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    METTL7A Downregulation Drives SLC1A5-Mediated Glutamine Competition to Promote Tumor Proliferation and Suppress CD8+ T Cell Immunity in Gastric Cancer
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    The mechanosensitive protein Zyxin influences Hippo signaling and tissue growth via adherens junctions and basal spot junctions in Drosophila
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  25. arxiv.org arxiv.org
    Modulating task outcome value to mitigate real-world procrastination via noninvasive brain stimulation
    4
    1. Public_Reviews 04 Aug 2026

      eLife Assessment

      This valuable cross-sectional longitudinal study leverages high-definition transcranial direct current stimulation to the left dorsolateral prefrontal cortex to examine its effect on procrastination behavior over an extended time span. The cross-sectional longitudinal study a testing of competing models provided solid evidence for how stimulating DLPFC impacts reveal-world procrastination behavior. Whether these results generalize to a larger population will be a significant future direction. This work will be of interest to those interested in cortical function, procrastination, and related states.

      Summary
    2. Public_Reviews 04 Aug 2026

      Reviewer #1 (Public review):

      Summary:

      The authors report the results of a tDCS brain stimulation study (verum vs sham stimulation of left DLPFC; between-subjects) in 46 participants, using an intense stimulation protocol over 2 weeks, combined with an experience-sampling approach, plus follow-up measures after 6 months.

      Strengths:

      The authors are studying a relevant and interesting research question using an intriguing design, following participants quite intensely over time and even at a follow-up time point. The use of an experience-sampling approach is another strength of the work.

      Comments on revised version.

      With the last round of revisions, the authors have now addressed my concerns.

      Review 1
    3. Public_Reviews 04 Aug 2026

      Reviewer #4 (Public review):

      Summary:

      The current study tested the effects of repeated sessions of tDCS targeting the DLPFC on procrastination behavior. The main outcome is that anodal versus sham DLPFC tDCS reduces procrastination behavior on both a short-term and a long-term scale up to six months after the stimulation sessions.

      Strengths:

      The current study tests competing models of procrastination with state-of-the-art high-definition transcranial electric stimulation. The study assesses stimulation effects on procrastination on both a short-term and a long-term scale, suggesting that repeated stimulation of the prefrontal cortex reduces procrastination on a time scale of up to six months.

      Weaknesses:

      The manuscript has already been reviewed and revised before, and it seems that the quality of the manuscript has substantially improved as a result of this revision process. I agree with the other reviewers that one must be cautious with drawing conclusions regarding the cognitive mechanisms underlying this effect, as many different cognitive functions are implemented by the DLPFC.

      One aspect of the current results that puzzles me is the strength of the current stimulation effects. Meta-analyses suggest that tDCS shows only small-to-moderate effect sizes (with Cohen's d around 0.5). While the authors report no effect sizes for their statistical models, the small p values, in combination with the unusually small sample size of 18 participants per group, suggests that the effect size must be rather large. Can the authors provide an estimate of the effect size of their stimulation effects? If they are considerably larger than to be expected, could the authors give an explanation for why their stimulation setup is showing much stronger effects than comparable high-definition tDCS studies on cognition or decision making?

      Regarding the strengths of the stimulation effects, I moreover found remarkable that the post-test procrastination rate was 100% in all (!) participants in the DLPFC group (figure 3F). I admit that it is hard to trust results that have no individual variation at all. This means that all participants are perfect responders to tDCS, which is again at variance what one typically expects for tDCS (where one usually has many non-responders). Do the authors have an explanation for this?

      In any case, I am surprised by the rather small sample size. Due to the small effect sizes for tDCS, it is common to have a minimum of 30 subjects per group in between-subject designs. According to G*Power, a between-subject design with 17 subjects per group could detect only relatively large effect sizes of Cohen's d = 0.99 (alpha = 5%, power = 80%, independent-samples t-test). As explained above, this is far above the effect size that can be expected for tDCS. In addition, small samples bear the risk that results strongly depend on outliers in the data, which might explain the strong effect size observed in the current study. The small sample size should be discussed as a major limitation of the current study and that the results need to be replicated by studies with larger sample sizes. Moreover, to rule out that the results are driven by outlier in the data, the authors should show individual data points in all plots showing empirical data.

      Related to this, in the figure showing individual data points (3B/F), I count only around 10 data points per tDCS group for the 18 participants per group. I ask the authors to modify the plot that the data points from all participants can be seen (for example, by adding some noise on the x-axis for participants with the same value on the y axis).

      Another surprising aspect of the data is that repeated sessions of tDCS change procrastination behavior up to six months after stimulation. Do the authors think that their tDCS setup leads to such long-lasting neuroplastic changes, and if yes, can they cite prior work where similar dosages of tDCS also showed such long-lasting effects? Or could the results be explained by learning effects, for example because participants in the DLPFC group learned during the repeated tDCS sessions that it feels internally rewarding to finish one's tasks instead of procrastinating them, and they still benefit from this kind of "learned industriousness" 6 months later? In any case, in my view it is important to be more specific about how seven sessions of tDCS can affect behavior half a year later.

      Lastly, the link to the data repository works, but I could not inspect the data because I was asked to request access to the data, which I did not do in order to remain anonymous.

      Review 2
    4. Public_Reviews 04 Aug 2026

      Author response:

      The following is the authors’ response to the previous reviews

      Public Reviews:

      Reviewer #1 (Public review):

      Summary:

      The authors report the results of a tDCS brain stimulation study (verum vs sham stimulation of left DLPFC; between-subjects) in 46 participants, using an intense stimulation protocol over 2 weeks, combined with an experience-sampling approach, plus follow-up measures after 6 months.

      Strengths:

      The authors are studying a relevant and interesting research question using an intriguing design, following participants quite intensely over time and even at a follow-up time point. The use of an experience-sampling approach is another strength of the work.

      Comments on revisions:

      Overall, I think the authors made many improvements to their manuscript. There are, however, still a number of concerns that first need to be addressed, since it is still not currently possible to fully evaluate the analyses, results, and conclusions presented in the paper. I list these points below:

      (1) The authors still use causal language where they must not use causal language. This is true for many places in the manuscript; I am highlighting here just a few places, but the authors nevertheless have to go carefully through the whole manuscript to change these instances.

      We sincerely thank the reviewer for this critical and well-taken point. We fully agree that our design (manipulating DLPFC excitability while measuring procrastination, task value, and aversiveness) does not directly measure or manipulate self-control, nor does it rule out alternative neurocognitive mechanisms. Accordingly, we have conducted a comprehensive, line-by-line revision of the entire manuscript to systematically replace causal claims with cautious, hypothesis-consistent language. In response, we have replaced all the wordings that may imply causal inferences, such as impair, cause, boost, by association-consistent phrasing. Furthermore, as you clearly raised below, we explicitly reframed self-control as a hypothesized theoretical construct rather than an empirically verified mediator throughout the whole re-revised manuscript. Please see specific revisions below:

      Abstract Section (Page 2, Line 53-59)

      “... a mediation analysis indicated a disassociable mechanism: the increase in task outcome value (but not task aversiveness) showed a statistical pattern consistent with accounting for the observed behavioral improvement. In conclusion, these findings are consistent with the hypothesis that enhancing DLPFC function may reduce procrastination by selectively amplifying the valuation of future rewards, not by simply reducing negative feelings about the task.”

      Introduction Section (Page 3, Line 83-86)

      “... Even worse, chronic procrastination has been consistently associated with poor general health conditions, such as immune system disruption, gastrointestinal disturbance, hypertension and cardiovascular disease (Sirois, 2015; Sirois, 2016).”

      Introduction Section (Page 4, Line 143-145)

      “Consistent with this framework, the left dorsolateral prefrontal cortex (DLPFC)—a region frequently implicated in value-based decision-making and top-down regulation—has been associated with procrastination. ...”

      Introduction Section (Page 4, Line 135-139)

      “... Also, given the integrative nature of prefrontal regulatory functions, we hypothesize a third pathway whereby both decreased task aversiveness and increased task-outcome value may jointly contribute to reduced procrastination, potentially reflecting coordinated downstream effects on valuation and affective processing.”

      Introduction Section (Page 5, Line 183-186)

      “... Thus, this study aims to clarify the brain-behavior association between DLPFC neuromodulation and procrastination, and to test whether observed changes in task valuation and aversiveness are consistent with theoretical models of top-down regulation.”

      Results Section (Page 11, Line 534-536)

      “... Thus, these findings are consistent with the view that neuromodulation of the left DLPFC is associated with reduced task aversiveness and increased task-outcome value.”

      Results Section (Page 11, Line 579-584)

      “... In summary, these findings identified a statistical pathway consistent with the theoretical model: neuromodulation of the left DLPFC was associated with increased task-outcome value, which in turn was associated with reduced procrastination.”

      Discussion Section (Page 12, Line 617-620)

      “On balance, our findings provide evidence consistent with the hypothesis that neuromodulation of the left DLPFC is associated with reduced procrastination, primarily through increasing task-outcome value rather than merely reducing task aversiveness. ...”

      Discussion Section (Page 13, Line 664-669)

      “... Building on this foundation, among several theoretical interpretations and cognitive pathways, our study showed the one plausible neurocognitive mechanism of procrastination: the cortical excitability of the DLPFC produced by active neuromodulation may engage prefrontal regulatory networks to increase task outcome value, which in turn is associated with reduced procrastination behavior, statistically supporting the theoretical accounts of temporal decision model (TDM, Zhang et al., 2019).”

      Discussion Section (Page 14, Line 755-762)

      “... Moreover, this study did not collect data for assessing participants' self-control at either baseline or post-neuromodulation. Accordingly, we explicitly note that self-control was not directly measured or manipulated in this study; the observed associations between DLPFC neuromodulation, task-outcome value, and procrastination are consistent with theoretical models positing a role for top-down regulatory processes, but do not constitute direct evidence that self-control mechanisms were engaged. This limitation precludes definitive conclusions about the unique contribution of self-control-related pathways versus alternative neurocognitive mechanisms.”

      Some examples:

      (a) In response to my comment (1) in the previous round, where the authors adjusted their text, the authors still use causal language in their last sentence "... procrastination behavior has been observed to impair general health..." Unless the cited study truly allowed causal conclusions, the causal language should be removed here as well.

      Thank you for pointing out this inappropriate phrasing. As you kindly suggested, we have reworded it as “Even worse, chronic procrastination has been consistently associated with poor general health conditions, such as immune system disruption, gastrointestinal disturbance, hypertension and cardiovascular disease” (Introduction Section, Page 3, Line 83-86).

      (b) The authors still make (causal) claims about the involvement of self-control in their observed results. To reiterate from the previous round of revisions: The authors cannot make any strong claims about the role of self-control processes because they do not directly measure self-control nor do they directly manipulate self-control or have a design that would rule out alternative mechanisms other than self-control. Therefore, their claims about self-control have to be toned down. It is laudable that the authors have added a statement towards the end of their discussion about not being able to make strong conclusions about the role of self-control. But the authors need to use similar careful wording not just at the end of the discussion but throughout the manuscript.

      We appreciate you reiterating this concern. In the re-revised manuscript, we have thoroughly removed or rewritten all the statements implying causal inferences, and have substantially toned-down claims for the roles of self-control in procrastination reduction from this neuromodulation. Please see instances for what we have replied to the Comment #1.

      (i) In the abstract, the authors use the formulation "...conceptualized roles of self-control on procrastination..." -- this wording is still too strong, suggesting that you actually studied self-control.

      Thank you for providing this specific instance. This inappropriate sentence has been removed.

      (ii) In the introduction (page 4, lines162-169), the way the authors formulate these sentences suggests that they directly measured self-control. Again, the authors need to make it explicit that they are not directly measuring self-control but its hypothesized down-stream consequences on valuations/behavior.

      Many thanks. This statement has been removed, and we have reworded it as “... Thus, this study aims to clarify the brain-behavior association between DLPFC neuromodulation and procrastination, and to test whether observed changes in task valuation and aversiveness are consistent with theoretical models of top-down regulation.” (Introduction Section, Page 5, Line 183-186).

      (iii) In the discussion, for example, on page 11, lines 555 and following, the authors write: "One major contribution this study has made is to disentangle the neurocognitive mechanism of procrastination by demonstrating that self-control could increase task-outcome value so as to reduce procrastination."

      As you kindly instructed, we have rewritten this statement as “One contribution of this study is to provide empirical evidence partially consistent with the temporal decision model (TDM), showing that increased task-outcome value—rather than decreased task aversiveness—was statistically associated with reduced procrastination following DLPFC neuromodulation.” (Introduction Section, Page 12, Line 625-628), which no longer implies any conclusions for the role of self-control in this study.

      Again, please be aware that you are NOT demonstrating that self-control does anything, since you only measure procrastination rates, outcome values, and task aversiveness. It is possible that mechanisms other than self-control might be relevant for this. Perhaps neuromodulation directly increases outcome values, without involvement of self-control processes. You simply cannot know that and therefore you cannot make those claims in the form that you are making them. You can write that the observed results are consistent with the idea that neuromodulation might have had an effect on self-control and this in turn might have affected outcome values. But you also need to make it explicit that, to substantiate these claims, you would need more direct evidence that indeed self-control was involved. These more careful formulations would not at all reduce the value of your work, but indeed they would rather demonstrate your carefulness in interpreting the results you obtained.

      We sincerely thank the reviewer for this exceptionally clear and constructive guidance. We fully agree that our study design does not measure or manipulate self-control, and therefore we cannot demonstrate that self-control processes are causally involved in the observed effects. As you correctly note, it is entirely possible that neuromodulation directly modulates outcome valuation or engages alternative neurocognitive pathways (e.g., attentional allocation, feedback learning, or affective processing) without invoking self-control mechanisms.

      In direct response, as we replied above, we have completely rewritten the whole revised manuscript to remove any assertions that we “identified” a role of self-control. The revised text now explicitly states as follow: (1) our findings merely are consistent with the theoretical hypothesis that DLPFC neuromodulation might engage prefrontal self-regulatory functions, which in turn influence outcome valuation; (2) we explicitly acknowledge that substantiating this specific pathway would require more direct evidence. Rather than single sentence, we have applied this careful, hypothesis-consistent framing systematically across the Abstract, Introduction, Results, and Discussion. As you suggested, these revisions more accurately reflect the interpretative boundaries of our data and demonstrate our commitment to rigorous, transparent scientific reporting. Please see specific cases for this revision above.

