our team morale. Creating that shared group consciousness makes the actual gameplay much more enjoyable. It is easy to see how these lighthearted conversations build a strong foundation of social cohesion.

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  51. socialsci.libretexts.org socialsci.libretexts.org
    13.2: Small Group Development
    2
    1. BraydenSteiner 08 Jul 2026
      The adjourning stage of group development occurs when a group dissolves because it has completed its purpose or goal

      I experience the adjourning stage frequently during group assignments in my online English/Rhetoric course. After few days of collaborating on a shared document and peer-reviewing each other's writing, submitting the final essay abruptly ends the group's purpose. We usually exchange a few quick messages of congratulations before completely dissolving the team. It is a very brief but necessary closure to a strictly task-oriented relationship.

    2. BraydenSteiner 08 Jul 2026
      During the forming stage, group members begin to reduce uncertainty associated with new relationships and/or new tasks through initial interactions that lay the foundation for later group dynamics.

      During my six and a half years in the Navy, I went through this forming stage repeatedly whenever I was assigned to a new unit or deployment. Initially, everyone is polite and cautious as we try to figure out each other's work habits and personalities. Those first few interactions are crucial for establishing a baseline of trust before the high-pressure tasks begin. Breaking the ice quickly always made the transition to actual operational work much smoother.

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  52. socialsci.libretexts.org socialsci.libretexts.org
    13.1: Understanding Small Groups
    2
    1. BraydenSteiner 08 Jul 2026
      Small groups exhibit interdependence, meaning they share a common purpose and a common fate.

      This concept perfectly describes how my Dungeons & Dragons group operates during our weekly sessions on Roll20. If my character, Ty'ruul, misses a critical spell or makes a tactical error, the rest of the party immediately suffers the consequences. We all share a common purpose of surviving the campaign, meaning our individual actions directly impact everyone else at the virtual table. Realizing this high level of interdependence makes me much more careful about my choices during combat.

    2. BraydenSteiner 08 Jul 2026
      Virtual groups take advantage of new technologies and meet exclusively or primarily online to achieve their purpose or goal.

      I participate in a highly active virtual group every time I log in to some of the online video games I enjoy. This allows me to coordinate gameplay with other players without ever interacting face-to-face. We rely entirely on voice communications and our digital environment to complete our objectives. It is amazing how much task cohesion we can build entirely through virtual channels.

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  53. www.biorxiv.org www.biorxiv.org
    A-type lamins anchor emerin at the inner nuclear membrane via two independent binding sites
    1
    1. josie.bircher 07 Jul 2026

      Really interesting paper! I love reading about the impacts of structural features generated by proteins (i.e. a lamin network) on protein:protein interactions. A few questions/thoughts: 1. In figure 1B, do you make anything of the puncta in the FLAG channel or the smaller puncta in the DAPI channel? 2. The linker region discovery is a very nice one! I was wondering, until I read your conclusion, whether there were any interesting disease-associated mutations in that region. It would be neat to track development of a mouse model with just the linker region disrupted in different ways to see if they don't make it through development. 3. I really loved your swapping strategy. It's really handy when biology provides a useful control protein. 4. Do you have a hypothesis for the strange spatial distribution of the LaB1(head+rod)-A(linker)-B1(tail) constructs? 5. How different are the A and and B1 linkers? especially if their NLS signals are similar, that's only like 20 amino acids left. It would be cool to see if there are any predicted structure differences/flexibilities between the two regions. It would also be informative to know how the lamin network structures might differ based on the inclusion of the different linker regions. 6. The section on lamin network stability at the end really made me rethink the whole lamin:emerin interaction story. Without having much prior knowledge on lamin, I wonder if the lamin:emerin interaction in vitro is based on a single lamin monomer interacting with emerin, or if it takes multiple to form a network. Is there a way you can drive formation or disintegration of the lamin network? That might even inform your pulldown data: if you pulldown lamin, then do something to disrupt a potential network, do you still pull down emerin? 7. I'm really curious about how the lamin network structure might differ between all of these different mutants. That would form a nice parallel to all of your emerin anchorage data.

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    biorxiv.org/content/10.1101/2025.09.01.673543v1
  54. zotiquest.substack.com zotiquest.substack.com
    The World Is the Rulebook
    2
    1. Thorah 07 Jul 2026
      What happens next? You don’t need a random event generator. You need to know how this world works, its physics, its politics, its people, its logic, well enough that the next thing follows naturally.

      Actually while I respect this concept I rather like the twists and wildcard rules in various games because they add something unexpected which in a game is really important for me to feel engaged when the game is supposed to not be deterministic. I really like to be suprised. In good measure mind but still.

    2. Thorah 07 Jul 2026
      They are not the enemy of originality. They are its infrastructure.

      Agreed. They're often neither but they're necessary. Every setting has the right to change things and oftentimes should but none very change everything and communicate that to a player so there necessary just a gravity is a necessary trope.

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    zotiquest.substack.com/p/the-world-is-the-rulebook
  55. s3.amazonaws.com s3.amazonaws.com
    S02_Cook.pdf
    1
    1. aidanchapin 07 Jul 2026
      From this perspective,then, archives are constructed memories about the past, about history, heritage, andculture, about personal roots and familial connections, and about who we are ashuman beings; as such, they offer glimpses into our common humanity. Yetmemory is notoriously selective—in individuals, in societies, and, yes, in archives.With memory comes forgetting

      My BA thesis was on the retention and creation of national identities among immigrants to America, particularly focused on Irish, Puerto Ricans, and Jews in New York. This reading reminded me a lot of the research I was doing on memory, identity creation, forgetting, and political mobilization, in part because I relied heavily on people like Benedict Anerson, and also because Cook discusses the ways in which memory and identity are political tools and products. While a lot of what I wrote was the ways in which different class factions created or mobilized these identities to present their particular interests as universal, I tried to also explain why this tactic worked, my explanation being that the process of selecting traits, events, and lineages out of the ever accumulating and complex manifold of history as meaningful and important, over other traits, events, and lineages, is an empowering and emotionally impactful thing to do, both as a group and as an individual. This selection also necessarily involves the creation and implementation of values, and a process of forgetting (which Cook also discusses). This process is as dangerous as it is powerful, but if we were incapable of selecting and forgetting, we would not be able to act (be it as immigrants, citizens, or archivists). While my thesis focused largely on nationalist parties, organized crime, secret societies, churches, and labor movements, it’s interesting to think about this stuff in the context of museums and archives. In the revised edition of Imagined Communities, Anderson actually adds two chapters, “Census, Map, Museum,” and “Memory and Forgetting” which I think are highly relevant to this piece. I did not touch on them in my thesis as much, as the diaspora groups in the time period I was writing about were not creating these institutions yet, but it’s cool to revisit it now while pursuing a library science degree. The other interesting thing about all this is that Cook isn’t only talking about the content of archives and identity formation (such as the early Irish republic trying to forge a coherent identity), but also about the archival community trying to find a universal identity that can paper over its internal differences toward a common goal. I have not thought about not explicitly political communities (like archivists) in this way before, although it makes perfect sense to do so in retrospect. Any institution has that potential and involves that process of selection and forgetting. In addition to Anderson’s book (or at least the aforementioned chapters), I highly recommend the short Nietzsche essay “On the uses and disadvantages of history for life,” which deals with the power granted from learning history and the simultaneous stupefying effect an overaccumulation of history can have on a person. While he’s talking about psychology, I think it’s interesting to think about it in the context of more practical questions archivists face when faced with the physical constraints of their disciplines. Both popular culture and archives laude preservation and remembering, so its thought provoking to read about the virtues of forgetting and destruction (even if you don’t agree)! I think of Rosenthal’s bug bag and water bottles here.