      (2) I am still puzzled by the power analysis. In the text, you write that a sample size of 18 participants (i.e., 9 per group) would be sufficient to achieve 80% power. I still feel this seems far too optimistic and hard to believe, but that is not my point here. While in the text, you write that you need 18 participants, the G*power output seems to suggest a sample size of 34, not 18. Why this contradiction? Or is it not contradictory? If it is not, then please explain it more fully.

      We appreciate you pointing out this critical typo. In the last round of revision, we mean that 18 participants per group are required to achieve at least 80% statistical power, rather than a total sample size, as shown by the GPower software. We are sorry for this critical typo to confuse you. As you correctly pointed out, the GPower indicated that the minimum sample size to reach 80% power is 34 (i.e., 17 per group). Thus, we selected 36 (i.e., 18 per group) participants as minimum sample size in case of potential drop-out. We have thoroughly corrected this typo, and double-checked no such numeric issues:

      Methods Section (Page 5, Line 234-237)

      “... statistical power was predetermined by G*Power at a relatively medium effect size (1-β err prob = 0.80, f = 0.25), indicating the total sample size at 34 (17 per group) to reach acceptable power. To account for potential attrition, we determined to recruit 36 participants, at least.”.

      (3) I have several comments about the mixed-effects analysis.

      First of all, I want to thank the authors for adding more details, things have become much clearer now. However, I still have a few questions and comments related to these analyses:

      (a) The variable Emotions was within-subjects, as far as I understood. Accordingly, Emotions should most likely be modelled with random slopes varying over participants (in addition to being modelled as a fixed effect).

      We thank you raising this reasonable concern on the mixed-effect linear modeling. Yes, the Emotions reflect daily baseline affect, which is modeled as covariates of no interests to adjust for daily emotional fluctuation (if any). In this vein, this baseline emotion score is included for each participant across all the sessions. Therefore, it should be modeled with random slopes as you assumed indeed.

      In response, we have remodeled this mixed-effects analysis by including the daily baseline emotion as random slopes varying over participants. After centering the variables, we estimated the revised models as “Procrastination Rate ~ Group * Treatment day + Age + Gender + SES + Emotions + (1 + Treatment day + Emotions || SubjectID)” and “Task execution willingness ~ Group * Treatment day + Age + Gender + SES + Emotions + (1 + Treatment day + Emotions || SubjectID)”. Notably, as you correctly assumed, fitting this complicated random-effect structure is likely to result in convergence failure, given the limited sample size in the present study. Therefore, we hypothesized the independence among random effects for model simplification. Consistent with this assumption, model comparisons indicated that the simplified models fit better than original ones (Procrastination Rate model, ∆AIC = -1.0, ∆BIC = -11.8, LRT, χ<sup>2</sup>(3) = 5.04, p = .17; Task-execution willingness model, ∆AIC = -5.5, ∆BIC = -16.4, LRT, χ<sup>2</sup>(3) = 0.51, p = .91).

      Taken together, as you kindly suggested, we have rebuilt the mixed-effect models by adding daily baseline emotion as random slopes varying over participants, and have demonstrated the consistent findings with the original one:

      Methods Section (Page 8-9, Line 412-419)

      “... Given the risks of convergence failure with the two correlated random-effects structure (i.e., treatment days and self-reported emotions), we hypothesized that the random effects are independent, leading to model simplification. Consistent with this assumption, model comparisons favored the simplified independent structure over the full correlated structure for both outcomes. For the actual procrastination model, the simplified model showed lower AIC (∆ = -1.0) and BIC (∆ = -11.8), with a non-significant likelihood ratio test (χ<sup>2</sup> (3) = 5.04, p = .17). For the task-execution willingness model, the simplified model was also preferred (∆AIC = -5.5, ∆BIC = -16.4; LRT: χ<sup>2</sup> (3) = 0.51, p = .91).”

      Results Section (Page 9-10, Line 469-489)

      “For procrastination willingness, results showed a statistically significant interaction effect between multi-session neuromodulations and groups (β = -7.84, SE = 1.80, t = -4.36, DF = 45.6, p < .001; Fig. 3A). In the post-hoc simple effect analysis, it demonstrated a significantly increased task-execution willingness (i.e., decreased procrastination willingness) after neuromodulation in the active neuromodulation group (NM-before: 35.65 ± 30.21, NM-after: 80.43 ± 19.92, Mean Diff = 41.79, SE = 7.58, DF = 103.4, t.ratio = 5.51, p < .0001, Tukey correction), but no such effects were identified in the sham control group (SC-before: 37.57 ± 26.46, SC-after: 47.35 ± 30.49, Mean Diff = 2.58, SE = 7.56, DF = 96.8, t.ratio = 0.34, p = .73, Tukey correction) (Fig. 3B-C). A linear uptrend for task-execution willingness was further observed across multiple sessions in the active NM group, indicating gradually increasing neuromodulation effects (Fig. 3D; p < .01, Mann-Kendall test). For actual procrastination behavior, changes to actual procrastination rates across all the sessions have been detailed in the Fig. 3E. Similarly, a statistically significant interaction effect was identified here (β = -7.37, SE = 2.40, t = -3.02, DF = 46.6, p = .004), and the simple effect analysis further revealed decreased actual procrastination rates after ms-tDCS in the active neuromodulation group (NM-before: 56.74 ± 39.10, NM-after: 0.00 ± 0.00, Mean Diff = 44.40, SE = 9.36, DF = 110.0, t.ratio = 4.74, p < .0001, Tukey correction), but no such prominent changes found in the sham control group (SC-before: 46.47 ± 40.76, SC-after: 33.35 ± 37.82, Mean Diff = 7.53, SE = 9.28, DF = 102.0, t.ratio = 0.81, p = .42, Tukey correction) (Fig. 3F-G).”

      (b) The analyses still cannot fully be evaluated as I cannot access the scripts and data. The authors mention that the scripts and data should be available via a link they provide (https://doi.org/10.57760/sciencedb.35140). However, when I try to access these materials via this link, no page opens; it seems the link is dead?

      Thank you very much for bringing this case to us. We checked this link and found it to be still active.

      To ensure accessibility for your evaluation, we have uploaded scripts and data into this online submission system. Please do let us know if you are still unable to access them. We are glad to send them to you by other available pathways. This link is a private access to you, and the repository would be openly available for other users upon the final publication.

      (c) What are the results and conclusions if you do not include the covariates of no interest? I.e., please re-run your main models without age, gender, SES, Emotions.

      Thank you for raising this question. As you clearly instructed, we have rerun main models without all those covariates. As shown in the table below, the results for the key predictors of interest (Group, Treatment day, and their interaction) remained largely unchanged in terms of effect size, direction, and statistical significance:

      Author response table 1.

      Comparison to statistics derived from model with covariates (i.e., age, gender, SES, Emotions) and without covariates

      (d) The authors mention that they use GLMMs, which would suggest generalized mixed-effects models, but they do not describe what family/distribution they used. Since they mention lmerTest and seem to report F-tests, my guess is that they used Gaussian models. However, both their DVs (procrastination rates and their ratings) are bounded variables and at least procrastination rates hit the lower boundary. That can mean that their analyses suffer from inflated Type 1 and/or Type 2 rates. Therefore, please repeat the analyses with an appropriate generalized mixed-effects model (perhaps a beta regression type of model?).

      We are very grateful to you for raising this crucial statistical point. As you correctly pointed out, we used the Gaussian distribution in estimating this model. We are sorry to confuse you due to the absence of reporting family/distribution we used. In the original manuscript, we meant “general” linear mixed-effect model, rather than “generalized” one. As you clearly and correctly raised, procrastination rates and willingness are technically bounded, and that procrastination rates frequently reached the lower boundary (0%) in the present study, which are in high risks to be inflated for Type 1 and/or Type 2 error.

      Thus, as you kindly suggested, a beta family distribution with logit function is used to reanalyze those main effects of interest. Results are tabulated in Author response table 2.

      Author response table 2.

      These convergent results confirm that the critical main effect (i.e., Group and Treatment day) and their interaction remain statistically significant across distributional specifications, and that our primary conclusions are not artifacts of the Gaussian assumption. Taken them together, as you kindly suggested, we have repeated the analyses with beta regression family distribution, which replicated our main findings, potentially supporting their statistical robustness.

      Following your suggestion, we have added those results derived from such sensitivity analyses into the revised manuscript:

      Methods Section (Page 9, Line 430--436)

      “... To examine whether our findings were sensitive to the distributional assumptions of the dependent variables, we re-analyzed the main models using an alternative distributional specification. Given that both procrastination rates (ranging from 0% to 100%) and task-execution willingness (measured on a 0-100 visual analog scale) are bounded continuous outcomes, and that procrastination rates frequently reached the lower boundary (0%) in the present study, a Beta regression model with a logit link function was employed for a sensitivity analysis.”

      Results Section (Page 10, Line 506-512)

      “... Furthermore, as a sensitivity analysis, we reran the main LMMs using Beta regression distribution with a logit link function, which is appropriate for the both bounded outcomes mentioned above (i.e., procrastination rate and procrastination willingness). The main effects (i.e., Group and Treatment day) and their interaction remained significant for both procrastination rate and willingness (see SI Results and Tab. S5), confirming that our findings are robust to alternative distributional assumptions.”

      (e) When reporting the results of the mixed-effects models, the authors report the regression coefficient, standard error, DFs and p value, but not the actual test statistic. Please add the information about the test statistic and report all degrees of freedom (in case of F tests that would be the degrees of freedom of the test and the residual degrees of freedom).

      We truly thank you for this nuanced reminder. As you suggested, we have added actual test statistics, including t-values and all degrees of freedom (DF). Please see specific instances below:

      Results Section (Page 9-10, Line 469-489)

      “For procrastination willingness, results showed a statistically significant interaction effect between multi-session neuromodulations and groups (β = -7.84, SE = 1.80, t = -4.36, DF = 45.6, p < .001; Fig. 3A). In the post-hoc simple effect analysis, it demonstrated a significantly increased task-execution willingness (i.e., decreased procrastination willingness) after neuromodulation in the active neuromodulation group (NM-before: 35.65 ± 30.21, NM-after: 80.43 ± 19.92, Mean Diff = 41.79, SE = 7.58, DF = 103.4, t.ratio = 5.51, p < .0001, Tukey correction), but no such effects were identified in the sham control group (SC-before: 37.57 ± 26.46, SC-after: 47.35 ± 30.49, Mean Diff = 2.58, SE = 7.56, DF = 96.8, t.ratio = 0.34, p = .73, Tukey correction) (Fig. 3B-C). A linear uptrend for task-execution willingness was further observed across multiple sessions in the active NM group, indicating gradually increasing neuromodulation effects (Fig. 3D; p < .01, Mann-Kendall test). For actual procrastination behavior, changes to actual procrastination rates across all the sessions have been detailed in the Fig. 3E. Similarly, a statistically significant interaction effect was identified here (β = -7.37, SE = 2.40, t = -3.02, DF = 46.6, p = .004), and the simple effect analysis further revealed decreased actual procrastination rates after ms-tDCS in the active neuromodulation group (NM-before: 56.74 ± 39.10, NM-after: 0.00 ± 0.00, Mean Diff = 44.40, SE = 9.36, DF = 110.0, t.ratio = 4.74, p < .0001, Tukey correction), but no such prominent changes found in the sham control group (SC-before: 46.47 ± 40.76, SC-after: 33.35 ± 37.82, Mean Diff = 7.53, SE = 9.28, DF = 102.0, t.ratio = 0.81, p = .42, Tukey correction) (Fig. 3F-G).”

      (f) Thank you for adding the analysis where you remove the last two sessions. But currently you present them in the manuscript without explaining/motivating why you do this. Please add this motivation, as otherwise it will be puzzling for the reader why you conduct these analyses.

      Thank you for this very practical requirement to clarify the motivation of reanalyzing main models from removing the last two sessions. Please see specific explanation as follow:

      Results Section (Page, Line 499-506)

      “... To systematically test whether such effects are biased by extreme data points or patterns, we reran the main LMMs by iteratively removing data from the last two sessions, which showed extraordinarily high effectiveness from neuromodulation (e.g., all the participants in the neuromodulation group had no actual procrastination behavior in session #6 and #7). Results showed the significant group*neuromodulation sessions interaction effects across all those nested models (removing session #6, #7 or both, all p < .05; see SI Results and Tab. S3-4), potentially indicating a statistical robustness from the data pattern.”

      (4) Mediation analysis

      In your manuscript, you present some mediation analyses. Please be aware that such mediation analyses cannot establish causality and they suffer from extremely high Type 1 error rates (see, e.g., https://datacolada.org/103). My suggestion would be to completely remove all mediation analyses. However, if you want to keep them, then you need to be extremely careful in how you present the results. You need to explicitly mention that you cannot derive any causal conclusions from them and that simulation studies have shown that such mediation analyses suffer from extremely high Type 1 errors.

      We sincerely thank you for this exceptionally important methodological guidance. We fully agree that mediation analyses, especially those based on observational measures rather than experimentally manipulated mediators, cannot establish causal pathways and are susceptible to inflated Type 1 error rates, as rigorously demonstrated in recent simulation studies (https://datacolada.org/103).

      As you kindly suggested, please allow us to retain those mediation analyses upon explicitly highlighting that this mediation statistical model cannot generate any causal conclusions. In response, we have systematically replaced all instances of “causal mediation” with “statistical mediation” or “exploratory mediation analysis”, and removed causal verbs (e.g., “depends on”, "drives", "explains") in favor of association-consistent phrasing (e.g., “is statistically mediated”, “aligns with the hypothesis that”) throughout the abstract, introduction, methods, results and discussion sections. Furthermore, in the Discussion section, we explicitly reiterated the limitations of extending this mediation associations to causal conclusions. Please see specific modifications underneath:

      Abstract Section (Page 2, Line 52-56)

      “... While the intervention is significantly associated with both decreased task aversiveness and increased perceived task outcome value, a mediation analysis indicated a disassociable mechanism: the increase in task outcome value (but not task aversiveness) showed a statistical pattern consistent with accounting for the observed behavioral improvement.”

      Methods Section (Page 9, Line 448-453)

      “... As these mediation analyses are based on observational measures rather than experimentally manipulated mediators, they do not establish causal pathways. Simulation studies have shown that such analyses can suffer from inflated Type 1 error rates. Results should therefore be interpreted as hypothesis-generating and statistically consistent with the proposed theoretical model, rather than as confirmatory evidence of causal mechanisms.”

      Methods Section (Page 9, Line 438-440)

      “... the Quasi-Bayesian mediation analysis was used to model the association between the effects of tDCS, task aversiveness/outcome and decreased procrastination.”

      Results Section (Page 11, Line 568-573)

      “As an exploratory analysis, results indicated that increased task outcome value was associated with changes in the task-execution willingness (δ = 21.73, p < .01; ζ = 11.25, p = .07, ρ = 32.99, p < .01, simulation = 1,000; see Fig. 5A) and real-world procrastination (δ = 30.75, p < .01; ζ = 3.05, p = .52, ρ = 33.81, p < .01, simulation = 1,000; see Fig. 5B), in the context of ms-tDCS neuromodulation. ...”

      Results Section (Page 11, Line 582-584)

      “... Nevertheless, all mediation findings are now explicitly labeled as “exploratory” and framed as quantifying statistical associations consistent with the TDM pathway, not causal mediation.”

      Discussion Section (Page 14, Line 747-755)

      “Notably, we explicitly acknowledge that exploratory Quasi-Bayesian mediation analyses, based on observational measures rather than experimentally manipulated mediators, cannot establish causal pathways and are susceptible to inflated Type 1 error rates as demonstrated in recent simulation studies. These findings should be interpreted strictly as hypothesis-generating and statistically consistent with the proposed theoretical model, rather than as confirmatory evidence of causal mechanisms. Substantiating the precise neurocognitive pathway will require future studies employing stronger causal designs, such as experimental manipulation of task valuation or longitudinal cross-lagged modeling. ...”

      As an example (but the mediation results are mentioned in several places, for example, also in the abstract): On page 10, lines 501-503: What you can causally conclude is that neuromodulation affects your measured variables (outcome values, procrastination rates, task aversiveness), but you cannot conclude that the effect of neuromodulation on procrastination rates causally operates via outcome values. Thus, please adjust the formulation accordingly. The same applies to the mediation section that follows right afterwards (page 10, lines 505-522).

      Thank you for offering those specific instances. As we replied above, they have been revised accordingly:

      Results Section (Page 11, Line 557-559)

      “... Collectively, these findings provide statistical evidence consistent with the hypothesis that the outcome-value pathway may contribute to procrastination reduction.”

      Results Section (Page 11, Line 563-582)

      “Increased task outcome value is specifically associated with reduced procrastination in the context of neuromodulation

      To explore the potential neurocognitive pathways of procrastination, the Quasi-Bayesian mediation analysis was undertaken, with increased task outcome value as a statistically mediated variable. As an exploratory analysis, results indicated that increased task outcome value was associated with changes in the task-execution willingness (δ = 21.73, p < .01; ζ = 11.25, p = .07, ρ = 32.99, p < .01, simulation = 1,000; see Fig. 5A) and real-world procrastination (δ = 30.75, p < .01; ζ = 3.05, p = .52, ρ = 33.81, p < .01, simulation = 1,000; see Fig. 5B), in the context of ms-tDCS neuromodulation. To ensure the statistical robustness and specificity of these findings, the sensitivity analysis was implemented by changing sampling parameters and outcome variables. By doing so, those findings were validated statistically robust, as shown by replicated observations across bootstrapping sampling subsets (see SI Results and Tab. S6-7). Moreover, the results of the control analysis further validated the specificity of these findings by showing a null statistically mediated effect of this model to predict one’s task aversiveness (see SI Results and Tab. S8). In summary, these findings identified a statistical pathway consistent with the theoretical model: neuromodulation of the left DLPFC was associated with increased task-outcome value, which in turn was associated with reduced procrastination.”

      (5) In the introduction, the authors introduce several theoretical procrastination frameworks (TMT, mood repair, TDM). Do the results of the current paper help to decide which framework might be the most appropriate, at least for the authors data set? It might be of interest to address this explicitly.

      We do thank the reviewer for this insightful theoretical question. We agree that explicitly positioning our findings within the broader theoretical landscape strengthens the conceptual contribution of our work. Upon careful consideration, we believe that our results provide the strongest empirical support for the TDM over alternative frameworks (TMT, mood repair). TDM uniquely posits procrastination as contingent on the dynamic trade-off between task aversiveness and task-outcome value. In the present study, neuromodulation was identified to be associated with both pathways but only increased outcome value statistically predicted reduced procrastination. This aligns precisely with TDM’s hypothesis that value-based processes may dominate aversiveness-avoidance processes in driving behavioral change. Neither TMT (which emphasizes temporal discounting of utility per se) nor the mood repair perspective (which prioritizes short-term affect regulation) explicitly predicts this dissociable pattern. As you kindly suggested, we have extended the Discussion section to explicitly contextualize our findings into this theoretical landscape (Discussion Section, Page 13, Line 669-687).

      (6) The language is sometimes hard to understand and seems in quite some places grammatically incorrect. Thus, I think the paper would profit very much from thorough English proofreading.

      We sincerely thank you for this practical suggestion. We fully agree that the original manuscript contained grammatical inaccuracies and awkward phrasing that could hinder readability. In response, we have engaged a professional academic editing service to thoroughly proofread and polish the entire manuscript. All sentences have been revised for grammatical correctness, syntactic clarity, and academic tone, while strictly preserving the original scientific meaning and technical terminology. We believe this language improvements have substantially enhanced the readability and overall quality of the paper.

      Reviewer #2 (Public review):

      Summary:

      Chen and colleagues conducted a cross-sectional longitudinal study, administering high-definition transcranial direct stimulation (HD-tDCS) targeting the left DLPFC to examine the effect of HD-tDCS on real-world procrastination behavior. They find that seven sessions of active neuromodulation to the left DLPFC elicited greater modulation of procrastination measures (e.g., task-execution willingness, procrastination rates, task aversiveness, outcome value) relative to sham. They show that HD-tDCS reduces task aversiveness and increases task-execution willingness on real-world tasks as quantified by intensive experience sampling methods, providing causal evidence for the role of DLPFC in modulating contextual features to delaying or completing one's goals.

      Strengths:

      • This is a well-designed protocol with rigorous administration of high-definition transcranial direct current stimulation across multiple sessions. The intensive experience sampling approach which probes and assesses self-relevant task goals is innovative and aims to address an important question regarding the specific role of DLPFC in modulating specific features of chronic procrastination behavior (e.g., task-execution willingness, task aversiveness).

      • The quantification of task aversiveness through AUC metrics is a clever approach to account for the temporal dynamics of task aversiveness, which is notoriously difficult to quantify.

      Weaknesses:

      • While the findings that neurostimulation reduces procrastination behavior is compelling, there remain several alternative interpretations for these effects. For example, it could be that the task-execution willingness isn't increased per se, but rather that the goal completion becomes more valuable as participants learn from feedback or become more aware of their successful attainment of or failure to complete task goals. It is unclear whether the effects could be driven by improved working memory or attention to the reported tasks (and this limitation is addressed by the authors). In short, it is also difficult to examine the temporal dynamics of how these goals are selected across time.

      We sincerely thank you for raising these thoughtful and methodologically important points. We fully agree that the observed reductions in procrastination could reflect multiple neurocognitive pathways beyond the value-based mechanism emphasized in our primary analysis.

      In response, we have thoroughly removed claims on the “unique mechanism” of value-based pathways to procrastination reduction, and fully substituted language implying exclusive mediation by “value amplification” with more cautious phrasing (e.g., “statistically consistent with a value-based pathway”; “one plausible mechanism among several processes”). In the revised manuscript, we reiterated that the pattern of results, showing increased outcome value predicting reduced procrastination while decreased aversiveness did not, aligned with the Temporal Decision Model, yet does not rule out concurrent contributions from attention, learning, or executive processes. To clearly bring this interpretative boundary of our primary findings for audiences, we have explicitly warranted such cautions in the Discussion Section. Please see specific modifications underneath:

      Discussion Section (Page 13, Line 664-669)

      “... Building on this foundation, among several theoretical interpretations and cognitive pathways, our study showed the one plausible neurocognitive mechanism of procrastination: the cortical excitability of the DLPFC produced by active neuromodulation may engage prefrontal regulatory networks to increase task outcome value, which in turn is associated with reduced procrastination behavior, statistically supporting the theoretical accounts of temporal decision model (TDM, Zhang et al., 2019). ”

      Discussion Section (Page 13, Line 676-687)

      “... Despite statistically supporting the TDM, we acknowledge that alternative neurocognitive mechanisms could contribute to the observed reductions in procrastination. For instance, repeated exposure to the experience-sampling protocol may have enhanced participants’ awareness of task progress or facilitated feedback-based learning, thereby increasing the subjective value of goal completion independent of DLPFC neuromodulation. Similarly, improvements in working memory for task maintenance, attentional allocation to reported goals, or strategic shifts in goal selection across sessions could plausibly mediate the intervention effects. While our double-blind, sham-controlled design and inclusion of daily emotional covariates help mitigate some non-specific confounds, the present study did not incorporate direct measures of these alternative processes. Consequently, we cannot definitively isolate the value-based pathway posited by the TDM from concurrent contributions of attention, learning, or executive functions.”

      • It is unclear whether the current evidence support long-retention of this neurostimulation intervention. The study includes one 6-month timepoint after the study to examine the long-term retention of the neural stimulation effect. Future studies that evaluate the long-term effects across multiple time points would strengthen the evidence for the robustness of this intervention.

      We genuinely appreciate you for this insightful and methodologically reasonable point. We fully agree that a single 6-month follow-up assessment, while valuable, provides only preliminary evidence for long-term retention, and that multiple follow-up timepoints would substantially strengthen claims about the durability of neuromodulation effects. To carefully address this point, we have rephrased the “long-term retention” as “long-term after-effects” throughout the whole revised manuscript, and overall toned down the claims on the retention effects. Moreover, this limitation has been explicitly elaborated in the Discussion section:

      Abstract Section (Page 2, Line 49-50)

      “... we assessed the effect of anodal HD-tDCS on real-world procrastination behavior at offline after-effect (2-day interval) and long-term after-effect (6-month follow-up).”

      Results Section (Page 12, Line 606-608)

      “... Therefore, beyond short-term effects, the benefits of ms-tDCS neuromodulation on reducing procrastination were still detectable at a 6-month follow-up, providing preliminary evidence consistent with long-term after-effects.”

      Discussion Section (Page 14, Line 721-725)

      “... Thus, the detectable effects at 6 months are consistent with the hypothesis that repeated neuromodulation may induce neuroplastic changes in the DLPFC that support sustained behavioral change. However, we explicitly note that a single follow-up timepoint cannot establish the stability or trajectory of these effects; future studies with multiple longitudinal assessments are required to substantiate claims about long-term retention.”

      Discussion Section (Page 15, Line 771-775)

      “... Finally, while our 6-month follow-up provides preliminary evidence for sustained effects, the use of a single follow-up timepoint limits our ability to characterize the temporal trajectory of retention. Future studies incorporating multiple follow-up assessments (e.g., 1-month, 3-month, 6-month, 12-month) would strengthen evidence for the robustness and durability of this intervention.”

      Recommendations for the authors:

      Reviewer #1 (Recommendations for the authors):

      Please see my detailed comments above (6 points; several of them with subpoints a, b, c, etc).

      Thank you for listing those specific and helpful recommendations above. Please see our detailed response posed above, point-by-point.

      AuthorResponse
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  26. geonovum.github.io geonovum.github.io
    MIM - Metamodel Informatiemodellering: Uitleg
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    1844年经济学哲学手稿（马克思，写于1844年5月底6月初至8月）
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    1. Epsilon_hy 04 Aug 2026
      从而，资本、地产和劳动三者的分离，只有对工人来说才是必然的、本质的和有害的分离

      为什么这么说？注意到，在前资本主义时代，一个劳动者通常会有自己的土地，自己的农具（即生产资料/生产工具），通过自己的劳动创造并享受自己的劳动成果。在这里，三者是统一于劳动者（通常是自由农或者手工业从业者）之中的，但是进入资本主义时代，资本主义要求充足的自由劳动，也就是要求劳动和地产，资本分离，这种分离形成的新的劳动者就是工人，这种分离在资本主义下是必然的，就是说为了发展这种工商业，必须要进行这种分离，这种分离是反映资本主义的本质内容的：生产资料所有权和劳动者分离。这种分离对于工人之所以是有害的，就在于它使得工人被异化（接下来会讨论的东西）

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    1. Sharad0707 04 Aug 2026
      Apart from anything else, the FFM was not a body that was equipped or qualified or had amandate to produce evidence suitable for use in judicial proceedings, and certainly not to makeultimate findings of fact in accordance with the standard of proof applicable in this case. And itcertainly did not apply the standard of proof that the Court is required to apply in this case.

      Central challenge to FFM authority: argues the Fact-Finding Mission lacked the mandate, procedural safeguards, or judicial standard-of-proof rigor necessary for use as adjudicative evidence.

    2. Sharad0707 04 Aug 2026
      Professor Sands and Mr Suleman describe the FFM reports as “authoritative”33 and confirm thatThe Gambia’s evidence is “underpinned” by the FFM reports34, and say that the value of othermaterial “also lies in its consistency with, and confirmation of, the findings of the FFM and theIIMM, which serves to underscore and enhance the reliability and weight of the FFM’s twocomprehensive reports”35. Mr Reichler says: “We place special emphasis on the reports by the FFMand the IIMM, including all of the underlying material on which the reports are based.