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    s3.amazonaws.com/files.commons.gc.cuny.edu/wp-content/blogs.dir/48911/files/2026/01/S02_Cook.pdf
  56. learn.zybooks.com learn.zybooks.com
    Section 4.9 - CS 001: Introduction to Computers and Programming | zyBooks
    1
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    learn.zybooks.com/zybook/PASADENACS001ShawSummer2026/chapter/4/section/9
  57. www.khanacademy.org www.khanacademy.org
    Introduction to gender in renaissance Italy (article) | Khan Academy
    3
    1. Zach_V 07 Jul 2026
      Men were expected to participate in all aspects of public life, to excel in learning, in their trade, in governance, and to do so with the aggressive and assertive behavior particular to their superior biological construction.

      I find this really funny cause credible studies have shown that time and time again, women are shown to live longer than men and are smarter as well.

    2. Zach_V 07 Jul 2026
      Men, who in renaissance Christian thought were created in the image of a male God, were believed to have a natural superiority over their female counterparts.

      That would explain why men back then thought they were God's greatest gift, because they were.

    3. Zach_V 07 Jul 2026
      "Fortune is a woman and if you wish to keep her under it is necessary to beat and ill use her; and it is seen she allows herself to be mastered by the adventurous rather than by those who go to work more coldly.

      This is just an abusive relationship. I'm relieved we moved past this era of humanity.

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    khanacademy.org/humanities/art-history-for-teachers/xeaa3470a:teaching-with-images/xeaa3470a:go-deeper-where-are-the-women-artists/a/introduction-to-gender-in-renaissance-italy
  58. www.biorxiv.org www.biorxiv.org
    2026.04.09.717238.full-html.html
    1
    1. MicaelaG 07 Jul 2026

      Hi this study effectively combines precision genome editing, stem cell disease modeling, and advanced biochemistry, utilizing rigorous controls to guarantee reproducibility. However, incorporating specific methodological improvements could significantly strengthen the authors' conclusions. First, performing a phenotypic rescue by reintroducing PSEN2 into the knockout lines is recommended to confirm direct causality and rule out off-target effects or culture adaptations. Second, utilizing single-cell resolution tools (e.g., FACS or single-cell RNA-seq) would better address potential cell heterogeneity within the 100-day culture. Finally, because conclusions regarding endo-lysosomal dysfunction rely strictly on static protein measurements, complementing these findings with dynamic functional assays (such as Bafliomycin A1 treatment or enzymatic probes) is highly recommended to definitively assess autophagic flux and actual lysosomal degradation. Refining the biochemical resolution would also clarify key processing pathways. In Figure 2A, the accumulation of amyloid precursor protein fragments is generically labeled as "APP CTFs." However, the low-resolution band fails to discriminate between CTF/beta and CTF/alpha, leaving it unclear which pathway is affected by PSEN1-KO. Replacing conventional Western blotting with high-resolution Tricine-SDS-PAGE and using ImageJ to quantify the exact CTF/beta and CTF/alpha ratio would resolve this ambiguity. Similarly, in Figure 1F, the claim that Nicastrin is immature due to a lack of glycosylation is based solely on a downward band shift. To definitively prove this, treating wild-type samples with PNGase F or Endo H to align the bands would provide the necessary biochemical confirmation. Lastly, the discussion's interpretation of APP processing warrants caution. Asserting that PSEN2 does not alter Aβ generation is premature without quantifying the intracellular amyloid pool, especially given PSEN2’s endo-lysosomal localization. Furthermore, the proposed compensatory mechanism remains speculative, as an increase in PSEN2 could shift the Aβ42:40 ratio toward more pathogenic forms. Happy to discuss if needed. Best wishes.

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    biorxiv.org/content/10.64898/2026.04.09.717238v1
  59. learn.zybooks.com learn.zybooks.com
    Section 4.8 - CS 001: Introduction to Computers and Programming | zyBooks
    1
    1. mendoza55982 07 Jul 2026
      4.8.1: While loops.

      I got all of these wrong because I was not carful to follow the numbers and especially what happens when the loop exits or does not enter the body.

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    learn.zybooks.com/zybook/PASADENACS001ShawSummer2026/chapter/4/section/8
  60. learn.zybooks.com learn.zybooks.com
    Section 4.8 - CS 001: Introduction to Computers and Programming | zyBooks
    2
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  61. Local file Local file
    Untitled document
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