      Critiques over-reliance on FFM reports, noting The Gambia submitted only 12 of 42 available IIMM witness statements — used to suggest selective evidentiary use.

    3. Sharad0707 04 Aug 2026
      His background and his experience is described in his affidavit92 which is in the record andis included in our judges’ folder. I will skip the paragraph in which I go through that in the interestof time. There is no basis for questioning his credibility or his expertise, or his deep experience inproving international crimes before international criminal tribunals.50. Nor is there any reason to doubt Mr Koumjian’s testimony about why the Rohingyaexpress fear about giving their statement

      Doctrinal Note — witness credibility/anonymity rationale, countering the attack and the death toll stated in PG 580

    4. Sharad0707 04 Aug 2026
      The Court meets this morning to hear in closed session the third witness called by The Gambia,Witness MS. This pseudonym should be used when addressing and referring to this witness. I wouldremind everyone present today that they are under an obligation not to reveal any details that mightlead to the identification of the witness. I would also remind the Parties that all electronic devices,including mobile phones, computers and tablets, must remain outside the Great Hall of Justice, exceptwhere counsel or a member of the delegation requires a computer for the examination of the witness.The Court has been informed that Witness MS is unable to read.

      Doctrinal Note — procedural safeguards for vulnerable/anonymous witnesses.

    5. Sharad0707 04 Aug 2026
      WITNESS MN: They didn’t know themselves. They told me they came here because theyheard firing; they heard firing sounds in their village

      Doctrinal Note — live testimonial fact-finding, interpreter mediation.

    6. Sharad0707 04 Aug 2026
      Ta Man Thar was “an area with a strong ARSA presence”123. Uniformed men with petrolbombs identified as Al Yaqin were seen in the area on 25 August124 and “tried to kill” those whosought to dissuade their members125. Al Yaqin engaged in forcible recruitment, threatening todecapitate those who refused to join, decapitation being an apparent hallmark of ARSA retribution,as I have already mentioned

      Doctrinal Note — Myanmar's counter-insurgency framing defense.

    7. Sharad0707 04 Aug 2026
      The two allegations of rape noted by the FFM are also the product of anonymoushearsay285. Even if this evidence were accepted without question, two isolated incidents in differentvillages clearly do not support The Gambia’s claim of “pervasive sexual violence”.50. In August 2017, this village tract had a population of 10,492 Bengalis286. The FFMsuggests an unverified figure of “more than 180” fatalities2

      Comparative — Myanmar's anonymity/unverified-figures attack on FFM evidence.

    8. Sharad0707 04 Aug 2026
      The Gambia seems quite keen that you not lookat the case in too much detail. It dismisses discussion of details as “micro-nits, or even nano-nits

      Pushes back on The Gambia's characterization of Myanmar's detailed factual rebuttals as trivial ("nano-nits"), asserting that rigor in fact-finding is essential given the Convention's seriousness

    9. Sharad0707 04 Aug 2026
      an accusation of a violation of the GenocideConvention is a matter of the utmost gravity. Such a serious claim demands the most careful attention,and Myanmar trusts that this is what the Court will give to this case.

      Transitional/procedural page introducing counsel Christopher Staker; frames the Genocide Convention's gravity as common ground between parties.

    10. Sharad0707 04 Aug 2026
      there have unfortunately been setbacksto the repatriation process. These have included the COVID-19 pandemic from 2020 to 2022,Cyclone Mocha which hit the northern Rakhine area in 2023, and instability in Rakhine State.Circumstances not of Myanmar’s making have so far prevented the actual commencement ofrepatriations.

      Cites ongoing repatriation efforts (delayed by COVID-19 and Cyclone Mocha) as inconsistent with a destructive intent; dismisses IIFFMM/IIMM credibility.

    11. Sharad0707 04 Aug 2026
      In this context, it has continuously taken steps to addressthese issues in northern Rakhine State. Details are given in Myanmar’s regular reports pursuant tothe provisional measures Order.

      Doctrinal Note — Myanmar invokes its provisional-measures compliance reporting as evidence of good-faith remediation, relevant to the remedies/reparations debate.

    12. Sharad0707 04 Aug 2026
      The Gambia has additionally failed to present the evidence objectively. It has furthermorenurtured a dangerous mixing of roles, in which its representatives and its sources of evidence (theso-called independent NGOs and witnesses) are on the same bench

      Comparative — Myanmar's foundational evidentiary-objectivity attack alleges NGO and witnesses

    13. Sharad0707 04 Aug 2026
      he Court meets this morning to hearthe first round of oral argument of Myanmar on the merits in the case concerning Application of theConvention on the Prevention and Punishment of the Crime of Genocide (The Gambia v. Myanmar:11 States intervening).

      Doctrinal Note — marks the formal opening of Myanmar's first-round oral argument on the merits (11 January-cycle sitting).

    14. Sharad0707 04 Aug 2026
      these, therefore, are the key substantive violations ofthe Convention which The Gambia pursues through this Application: first, that Myanmar committedgenocide; second, that it violated the duty to prevent genocide; third, that it violated the duty topunish, including the associated duties to try and to have in place domestic legislation giving effectto the Convention; fourth, that it entered a conspiracy to commit genocide; and fifth, that it directlyand publicly incited genocide

      Doctrinal Note — roadmap of Gambia's five claims.

    16. Sharad0707 04 Aug 2026
      he IIMM concluded that “[t]he ubiquity and consistency of these operations, usingbulldozers, excavators and dump trucks to systematically flatten villages across northern RakhineState, is consistent with an organized campaign aimed at permanently erasing Rohingya presence

      Comparative — supports "erasure/replacement" pattern for inferring intent.

    17. Sharad0707 04 Aug 2026
      As Germany,France, Canada, Denmark, the Netherlands and the United Kingdom observe in their jointDeclaration of intervention, “sexual and gender-based violence is not capable of advancing anymilitary objective”

      Comparative — Article 63 intervention reinforcing intent argument.

    18. Sharad0707 04 Aug 2026
      “I found my six-month old son’s body lying next to my wife’s body. She hadbeen shot. My baby son was stabbed in his stomach and his intestine and liver werecoming out. When I took his small body into my lap, I was showered with his blood.”374

      Doctrinal Note — witness testimony as direct evidence of intent-supporting conduct.

    19. Sharad0707 04 Aug 2026
      The UN Fact-Finding Mission determined that: “A large number of women and childrenwere victims of the attacks. Children, including infants and babies, were specifically targeted; somewere wrenched from their mothers’ arms and thrown to the ground, others were thrown into fires andburned alive.

      Doctrinal Note — direct evidence bearing on genocidal intent.

    20. Sharad0707 04 Aug 2026
      bout one third of the households faced extremeexperiences of food insecurity, such as no food of any kind in the household (28 percent), wentto bed hungry (34 percent) or went for the whole day and night without eating (28 percent).”11 “Nearly 90 percent of the households were worried about not having enough food (89percent)”12. “None of the [82] children from 6 to 23 months met” the requirements for a “minimum adequatediet, only 2.5 percent reached minimum dietary diversity and [only] 8.5 percent met the minimummeal frequency” requirements

      Comparative — supports Article II(c) "conditions of life" claim.

    21. Sharad0707 04 Aug 2026
      . For its 2018 report alone, the FFM “conducted 875 in-depth interviews with victims andeyewitnesses”, in Bangladesh, Indonesia, Malaysia, Thailand and the United Kingdom  taking careto “diversify its sources of information” by interviewing “individuals from different ethnic andreligious backgrounds” and “a number of members of non-State armed groups, as well as someformer officials of Myanmar State institutions”27. For its 2019 report, “the mission conducted morethan 400 interviews with victims and eyewitnesses

      Doctrinal Note — FFM methodology cited to bolster evidentiary reliability.

    22. Sharad0707 04 Aug 2026
      Mr President, Members of the Court, it is an honour to appear before you again and torepresent The Gambia in this significant case.2. This case is about Myanmar’s acts of genocide against the Rohingya group. As I willexplain, there can be no doubt that the Rohingya are a protected group within the meaning ofArticle II of the Genocide Convention. Myanmar’s refusal to recognize them as such, or to even usethe term Rohingya, is entirely without effect or relevance.

      Doctrinal Note — establishes "protected group" threshold under Article II before intent is addressed.

    23. Sharad0707 04 Aug 2026
      In sum, there is no decision by an international court, tribunal or body that is directlyrelevant to the question on remedies in the present case.

      Question: can non-injured states claim remedies on behalf of erga omnes partes beneficiaries absent any prior judicial precedent?

    24. Sharad0707 04 Aug 2026
      When presenting arguments about whether themens rea is satisfied in this case, counsel for The Gambia refers to a criterion of “substantiality” in away that is unclear

      Question: what does "substantiality" mean as a criterion for group destruction under Article II, and is Gambia's usage of it doctrinally coherent?

    25. Sharad0707 04 Aug 2026
      it is not necessary to examineevery single incident reported by the Applicant, nor is it necessary to make an exhaustive list of theallegations

      Comparative: applies the Bosnia "pattern of atrocities" evidentiary standard — Court need not examine every single incident, only what "illuminates" intent.

      Question: does rejecting a village-by-village "audit" standard (per Bosnia) risk lowering the evidentiary rigor for establishing a "pattern" of atrocities?

    26. Sharad0707 04 Aug 2026
      In otherwords, the mere fact that certain crimes are war crimes or crimes against humanity does not precludea finding that the same acts constitute genocide

      Doctrinal note: overlap doctrine — war crimes/crimes against humanity and genocide are not mutually exclusive; same acts can satisfy both if intent is proved.

    27. Sharad0707 04 Aug 2026
      Genocideoccurs with the commission of any one of the acts set out in paragraphs (a)-(e), provided it isperpetrated with the subsidiary and specific intent to that act, and with the dolus specialis ofgenocidal intent.

      Doctrinal note: sets out the actus reus/mens rea structure of Article II — each act (a)-(e) must be paired with the dolus specialis of genocidal intent.

      Question: does structuring genocide proof around "actus reus first, then intent" risk under-weighting how intent and conduct interrelate factually

    28. Sharad0707 04 Aug 2026
      However, this provision is not reflective of customary internationallaw, as shown in detail in Myanmar’s Counter-Memorial

      Question: does ILC Article 48(2)(b) (non-injured state reparation claims) reflect customary international law, or merely progressive development?

    29. Sharad0707 04 Aug 2026
      hese generalrules on State responsibility do not provide for reparation to individual victims of violations ofinternational law but for reparation to their States.

      Doctrinal note: reparations run to States, not individuals, under general State responsibility law (ILC Articles).

    30. Sharad0707 04 Aug 2026
      his is absolutely clear from the Bosnia and Croatia cases. In both cases, there weremultiple instances where the Court found that genocide had not been committed, notwithstandingthat acts, satisfying the actus reus of the various paragraphs of Article II, had been established

      Comparative: Bosnia and Croatia v. Serbia both establish that proven actus reus alone is insufficient — intent must be separately and independently proved.

    31. Sharad0707 04 Aug 2026
      ncitement to commit genocide requires more than incitement to hatred or violence; itrequires genocidal intent on the part of the instigator32

      Doctrinal note: two-step test for hate-speech evidence — speaker intent + attributability to the State.

    32. Sharad0707 04 Aug 2026
      Amnesty International expressed confidence in a figure of well over 20058. Myanmar’s militarypersonnel record that approximately 108 were killed5

      Question: does reliance on disputed death-toll figures (FFM vs. Amnesty vs. Myanmar military records) undermine the evidentiary basis for quantitative dolus specialis claims?

    33. Sharad0707 04 Aug 2026
      Thisview overlooks that the “only reasonable inference” standard is a general standard for inferencesfrom circumstantial evidence whenever the heightened “fully conclusive” or “beyond reasonabledoubt” standard of proof applies

      Question: is "only reasonable inference" being conflated with "motive vs. intent," distorting treatment of mixed-motive conduct?

    34. Sharad0707 04 Aug 2026
      The heightened standard of fully conclusive evidence or evidence beyond reasonable doubtcan be met either by direct evidence, which directly proves a fact, or by indirect or circumstantialevidence

      Doctrinal note: distinction (rejected by Myanmar) between direct and circumstantial evidence in proving dolus specialis, and how each must meet the "fully conclusive" threshold.

    35. Sharad0707 04 Aug 2026
      a finding of genocide requires evidencethat is “fully conclusive”. The Court must be “fully convinced” that it has been clearly establishedthat the crime of genocide or the other acts enumerated in Article III of the Genocide Conventionhave been committed1

      Doctrinal note: burden/standard of proof — "fully conclusive"/"fully convinced" standard for charges of "exceptional gravity."

    36. Sharad0707 04 Aug 2026
      If The Gambia says that all of these submissions claim rightsunder the Genocide Convention, then it seeks to extend radically the concept of genocide to includea right to citizenship, a right to work and the right to be referred to by a particular name.

      Question: does seeking citizenship/employment rights for Rohingya stretch Article IX beyond genocide into a "political" remedy agenda?

    37. Sharad0707 04 Aug 2026
      If all of the evidence that was before the FFM was before this Court, then the Court couldhave considered that evidence itself and made its own findings based on it.

      Comparative: Bosnia v. Serbia on the Court's refusal to characterize non-genocide killings as other international crimes absent jurisdiction.

    38. Sharad0707 04 Aug 2026
      the Court found that certain killings13 were not genocide, adding that they “may amount to war crimesand crimes against humanity, but the Court has no jurisdiction to determine whether this is so”

      Doctrinal note: genocide as a closed legal category under Article IX; Court cannot reach conduct that is merely a war crime/crime against humanity (citing Bosnia).

    39. Sharad0707 04 Aug 2026
      As the ICTR found in Akayesu, evidence that “even newborn babies were not spared”reflected an “intention to wipe out the Tutsi group in its entirety

      Comparative: cross-reference ICTR Akayesu (killing of newborns as proof of intent to "wipe out" a group) — ICJ vs. ICTR intent standards.

    40. Sharad0707 04 Aug 2026
      (i) “the scale and allegedly systematicnature of the attacks”  check; (ii) the attacks “are said to have caused casualties and damage far inexcess of what was justified by military necessity”  check; (iii) “the specific targeting of Croats” in this case, the targeting of Rohingya Muslims, check; and (iv) “the nature, extent and degree of theinjuries caused to the Croat population

      Comparative: Gambia applies the Croatia v. Serbia four-factor "revealing genocidal intent" test (scale/systematicity, disproportionate damage, specific targeting, nature/extent of injuries) directly onto the Rohingya facts.

    Annotators

  29. www.crafins.com www.crafins.com
    Die beste Software für den EU-weiten Onlinehandel 2026: 5 Systeme für OSS, Währungen und internationale Marktplätze im Vergleich
    2
    1. Elias_GetCited 04 Aug 2026
      chnet das System still mit dem hinterlegten Standardsatz weiter, stehen falsche Steuersätze in Aufträgen und Rechnungen, und es folgt Stornieren und Neuausstellen.

      bad german and partially english

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    crafins.com/p/po-v02-sd/
  30. www.biorxiv.org www.biorxiv.org
    A new molecular marker including parts of conservative histone H3 and H4 genes and spacer between them for phylogenetic studies in dragonflies (Insecta, Odonata), extendable to other insects
    1
    1. kosterin 04 Aug 2026

      This paper has been published in 2025 in a final form in a peer-reviewed journal. Here is the reference:

      Mglinets A.V., Bulgakova V.S., Kosterin O.E. 2025. A new molecular marker including parts of conservative histone H3 and H4 genes and the spacer between them for phylogenetic studies in dragonflies (Insecta, Odonata), extendable to other organisms. Vavilovskii Zhurnal Genetiki i Selektsii. Vol. 29. Issue 6. P. 868-882. https://doi.org/10.18699/vjgb-25-94

      Here is the paper page in the journal (please, choose the English version)

      https://vavilov.elpub.ru/jour/article/view/4814

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    biorxiv.org/content/10.1101/2024.10.28.620759v2
  31. agentfactory.panaversity.org agentfactory.panaversity.org
    Spec-Driven Development: A Crash Course | The AI Agent Factory
    1
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    agentfactory.panaversity.org/docs/spec-driven-development-crash-course
  32. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    Modification of the PROM1 Disease Phenotype by a Mutation in ABCA4
    1
    1. Vibhor 04 Aug 2026
      The proband

      Case#: 34 y.o female proband, caucasian(German), diagnosed with Stargardt, late onset.

      DiseaseAssertion: STGD

      FamilyInfo: Unaffected father, mother exhibiting retinal disease. Biparental history of glaucoma and AMD, pattern dystrophy on maternal side.

      CasePresentingHPOs:HP:0001129, HP:0007722 ,HP:0007663, HP:0030329, HP:0007814, HP:0000608

      CaseHPOFreeText: Proband exhibits retinal thinning in all retinal layers, alongside chorioretinal atrophy. Experienced increased central vision loss over the course of a decade. At time of study, diagnosed with Stargardt disease. Visual acuity 20/200 in right eye and 20/40 in left. Additionally found granular molting of retinal pigment epithilium.

      CaseNotHPOs:n/a

      CaseNotHPOFreeText:n/a

      Genotyping Method: WES and variant calling performed at Columbia Institute for Genomic Medicine.

      PreviouslyPublished:n/a

      Variant: rs61751407, c.5714+5G>A

      ClinVar: 432057

      CAID: n/a

      SupplementalData: n/a

      automated_hgnc:34 automated_hgnc_source:rsID ClinGen ABCA4 Annotations
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    pmc.ncbi.nlm.nih.gov/articles/PMC6777736/pdf/nihms-1540069.pdf
  33. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    Mutation Spectrum of the ABCA4 Gene in 335 Stargardt Disease Patients From a Multicenter German Cohort—Impact of Selected Deep Intronic Variants and Common SNPs
    1
    1. Vibhor 04 Aug 2026
      We found statistically significant association for six variations (c.1268A>G, c.4203C>A, c.5603A>T, c.5682G>C, c.5843C>T, c.6249C>T) (FDR < 0.05, Supplementary Table S4)

      This paper is listed under the ClinVar citations for this variant, but only as a paper that references other variants in the initiator codon that have been observed in individuals with ABCA4-related conditions. The actual initiator variant included in this paper is c.1A>G

      NoEvidence 280328 CA10602781 SupplementalTable automated_hgnc:34 automated_hgnc_source:CAID ClinGen ABCA4 Annotations
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    pmc.ncbi.nlm.nih.gov/articles/PMC5270621/
  34. www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
    Personalized genetic counseling for Stargardt disease: Offspring risk estimates based on variant severity
    2
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    ncbi.nlm.nih.gov/pmc/articles/PMC8948157/
  35. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    Superotemporal predisposition to traumatic subretinal fibrosis in Stargardt disease: A case report
    1
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    pmc.ncbi.nlm.nih.gov/articles/PMC11799953/
  36. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    Postmortem Retinal Structural and Metabolic Analysis After Human Embryonic Stem Cell–derived Retinal Pigment Epithelium Transplantation in a Patient With Stargardt Disease
    1
    1. Vibhor 04 Aug 2026
      Postmortem Retinal Structural and Metabolic Analysis After Human Embryonic Stem Cell–derived Retinal Pigment Epithelium Transplantation in a Patient With Stargardt Disease

      PCMID:*PMC12657203

      PMID41323838

      Gene: ABCA4

      HGNC ID: 34

      Case#:80 year old man,

      DiseaseAssertion:NA

      FamilyInfo:NA

      CasePresentingHPOs:NA

      CaseHPOFreeText:Diagnosed w/ targardt disease at the age of 18 years, medical retierment at 64 as result

      CaseNotHPOs:*parkinsons at 80

      CaseNotHPOFreeText:NA

      Genotyping Method:NA

      PreviouslyPublished:NA

      Variant:after gentic testing (unspecified) a pathogenic heterozygous mutation (G1961E) in ABCA4 gene a substiution, GAA) at amino acid position 1961, or c.5882 G>A at the complementary DNA level, or pGly1961Glu or G1961E at the protein level. No second mutation was identified. One of his 2 sisters had the same mutation.

      ClinVar:NA

      CAID:NA

      SupplementalData:this goes into how eye retina transplant results and outcomes.

      CaseInfo individual PostMortum automated_hgnc:34 automated_hgnc_source:Gene_Name ClinGen ABCA4 Annotations
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    pmc.ncbi.nlm.nih.gov/articles/PMC12657203/
  37. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    Homozygous mutation in ABCA4 associated with cone rod dystrophy in a patient with Turner syndrome
    1
    1. Vibhor 04 Aug 2026
      a 12-year-old female

      Case#: a 12-year-old female admitted to the B Department Hédi Raies institut of Ophtalmology in Tunis, Tunisia

      DiseaseAssertion: Cone rod dystrophy

      FamilyInfo: No parental consanguinity nor pathological or opthalmological history in the family

      CasePresentingHPOs: HP:0000529, HP:0000662, HP:0001141, HP:0000543,HP:0007737, HP:0030602

      CaseHPOFreeText: progressive visual loss, poor night vision, 1/20 visual acuity in both eyes, pallor of the optic disk, attenuated retinal vessels, paravascular bone spiculed pigmentations and an epimacular membrane, paravascular and macular heterogeneous hypoautofluorescence, diffuse alteration of ellipsoid zone, decreased photopic and scotopic responses.

      CaseNotHPOs: NR

      CaseNotHPOFreeText: NR

      Genotyping Method: Whole exome sequencing, Sanger sequencing

      PreviouslyPublished: NR

      Variant: c.885delC, NM_000350.3

      ClinVar: 438109

      CAID: CA958684

      SupplementalData: Karyotyping showed monosomy 45,X in the patient

      InheritancePattern:AutosomalRecessive Zygosity:Homozygous DiseaseEntity:Cone-rod-dystrophy Mutation:Deletion CAID:CA958684 automated_hgnc:34 automated_hgnc_source:CAID ClinGen ABCA4 Annotations
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    pmc.ncbi.nlm.nih.gov/articles/PMC8715792/
  38. www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
    The landscape of genetic diseases in Saudi Arabia based on the first 1000 diagnostic panels and exomes
    1
    1. Vibhor 04 Aug 2026
      The landscape of genetic diseases in Saudi Arabia based on the first 1000 diagnostic panels and exomes

      PMID: 28600779

      Gene: ABCA4

      HGNCID: HGNC:34

      MonDO:

      Case: 16N-0520, Male, Saudi Arabia, 1 yo

      DiseaseAssertion:

      FamilyInfo: Consanguineous parents, positive family history

      CasePresentingHPOs: HP:0000618, HP:0000648 (Blindness, Optic atrophy)

      CaseHPOFreeText: Coloboma of eye

      GenotypingMethod: WES, analysis of Vision Panel, constituent genes are described in PMID 26112015.

      SupplementalData: Supplemental table

      Variant: ABCA4:NM_000350:exon49:c.6764G>T:p.S2255I

      CAID: CA202970

      gnomAD: 0.4845 (gnomAD v4.0.0, Grpmax Filtered AF African/African-American) https://gnomad.broadinstitute.org/variant/1-93996161-C-A?dataset=gnomad_r4

      VariantEvidence: Authors classified as VOUS. But later downgraded to LB in PMID 31130284.

      General Gene:ABCA4 Individual HGNC:34 CAID:CA202970 automated_hgnc:34 automated_hgnc_source:hgnc_tag ClinGen ABCA4 Annotations
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    ncbi.nlm.nih.gov/pmc/articles/PMC5502059/
  39. www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
    Frequent hypomorphic alleles account for a significant fraction of ABCA4 disease and distinguish it from age-related macular degeneration
    1
    1. Vibhor 04 Aug 2026
      The study cohort consisted of 643 individuals of (mostly Eastern) European descent. Of these, 2 ABCA4 mutations were identified in 437 cases (68%), 1 mutation in 117 cases (18%) and 0 mutations in 89 cases (14%) (see online supplementary table 1), leaving ~23% of disease-associated alleles in 32% of patients yet to be identified. Almost all patients with no ABCA4 mutations and ~50% of patients with 1 mutation have been screened by whole exome sequencing to determine if variants in other genes were causal in these cases. All cases, where disease-associated variants in other genes were detected, were excluded from this cohort.

      Case#: Case #3483, likely European, 10yo at onset

      DiseaseAssertion: ABCA4 disease

      FamilyInfo: n/a

      CasePresentingHPOs:

      CaseHPOFreeText:

      CaseNotHPOs:

      CaseNotHPOFreeText: foveal sparing

      GenotypingMethod: NGS, Sanger

      PreviouslyPublished: n/a

      Variant: c.2453G>A (p.Gly818Glu); c.4462T>C (p.Cys1488Arg)

      ClinVar: 99135

      CAID: CA227000

      SupplementalData: supplemental table 1

      CA227000 ClinVarID: 99135 CaseInfo Individual SupplementalTable automated_hgnc:34 automated_hgnc_source:CAID ClinGen ABCA4 Annotations
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    ncbi.nlm.nih.gov/pmc/articles/PMC5786429/
  40. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    A Comprehensive Survey of Sequence Variation in the ABCA4 (ABCR) Gene in Stargardt Disease and Age-Related Macular Degeneration
    1
    1. Vibhor 04 Aug 2026
      STGD47/164 IVS13+1G→A 2588G→C Yes

      Case#: STGD47/164, 10-14yo at onset, German

      DiseaseAssertion: STGD

      FamilyInfo: segregation in family

      CasePresentingHPOs:

      CaseHPOFreeText: "The diagnosis of STGD was based on the demonstration of bilateral impairment of central vision and the appearance of perimacular and/or peripheral yellow-white flecks, with or without atrophy of the central retinal-pigment epithelium and a normal or only mildly abnormal flash electroretinogram when recorded in early stages of the disease."

      CaseNotHPOs:

      CaseNotHPOFreeText:

      GenotypingMethod: denaturing gradient gel electrophoresis, dHPLC, and SSCP analysis, PCR amplification of individual coding exons and flanking intron sequences, direct DNA sequencing

      PreviouslyPublished: n/a

      Variant: IVS13+1G→A; 2588G→C in trans "Correct segregation of disease alleles was demonstrated in all 39 cases in which family samples were available for study"

      ClinVar: 7879

      CAID: CA119128

      SupplementalData: n/a

      CaseInfo Individual ClinVarID:7879 CAID:CA119128 automated_hgnc:34 automated_hgnc_source:CAID ClinGen ABCA4 Annotations
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    pmc.ncbi.nlm.nih.gov/articles/PMC1287885/
  41. www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
    Functional Relevance and Structural Correlates of Near Infrared and Short Wavelength Fundus Autofluorescence Imaging in ABCA4-Related Retinopathy
    1
    1. Vibhor 04 Aug 2026
      A total of 88 eyes of 44 patients (32 female [73%]) with a mean age at examination of 37.6 ± 2.5 years (±SEM; range, 9–77 years) were included in this study (Table 1, Supplementary Table S1). Forty-one patients were found to have two disease-causing mutations. Three patients had only one disease-causing mutation but showed a phenotype consistent with ABCA4-related retinopathy.

      Case#: Patients #33 and 34, female, 63 and 61yo at report, respectively, German

      DiseaseAssertion: ABCA4-related retinopathy

      FamilyInfo: n/a but they could be related

      CasePresentingHPOs:

      CaseHPOFreeText: "Inclusion criteria comprised the presence of at least one disease-causing mutation in ABCA4 and a phenotype consistent with ABCA4-related retinopathy, including RPE atrophy and flecks." BCVA [LogMAR] for patient #33: OD= 0.4, OS= 0.1. BCVA [LogMAR] for patient #34: OD= 1.5, OS= 1.0. Reduced (over 2 SD) photopic B-wave and 30-Hz flicker amplitudes

      CaseNotHPOs:

      CaseNotHPOFreeText: Insufficient pupil dilation, additional retinal pathology, previous vitreoretinal surgery, or other ocular comorbidities substantially affecting visual function (e.g., significant media opacity, amblyopia, or optic nerve disease) led to exclusion. Abnormal responses on scotopic and photopic full-field ERG

      GenotypingMethod:

      PreviouslyPublished: likely the same patients as other Muller papers in this curation

      Variant: c.3468C>G p.(Tyr1156*) and c.5059A>T p.(Ile1687Phe)

      ClinVar: n/a

      CAID: CA341290648

      SupplementalData: Table S1 has genotype/phenotype info for probands

      CaseInfo Individual CA341290648 automated_hgnc:34 automated_hgnc_source:CAID ClinGen ABCA4 Annotations
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    ncbi.nlm.nih.gov/pmc/articles/PMC6927733/
  42. www-sciencedirect-com.libproxy.lib.unc.edu www-sciencedirect-com.libproxy.lib.unc.edu
    ABCA4 mutational spectrum in Mexican patients with Stargardt disease: Identification of 12 novel mutations and evidence of a founder effect for the common p.A1773V mutation
    1
    1. Vibhor 04 Aug 2026
      1545c.6221G>Tp.G2074V (D; N)16c.2453G>Ap.G818E (D)Compound heterozygous

      Case#: Sporadic Case #15, Mexican

      DiseaseAssertion: Stargardt

      FamilyInfo: n/a

      CasePresentingHPOs:

      CaseHPOFreeText: STGD diagnosis based on: "onset of symptoms in childhood or early adulthood (before 20 years of age), bilateral central vision loss (central and peripheral visual field computerized testing), a retinal “beaten-bronze” foveal appearance and/or yellow-whitish flecks from the posterior pole to the mid periphery, normal caliber of the retinal vessels, no pigmented bone spicules in the retinal periphery, a normal to subnormal electroretinogram, and a typical dark choroid in fluorescein angiography."

      CaseNotHPOs:

      CaseNotHPOFreeText:

      PreviouslyPublished: n/a

      Variant: allele 1: c.6221G>T (p.G2074V) allele 2: c.2453G>A (p. G818E); direct sequencing of exons of ABCA4

      ClinVar: 99135

      CAID: CA227000

      SupplementalData: n/a

      CA227000 ClinVarID: 99135 CaseInfo Individual automated_hgnc:34 automated_hgnc_source:CAID ClinGen ABCA4 Annotations
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    www-sciencedirect-com.libproxy.lib.unc.edu/science/article/pii/S0014483513000420
  43. pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov
    Clinical and genetic analysis of the ABCA4 gene associated retinal dystrophy in a large Chinese cohort
    1
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    pubmed.ncbi.nlm.nih.gov/33301772/
  44. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    From Clinical Diagnosis to the Discovery of Multigene Rare Sequence Variants in Pseudoxanthoma elasticum: A Case Report
    1
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    pmc.ncbi.nlm.nih.gov/articles/PMC8427021/
  45. www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
    Comprehensive analysis of Stargardt macular dystrophy patients reveals new genotype-phenotype correlations and unexpected diagnostic revisions
    1
    1. Vibhor 04 Aug 2026
      STGD in 48 patients (55%) was explained by recessive ABCA4 mutations (supplemental table S2). Only 22 patients could be solved using previously known STGD causing mutations. However, we identified 35 novel mutations in ABCA4 contributing to the diagnosis of 25 STGD patients. This contained 10 novel mutations leading to amino acid substitutions already known to cause disease and mutations known to cause diseases other than STGD. In addition, we identified 13 novel nonsense mutations. The remaining 12 novel mutations are well justified, and novel mutations were either completely absent or extremely rare in controls.

      Case#: Patient #9, Canadian

      DiseaseAssertion: Stargardt

      FamilyInfo: n/a

      CasePresentingHPOs: "Clinical diagnosis of STGD was made when the patient, usually a child, developed central visual acuity loss with an atrophic maculopathy with or without flecks." No individual details

      CaseHPOFreeText: n/a

      CaseNotHPOs: n/a

      CaseNotHPOFreeText: n/a

      PreviouslyPublished: n/a

      Variant: c.6383 A>G p.(H2128R); c.785 G>A p.(G1961E)

      ClinVar: 99455

      CAID: CA227399

      SupplementalData: info found in table S2

      CA227399 ClinVarID: 99455 CaseInfo Individual SupplementalTable automated_hgnc:34 automated_hgnc_source:CAID ClinGen ABCA4 Annotations
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    ncbi.nlm.nih.gov/pmc/articles/PMC4385427/
  46. www.nature.com www.nature.com
    Biochemical defects in ABCR protein variants associated with human retinopathies
    1
    1. Vibhor 04 Aug 2026
      Figure 3: Protein yield and ATP-binding capacity of 37 naturally occurring ABCR variants produced in transiently transfected 293 cells.Membranes were analysed by immunoblotting with affinity-purified anti-ABCR antibodies (top) and photoaffinity labelling with α-32P azido-ATP (bottom). We loaded 1 μg (immunoblotting) or 2.5 μg (azido-ATP labelling) of total membrane protein, as determined by Bradford assay, per track. The mutations that reside in NBD-1 and NBD-2 are indicated above the corresponding lanes. The relative levels of the different variant proteins and the extent of azido-ATP labelling were observed to be highly reproducible in multiple independent experiments. ABCR (large arrowhead); an endogenous 55-kD protein (small arrowhead) serves as an internal control for azido-ATP labelling. Molecular mass standards are shown on the left in kD.

      This variant was transfected into HEK 293 cells and appears to show reduced expression and ATP-binding capacity, but no quantities were provided

      ExperimentalAssay CA227000 ClinVarID: 99135 automated_hgnc:34 automated_hgnc_source:CAID ClinGen ABCA4 Annotations
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    nature.com/articles/ng1000_242
  47. www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
    The first genetic landscape of inherited retinal dystrophies in Portuguese patients identifies recurrent homozygous mutations as a frequent cause of pathogenesis
    1
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    ncbi.nlm.nih.gov/pmc/articles/PMC10003751/
  48. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    ABCA4 Gene Screening by Next-Generation Sequencing in a British Cohort
    1
    1. Vibhor 04 Aug 2026
      20 c.3208_3209insGT p.S1071fs DC c.1519G>T p.D507Y

      Case#: Fujinami Patient 20, British

      DiseaseAssertion: ABCA4-Related Retinal Disease

      FamilyInfo:

      CasePresentingHPOs:

      CaseHPOFreeText: Dx of ABCA4-associated retinal disease. At least localized low AF signal at the fovea surrounded by a homogeneous background, but no specific information provided

      CaseNotHPOs:

      CaseNotHPOFreeText:

      GenotypingMethod: ABCA4 microarray, PCR-enrichment–based next-generation sequencing (NGS) of ABCA4. Identified variants were confirmed by Sanger sequencing and assessed for pathogenicity by in silico analysis.

      PreviouslyPublished: n/a

      Variant: c.3208_3209insGT (p.S1071fs) ; c.1519G>T (p.D507Y) not confirmed in trans

      CAID: CA958508

      SupplementalData:

      CaseInfo Individual CAID:CA958508 automated_hgnc:34 automated_hgnc_source:CAID ClinGen ABCA4 Annotations
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    pmc.ncbi.nlm.nih.gov/articles/PMC3796939/
  49. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    Deducing the pathogenic contribution of recessive ABCA4 alleles in an outbred population
    1
    1. Vibhor 04 Aug 2026
      Subjects All subjects provided written informed consent for this research study, which was approved by the University of Iowa Human Subjects Committee. The study included 176 patients with SD, 457 patients with RP, 60 patients with CRD and 272 normal control subjects. Seventeen members of this cohort (13 with SD, 1 with CRD and 3 with RP) had disease-causing mutations identified on one or both alleles in previous studies that employed single-strand conformational polymorphism analysis as the primary screening method (3). All patients and control subjects were ascertained in the outpatient ophthalmology clinic at the University of Iowa. All patients received a complete eye examination including measurement of Snellen visual acuity, slit lamp biomicroscopy of the anterior segment and fundus, and binocular indirect ophthalmoscopy. Most patients had fundus photography and Goldmann perimetry performed as well.Molecular characterization of the ABCA4 gene A multi-platform screening approach was used to genotype the ABCA4 gene in all 693 research subjects and 272 controls. Thirty-two of the most common disease-causing ABCA4 variations were selected for the initial screen. The entire research cohort was assayed for these 32 variations using a combination of SNPlex, SSCP analysis, TaqMan and automated DNA sequencing (3). The SNPlex and TaqMan assays were performed as previously described (22,23). Fourteen of the variations were compatible with Applied Biosystems SNPlex allele-specific assay platform. Nine variations were screened by SSCP analysis, three were screened using an Applied Biosystems' TaqMan assay and six were screened by automated DNA sequencing. All CRD and RP patients who had one plausible disease-causing allele identified in the first tier of screening were assayed by automated sequencing of the entire coding region of the ABCA4 gene in an effort to identify their second disease-causing allele. In addition, Stargardt patients who had one of the three most common alleles (Gly863Ala, Gly1961Glu or IVS38-10) were also sequenced through the entire coding region of the ABCA4 gene.Visual acuity The best-corrected visual acuity was recorded in each patient's medical record as a Snellen fraction (normal = 20/20). Before statistical analysis, these values were converted to the logarithm of the minimal angle of resolution (logMAR) by calculating the base 10 logarithm of the Snellen fraction [e.g. normal = log(20/20) = 0]. For patients with multiple hospital visits, the acuity measurements taken closest to the patient's 27th birthday were used for the statistical analysis. Values from the left eye and right eye were averaged.Visual field volume scores Goldmann visual fields were scanned with a Sharp scanner and analyzed with ImageJ software (available at http://rsbweb.nih.gov/ij/) as follows: transparent layers were added to each field, and the isopters of the visual fields were manually traced onto these layers. Each isopter was assigned a z-axis value according to relative luminous energy of the stimulus (I2e = 100, I3e = 31.7, I4e = 10, III4e = 0.49, V4e = 0.024, no detection = 0). The volume scores were calculated by multiplying the area of each isopter by its associated z-axis value and then summing the values for all isopters. For patients with multiple hospital visits, the visual field measurements taken closest to the patient's 27th birthday were used for the statistical analysis. Values from the left eye and right eye were averaged.Statistical analyses The frequencies of disease-causing alleles observed among the three groups of retinal disease patients were compared with the frequency in controls using Fisher's exact test. The phenotype of each patient was assumed to result from the additive effect of two alleles and one or more additional factors that were cumulatively represented by a single residual value for each subject. The values for the quantitative contribution of each allele were estimated using a multiple linear regression analysis (24). Specifically, to dissect the effect of each allele, we decomposed the mean phenotype of a person whose genotype consists of allele i and allele j into ai + aj, where ai is the effect of the i-th allele. To do this, we created a vector Yva of length 51 containing the average logMAR visual acuities for each subject, and a 51x16 matrix, X. Each cell of this matrix, Xij, indicated the number of occurrences of the j-th allele for each subject i. This system of 51 equations was solved with multiple linear regression to give estimates of a, using the statistics program R (available at http://www.R-project.org). To verify the allelic data, each row of X summed to 2, and each column summed to the corresponding number of occurrences of each allele for this cohort. These calculations were performed in the same manner for Yvol, the vector of containing each subject's visual field quantitative phenotype. The estimates of a, the coefficients for each allele, for both Yva and Yvol are given in Table 1.

      Case#: Patient on line 28, US

      DiseaseAssertion: retinitis pigmentosa (RP)

      FamilyInfo:

      CasePresentingHPOs:

      CaseHPOFreeText:

      CaseNotHPOs:

      CaseNotHPOFreeText:

      GenotypingMethod: Thirty-two of the most common disease-causing ABCA4 variations were selected for the initial screen. The entire research cohort was assayed for these 32 variations using a combination of SNPlex, SSCP analysis, TaqMan and automated DNA sequencing. All CRD and RP patients who had one plausible disease-causing allele identified in the first tier of screening were assayed by automated sequencing of the entire coding region of the ABCA4 gene in an effort to identify their second disease-causing allele. In addition, Stargardt patients who had one of the three most common alleles (Gly863Ala, Gly1961Glu or IVS38-10) were also sequenced through the entire coding region of the ABCA4 gene.

      PreviouslyPublished: n/a

      Variant: c.6601_6602del (p.Arg2201AlafsTer?) "Glu2200del2 aggGA"; c.5461-10T>C "IVS38-10 T>C"

      CAID: CA227421

      SupplementalData: genotype in supplemental table 1

      CAID:CA227421 CaseInfo Individual SupplementalTable automated_hgnc:34 automated_hgnc_source:CAID ClinGen ABCA4 Annotations
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    pmc.ncbi.nlm.nih.gov/articles/PMC2935854/
  50. pmc.ncbi.nlm.nih.gov pmc.ncbi.nlm.nih.gov
    High-Throughput Sequencing to Identify Mutations Associated with Retinal Dystrophies
    1
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    pmc.ncbi.nlm.nih.gov/articles/PMC8391535/
  51. biol2022.github.io biol2022.github.io
    Week 1: Getting started – BIOL2022
    1
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    biol2022.github.io/BEDA-handbook/module01/102-week01.html
  52. Local file Local file
    9781439064184.pdf
    1
    1. lucasalopz 04 Aug 2026
      It follows that r9 2 r 5 0

      Is this the correct logic?

      if r' - r > 0, then $$ 0 \leq r' \le b $$ is not true. Since b divides r' - r, then if r' = r, then q' = q.

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  53. www.medrxiv.org www.medrxiv.org
    Rethinking intensity: Repetitive transcranial magnetic stimulation across ethnic populations
    1
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    medrxiv.org/content/10.1101/2025.02.22.25322728v1
  54. www.biorxiv.org www.biorxiv.org
    An integrated human forebrain organoid reveals microglia-mediated CD8⁺ T cell recruitment and neuroimmune dysfunction in Alzheimer's disease pathology
    3
    1. Public_Reviews 04 Aug 2026

      eLife Assessment

      This study presents a valuable human organoid platform for investigating neuron-immune interactions in Alzheimer's disease and modeling the interplay between innate and adaptive immunity in the context of amyloid pathology. The system has the potential to advance the field by enabling the study of human-specific neuroimmune interactions that are difficult to recapitulate in rodent models; however, the evidence supporting several central conclusions remains incomplete. Key claims, including the causal role of microglia-derived chemokines in T cell recruitment and the existence of a neuroinflammatory feedback loop, rely primarily on correlative observations and lack the mechanistic experiments necessary to establish causality; in addition, a major confounding factor, the non-autologous nature of the cellular components, is not adequately addressed. Despite these limitations, the study will be of considerable interest to researchers in neuroimmunology and Alzheimer's disease.

      Summary
    2. Public_Reviews 04 Aug 2026

      Reviewer #1 (Public review):

      Summary:

      A growing body of evidence indicates that Alzheimer's disease is not simply a disease of neurons accumulating toxic protein aggregates, but one in which the immune system, both its resident brain component and its circulating peripheral arm, plays an active and sustained role. Understanding how these two immune compartments interact with one another and with diseased neural tissue has been hampered by the fact that the mouse immune system differs fundamentally from the human one in ways likely to matter for disease progression. The authors set out to address this gap by building a modular laboratory model that brings together three human cell types in a three-dimensional setting: brain organoids derived from human stem cells to provide a neural substrate, stem cell-derived brain immune cells (microglia) to represent the resident immune compartment, and circulating immune cells (CD8-positive T cells) harvested from human blood to represent the peripheral adaptive immune response. By exposing this tri-cellular system to a toxic form of amyloid protein, the hallmark aggregating molecule of Alzheimer's disease, the authors aimed to dissect, step by step, how microglia respond to amyloid stress, what inflammatory signals they release as a consequence, and whether those signals are sufficient to attract T cells into the neural environment. They further aimed to test whether blocking the molecular receptors that guide T cell movement could interrupt this process, with the broader goal of positioning the platform as a tool for human-relevant drug screening.

      Strengths

      The conceptual architecture of the platform is one of its clearest strengths. The decision to add immune components in a stepwise, modular fashion, first characterising the neural response to amyloid, then adding microglia, then adding T cells, makes it possible to attribute observed changes to specific cellular contributions in a way that a more complex all-at-once model would not allow. This staged design is well thought-through, and its logic is clearly communicated. The combination of single-cell transcriptional profiling, calcium imaging for real-time functional readouts, transwell migration assays, and protein secretion measurements gives the study a genuinely multi-modal character that goes beyond what purely transcriptomic or purely imaging-based approaches can offer. The observation that T cells failed to migrate toward amyloid-treated organoids in the absence of microglia is a clean and conceptually important result, clearly supporting the idea that the resident immune response acts as an intermediary between amyloid pathology and the recruitment of peripheral immune cells. The identification of specific chemokine receptor pathways mediating T cell movement and the demonstration that pharmacological blockade of those receptors reduces migration and provide a degree of mechanistic resolution useful for thinking about future therapeutic strategies.

      Weaknesses

      Despite these strengths, several aspects of the work as presented substantially limit the confidence one can place in its conclusions.

      The most consequential issue concerns the origin of the cells used in the model. The three cellular components: the brain organoids, the microglia, and the T cells are derived from genetically unrelated individuals. The T cells, in particular, come from healthy blood donors unrelated to the stem cell lines used to generate the neural tissue. This means the immune cells and the tissue they are interacting with carry different molecular identity markers (the proteins that the immune system uses to distinguish self from non-self). In this setting, any T cell activation or directed movement could reflect a generic rejection-like response to foreign tissue rather than a disease-relevant, chemokine-directed recruitment process. This is not a subtle concern: it represents a fundamental ambiguity at the heart of the model's central finding, and it is not acknowledged anywhere in the manuscript. For the transwell migration data to be interpretable as a model of Alzheimer's disease rather than of immune incompatibility, the authors would need to demonstrate that migration is driven by the specific chemokine environment and not by the genetic mismatch between cells, for example, using cells from the same donor or from matched donors, or by showing that blocking identity-marker recognition does not alter migration.

      A related concern is that the T cells used are from healthy individuals, whereas T cells from people with Alzheimer's disease are known to differ in their activation state, surface receptor expression, and functional behaviour. The platform cannot yet claim to model the specific T cell biology of Alzheimer's disease until disease-relevant T cells are incorporated.

      Beyond this foundational issue, the study frequently describes findings in causal terms that the experimental design does not support. The resident immune cells are said to "drive" T cell recruitment and "establish" a feedback loop. These are strong mechanistic claims. The evidence presented indicates that when microglia are present, more T cells migrate, and that blocking T cells receptors reduces migration. What is missing is direct evidence that the specific molecules measured, particularly the chemokines CCL4 and CCL5, are the agents responsible, as opposed to other signals also present in the conditioned environment. No experiment directly neutralises these chemokines to test whether their removal is sufficient to abolish T cell recruitment. Without such an experiment, the receptor-blocking data show only that the receptors matter, not that the measured ligands are the ones activating those receptors.

      The abstract describes one particular molecule, CXCL10, as a contributor to T cell recruitment, but the data in the paper itself show no significant change in CXCL10 levels between conditions. This discrepancy between the abstract and the results is misleading to readers who may not read the figures in detail.

      The single-cell sequencing data, which form the basis for claims about changes in cell populations following amyloid treatment or microglia addition, are presented without validation of the cell type labels against established reference datasets from human brain tissue. The proportional shifts in cell populations between conditions (Figures 1H and 3E) are described as significant findings but are shown without any statistical test appropriate for this type of compositional data. Comparisons of cell-type proportions derived from single-cell sequencing require specialised statistical approaches that account for the interdependence of proportions and the variability between samples; standard tests are not appropriate here, and none are applied.

      There is also an unresolved inconsistency in the age at which the organoids were analysed by single-cell sequencing: the text states day 90, while the figure legend states day 60, and the methods section contains a passage describing experimental conditions (including a cholesterol treatment and a drug called semaglutide) that are entirely unrelated to this study and appear to have been copied from a different manuscript. These issues raise concerns about the rigour of the manuscript preparation and should be corrected.

      Finally, the sample sizes underpinning several key conclusions are small (typically three to four organoids per group), particularly for the protein-secretion measurements used to identify the inflammatory signals responsible for T cell recruitment. While organoid studies are inherently limited in scale, the strength of the mechanistic claims made here would benefit from larger sample size or independent experimental replication.

      Conclusion:

      The authors have built a platform that is conceptually well-conceived and generates data consistent with a role for microglia in bridging amyloid pathology and T cell recruitment. In that sense, they have made meaningful progress toward their stated aims. However, the platform, as described, cannot yet deliver the human-specific mechanistic insight it claims to provide, primarily because the non-autologous configuration of the model introduces an uncontrolled variable that confounds the interpretation of the immune interaction data. The claim to have provided "the first human-specific mechanistic demonstration" of microglial activation as a bridge between amyloid pathology and adaptive immune recruitment is not supported by the evidence presented. The data are consistent with this interpretation but do not establish it.

      The general approach, building increasingly complex human neural-immune models by adding components in a controlled, stepwise manner, is a valuable direction for the field and one that other groups working on neuroinflammation will find useful to consider. The combination of live calcium imaging and transcriptional profiling in the same experimental system is a practical contribution that demonstrates the kind of multi-modal readout this class of model can support. If the autologous confound is resolved in future iterations and if the mechanistic claims are grounded in more direct experimental evidence, this type of platform could become a genuinely useful tool for investigating human neuroimmune biology and for screening candidate therapeutic compounds in a human-relevant context. As currently presented, however, readers and researchers considering adopting this approach should be aware that the immune interaction data may reflect genetic mismatches between cell sources rather than disease-specific biology, and that the causal conclusions drawn from the chemokine and migration data go beyond what the experiments can support.

      Review 1
    3. Public_Reviews 04 Aug 2026

      Reviewer #2 (Public review):

      Summary:

      In this study, the authors developed a human forebrain organoid model incorporating both iPSC-derived microglia and CD8⁺ T cells, enabling them to recreate and investigate multicellular aspects of AD pathology in a human-relevant system.<br /> Their findings show that microglia help clear amyloid-β deposits, but they also promote inflammatory responses. Activated microglia recruit CD8⁺ T cells by releasing the chemokines CCL4, CCL5, and CXCL10, which signal through the receptors CCR1/CCR5 and CXCR3. Pharmacological inhibition of CCR5 or CXCR3 prevents T-cell recruitment and alters autophagy pathways in a microglia-dependent manner.

      Strengths:

      The study presents a versatile human organoid platform for investigating neuron-immune interactions in Alzheimer's disease. It highlights the critical role of microglia-driven recruitment of CD8⁺ T cells in sustaining neuroinflammation and identifies CCR5 and CXCR3 signaling pathways as promising therapeutic targets for neuroinflammatory conditions.

      This study is interesting and presents novel findings supported by state-of-the-art approaches, including single-cell RNA sequencing, a three-dimensional cerebral organoid model, and co-culture systems involving two distinct immune cell populations.

      Weaknesses:

      Several aspects of the study require clarification and further improvement. For example:

      (1) Figure 1H is missing statistical analyses.

      (2) The scRNA-seq analysis shows a reduction in the proportion of cells occupying transcriptional states associated with later pseudotime values, which the authors interpret as evidence that Aβ treatment inhibits neuronal maturation. However, the data presented do not appear sufficient to support this conclusion. An alternative explanation is that Aβ preferentially affects the survival of more mature neuronal populations, leading to their depletion, consequently, an apparent enrichment of cells at earlier pseudotime states. Therefore, the observed pseudotime shift does not necessarily demonstrate impaired maturation per se. The authors should revise the interpretation of these results in the first paragraph and either provide additional evidence supporting a maturation defect or discuss alternative explanations such as selective loss of mature neurons.

      (3) A similar concern applies to the scRNA-seq data presented in Figure 3. The authors interpret the shift toward later pseudotime states in the presence of microglia as evidence of enhanced neuronal maturation. However, the data do not exclude alternative explanations. For instance, microglia may preferentially promote the survival of more mature neuronal populations or protect them from cell death, thereby increasing their relative abundance in the dataset. Consequently, the observed pseudotime distribution cannot be taken as direct evidence of enhanced maturation. The authors should revise their interpretation accordingly and discuss the possibility that the observed effect reflects differential survival rather than accelerated neuronal maturation.

      (4) In Figures 4A-E, the authors should report the levels of the secreted proteins in pg/mL instead of relative values, as this would better reflect the actual amounts produced. In Figure 4H, the inhibitor-treated control T-cell samples should be included. Furthermore, it should be explicitly stated that the inhibitor-treated data points currently shown refer to T cells cultured in the presence of myeloid Aβ.

      Review 2
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    biorxiv.org/content/10.64898/2026.05.25.727443v1
  55. access.infobase.com access.infobase.com
    Article: Culturally responsive teaching in a globalized world (Aug. 2019)
    2
    1. Annotating4Sch00l 04 Aug 2026
      Hence, providing relevant cultural training and professional development for aspiring and experienced teachers becomes even more important.Such training needs to extend beyond traditional multicultural education approaches, or what has been called a “tourist” curriculum characterized by occasional or “highlight” additions.Instead, training for teachers must model a multi-dimensional approach that includes integrating content from diverse cultures and experiences, and critically examining how cultural identity impacts learning.

      Important to find those to become accustomed to new ideas and be open to the idea

    2. Annotating4Sch00l 04 Aug 2026
      more research is being devoted to understanding and supporting conditions for equitable learning. Culturally responsive teaching (CRT) is one idea to support these conditions. CRT is concerned with teaching methods and practices that recognize the importance of including students’ cultural backgrounds in all aspects of learning.To date, much focus in the field of CRT draws attention to the need for a greater diversity of role models and learning experiences in the classroom, and an expansion of teachers’ capacities to truly support and affirm diverse students.

      YOU MUST MAKE THE STUDENT FEEL COMFORTABLE WITH WHO THEY ARE

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    access.infobase.com/article/2065236-culturally-responsive-teaching-globalized-world-aug-2019
  56. docs.docker.com docs.docker.com
    Develop with containers
    1
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    docs.docker.com/get-started/introduction/develop-with-containers/
  57. indy.peergos.me indy.peergos.me
    /Wiki/Pad/b/about.html
    5
    1. gyuri 04 Aug 2026
      next steps

      And of course the roundtrip from Peergos CryptPad document to Mind/graph TrailScape and TrailPlex and MEMEpleX and the serch engine for it will be developed as extra capabilities added to Indywii so they will be available in any future app developed on the Indyweb

    2. gyuri 04 Aug 2026
      notation processor

      Extensibale self describing self creating edtiro just like Emacs

      Except that we do not need to create folder structures for javascript files but flip that and set things up so that in every folder we can add javascript that is required to make the specific capabilities needed in tht folder to be available callable imported and developed right whre they are to be used

      Since we are also leveraging IPFS any code that is developed in one context can be referenced from anywhere else This is posssible because every app would have the smae universal extensile setup that is added to IndyWiki as the seed App

    4. gyuri 04 Aug 2026
      appropriately named subfolders

      The folder structures elaborated in the course of this slef documenting development process

      will be a mirrored in the Wiki, so there will always be a dynamic eventually constistent roundtrip between work done on the MidDrive Side (Drive is any fodler/file system like Google Drive, Peergos, Cyptpad etc) and on the IndyWiki side

    5. gyuri 04 Aug 2026
      MindGraph

      MindGraph powered WikiNizer and lead to the deelopment of the symmathetic metamorphic metadesign notaion

      Indiwiki uses trailMarks, so there is a need to etend Indy/wiki with full support for trailMarks in a homoiconinc self-describing self exlicating self-creating way

      The intended interpretation of the notation can thus be added peiecmeal in an instance first dynamic lively metamorphic environment

      where desritpiosn formulation of requirements specification and documented use cases can gadually refined with judicios formulation of required functions gradually into working system

      eventual consistent eventual complete working interactive affordances

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  58. es.wikipedia.org es.wikipedia.org
    Jerome Bruner - Wikipedia, la enciclopedia libre
    3
    1. Alejandrouss 04 Aug 2026
      constructivismo

      En su teoría estamos hablando de un rol activo del estudiante, donde el rol profesor estudiante deja de ser unidireccional y debe retarse a los modelos bidireccionales y con reflexividad, sobre todo en épocas en donde, para uno, es muy difícil que pueda elegir su maestro, así mismo el hecho de contrargumentar no me parece un hecho desafiante sino una nueva perspectiva al conocimiento brindado en un espacio, platon y aristoteles se distancian bastante y aun asi son maestro y alumno.

      conocimiento
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  59. www.planalto.gov.br www.planalto.gov.br
    Constituição
    1
    1. BeaHolanda 04 Aug 2026
      o servidor titular de cargo efetivo que tenhacompletado as exigências para a aposentadoria voluntária e que opte por permanecer em atividade poderá fazer jus a um abono de permanência equivalente, no máximo, ao valor da sua contribuição previdenciária, até completar a idade para aposentadoria compulsória.

      Abono de permanência! casos de aposentadoria voluntária. CF- "incentivo $" será no máximo até o valor de sua contribuição previdenciária.

      no Ceará- igual ao valor da sua contribuição no RPPS

      deve manifestar FORMALMENTE o interesse em permanecer no cargo

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    planalto.gov.br/ccivil_03/constituicao/constituicao.htm
  60. mutabit.com mutabit.com
    Markdown: Documentación ágil y estructurada
    7
    2. Alejandrouss 04 Aug 2026
      StackOverflow

      es una estructura de datos. Piensa como un montón de platos, solo puedes agregar más platos en la parte superior o quitar el plato superior (lo llamamos LIFO: Último en entrar, primero en salir), pero en este caso, los platos son en realidad datos en la memoria de la computadora.

      En teoría, podríamos agregar tantos datos a una pila como queramos, pero la memoria es finita, por lo que establecemos un límite al tamaño de la "pila de datos". Cuando intenta agregar datos a una pila que está llena, se produce un desbordamiento de la pila. Dependiendo de la implementación de la pila, el programa evitará que se agreguen más datos o los datos se agregarán a una ubicación inesperada de la memoria, lo que generará todo tipo de problemas inesperados. - > sacado conversacion reddit

      definicion
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    mutabit.com/repos.fossil/documentaton/doc/3637fc87/es/capitulos/markdown-intro.html
  61. mutabit.com mutabit.com
    Cardumem Wiki: Top-level Files of 125ff72321
    1
    1. nitaigouranga 03 Aug 2026
      So, how a new syntax can make more explicit the Hipertextual Algebra we talked before and empower memory/knowledge hypertextual/hypermedia practices? Cardumem is an exploration of that inquiry.

      Es pregunta inicial respecto a la nueva sintaxis de Cardumen me parece muy valiosa ya que apunta a la accesibilidad, unos de los aspectos centrales de la clase. Qué tan accesible es un proyecto que desarrollamos también se manifiesta en el lenguaje, así que buscar la manera de hacer más explícito lo que se quiere comunicar, sin reducirlo necesariamente a algo simple, apunta a ese camino.

      accesibilidad
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  62. mutabit.com mutabit.com
    Hypothesis: lectura anotada social e hipertextual
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    mutabit.com/repos.fossil/unisema/doc/49dcd6/tema/hypothesis.html
  63. www.biorxiv.org www.biorxiv.org
    DishCam: an open-source 3D-printed darkfield imager for microbial colonies and small organisms on Petri dishes
    1
    1. ryan_lane 03 Aug 2026

      Hello, thanks for sharing this work -- your darkfield images are impressive for such an inexpensive setup and it's awesome how open you've been with all the files, BOM, and instructions. Makes it super easy to actually build on.

      I was wondering if you could confirm the effective pixel size at the sample plane for the 12mm and 16mm lens setups? Knowing the IMX477 chip is 1.55 µm and you're capturing the full 90mm dish at 4056×3040, I'm guessing it's something like ~20-30 µm/pixel, but would love the actual number.

      Thanks for putting this together!

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    biorxiv.org/content/10.64898/2026.07.14.738485v1
  64. www.youtube.com www.youtube.com
    W CO INWESTUJĘ W 2 połowie 2026? Jak zarządzam portfelem 3,7 mln. PLN, żeby wygrać z S&P 500?
    1
    1. pyxelr 03 Aug 2026
      W CO INWESTUJĘ W 2 połowie 2026? Jak zarządzam portfelem 3,7 mln. PLN, żeby wygrać z S&P 500?

      1. Wyniki portfela i główny cel

      • Wyniki: Po prawie 7 latach inwestowania portfel o wartości 3,7 mln PLN pobił swój główny benchmark S&P 500, a także wyprzedził indeks NASDAQ 100.
      • Zarządzanie ryzykiem: Portfel łączy wysokie stopy zwrotu z niską zmiennością (np. przy 20% spadku S&P 500 w 2025 r. ten portfel zaliczył spadek jedynie o ok. 2,5%).
      • Filozofia: Priorytetem jest przetrwanie na rynku w perspektywie kolejnych 10 lat, a nie krótkoterminowe ściganie się na rekordowe stopy zwrotu za wszelką cenę.

      2. Polska Giełda (GPW) – podejście i selekcja spółek

      • Koncentracja: Polska część została zebrana z 26 do około 15 spółek i planowana jest dalsza powolna koncentracja wokół podmiotów jakościowych.
      • Sentyment: Nastawienie neutralne z małym plusem – po 4 latach hossy wyceny jakościowych spółek są już wyższe, a potencjał na łatwe zyski uległ zmniejszeniu (tryb Wait and See).
      • Główne pozycje: Digital Network, Synthaverse (Synectik), Cyberfolks, XTB.
      • Ochrona przed walutą: Szukanie spółek zarabiających w EUR/USD (Cyberfolks, Vercom, Asbis), co stanowi zabezpieczenie na wypadek ewentualnego osłabienia złotego. Unikanie czystych importerów zyskujących wyłącznie na silnym PLN.
      • Sektory na celowniku: Dystrybucja elektroniki (AB, Asbis), cyberbezpieczeństwo oraz przemysł/budownictwo zyskujące na modernizacji sieci energetycznych, obronności i infrastruktury (Kęty, Cognor).

      3. Globalna Technologia i Sztuczna Inteligencja (~16% portfela)

      • Teza inwestycyjna: Sztuczna inteligencja to realna rewolucja technologiczna, w którą największe firmy pompować będą gigantyczny kapitał przez lata.
      • Struktura części technologicznej:
        • Global Equity Momentum (GEM): Ekspozycja przez ETF na rynki wschodzące (ponad 50% wagi to technologia, głównie półprzewodniki).
        • Portfel scoringowy: Wyselekcjonowane spółki z sektora amerykańskich półprzewodników.
      • Podążanie za Capexem: Kapitał trafia obecnie do dostawców sprzętu i półprzewodników, ponieważ tam płyną ogromne wydatki inwestycyjne hyperskalerów (np. Alphabet wyda ok. 200 mld USD na Capex w 2026 r.).
      • Planowana rotacja: Pod koniec 2026 lub w 2027 roku planowana jest realizacja zysków z półprzewodników i przenoszenie kapitału bezpośrednio do hyperskalerów (Alphabet, Amazon).

      4. Portfel Nieruchomości / REIT-y (~10% portfela)

      • Obecny stan: Najsłabiej zachowująca się część portfela pod względem stopy zwrotu, ale nadal na plusie w PLN i USD.
      • Rola w portfelu: Klasa aktywów nieskorelowana z technologią, mająca wygładzać obsunięcia całego portfela podczas spadków na NASDAQ.
      • Kluczowe pozycje: Equinix (budynki pod centra danych) oraz CareTrust (nowoczesne domy opieki dla seniorów) – spółki wpisane w silne megatrendy.
      • Katalizatory poprawy: Wchłonięcie nadpodaży z lat zerowych stóp procentowych, ustabilizowanie warunków makro oraz listopadowe wybory do Kongresu USA.

      5. Ryzyka makroekonomiczne i podejście do spadków

      • Ryzyka: Konflikt na Bliskim Wschodzie (Iran), rosnące ceny ropy, obawy inflacyjne i opóźnienia w obniżkach stóp procentowych.
      • Strategia działania: Wskaźnik C/WK (Forward P/E) dla S&P 500 spadł poniżej 20 (blisko 10-letniej średniej). Twórca zadeklarował chęć regularnego dokupowania na spadkach i budowania pozycji bez ścigania rosnących kursów.

      6. Przegląd alokacji portfela

      • Akcje GPW (Największy udział)

        • Strategia: Nastawienie selektywne, stawianie na spółki jakościowe oraz eksporterów.
        • Główny cel: Stabilny wzrost kapitału oraz generowanie dywidend.

      • Globalna Technologia / AI (~16% portfela)

        • Strategia: Mocno bycze nastawienie; inwestowanie w półprzewodniki z planem późniejszej rotacji w hyperskalerów.
        • Główny cel: Maksymalizacja stopy zwrotu i bicie indeksu S&P 500.

      • REIT-y / Nieruchomości (~10% portfela)

        • Strategia: Cierpliwe przeczekanie dołka cyklu w defensywnym sektorze.
        • Główny cel: Dywersyfikacja risk-off oraz wygładzanie zmienności całego portfela.
      investing polish YouTube
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  65. www.youtube.com www.youtube.com
    To świetny czas na ZAKUP tej spółki! BigTechy po wynikach
    1
    1. pyxelr 03 Aug 2026
      To świetny czas na ZAKUP tej spółki! BigTechy po wynikach
      • Wyniki Meta Platforms: Przychody w Q2 wyniosły blisko 61 mld USD (+28% r/r), napędzane wzrostem przychodów z reklam o 27%. Ze względu na znaczny wzrost kosztów oraz podniesienie prognozy CapEx na 2026 rok do 130–145 mld USD wolne przepływy pieniężne (FCF) uległy mocnemu ograniczeniu, powodując spadek kursu akcji, który autor uznaje za okazję inwestycyjną.
      • Wyniki Microsoft: Przychody wzrosły o 18% r/r do 90 mld USD, a zysk netto o 31% do niemal 36 mld USD. Segment Azure zanotował wzrost o 43% r/r, przekraczając po raz pierwszy poziom 100 mld USD rocznych przychodów, podczas gdy portfel podpisanych kontraktów (RPO) skoczył o 84% do 678 mld USD.
      • Wyniki Amazon: Przychody wzrosły o 20% r/r do ponad 200 mld USD, a zysk operacyjny o 43% do 27,5 mld USD. Wzrost chmury AWS przyspieszył do 37% r/r, generując ponad 60% zysku operacyjnego całej grupy. Prognoza CapEx na 2026 rok została podniesiona do 220 mld USD z powodu olbrzymiego zapotrzebowania na infrastrukturę AI.
      • Wydatki CapEx gigantów technologicznych: Cztery największe spółki technologiczne planują wydać w 2026 roku łącznie 735–760 mld USD na inwestycje w infrastrukturę i serwery. Mimo obaw rynku o krótkoterminową rentowność, popyt na moc obliczeniową przewyższa obecne możliwości produkcyjne.
      • Strategia i ruchy w portfelu autora: Autor planuje dokupić akcje Meta Platforms po spadkach. Zwraca również uwagę na dynamiczny wzrost wartości posiadanych akcji Nebius oraz na nieudaną próbę zakupu Aehr Test Systems z powodu nagłego skoku kursu.
      investing AI polish YouTube
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  66. www.youtube.com www.youtube.com
    5 spółek, które mogą czekać OGROMNE wzrosty
    1
    1. pyxelr 03 Aug 2026
      5 spółek, które mogą czekać OGROMNE wzrosty
      • Analiza rynku półprzewodników i AI: Wyniki finansowe gigantów takich jak TSMC i ASML pokazują, że hossa na sztuczną inteligencję wchodzi w nową fazę – popyt rozszerza się z samych akceleratorów GPU na procesory CPU, pamięci HBM/DDR, układy sieciowe i zaawansowane pakowanie.
      • Wyniki i plany TSMC: Podniesienie prognozy wzrostu przychodów na 2026 rok do ponad 40% r/r oraz zwiększenie CapEx-u do 60–64 mld USD. Wciąż kluczowym wąskim gardłem dla klientów pozostaje dostępność zaawansowanego pakowania (np. CoWoS).
      • Wyniki i plany ASML: Podniesienie prognozy przychodów na 2026 rok do 43–45 mld EUR, znaczny wzrost sprzedaży systemów dla pamięci (+75%) oraz logiki (+25%). Produkcja maszyn Low-NA EUV na 2027 rok jest niemal całkowicie wyprzedana.
      • Przegląd 5 spółek z potencjałem wzrostu:
        • Alphabet (Google): Silna pozycja finansowa, ogromny backlog w segmencie chmury/data center oraz rekordowe wykorzystanie narzędzi AI mimo niedawnych roszad kadrowych.
        • Amkor Technology: Lider w obszarze zewnętrznego pakowania i testowania półprzewodników (OSAT), posiadający 10-letnie partnerstwo z TSMC oraz nową fabrykę w Arizonie.
        • Aehr Test Systems: Producent urządzeń do testowania i wygrzewania chipów (Burn-in), charakteryzujący się rekordowymi zamówieniami, ale i wysoką zmiennością kursu.
        • Nvidia: Dominujący dostawca GPU/CPU dla AI z nadchodzącą generacją Rubin, uznawany za atrakcyjną pozycję długoterminową po korektach cenowych.
        • Meta Platforms: Szybko rozwijająca się spółka technologiczna, wymieniana jako jeden z najtańszych podmiotów z grupy Big Tech pod kątem wyceny.
      investing semiconductors AI polish YouTube
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  67. www.whitehouse.gov www.whitehouse.gov
    Science: A New Golden Age
    7
    1. brianmapes 03 Aug 2026
      a double-blind process that removes career history, cutting against elitism and leveling the playing field for younger or less prominent researchers.

      naive, in lots of small fields: the number of people who can judge well a detailed proposal without basically seeing through the blinds is tiny or perhaps negative

    2. brianmapes 03 Aug 2026
      When a funding agency can support only one proposal in ten, the noise begins to drown out the signal. All too often, consensus-driven panels fund the least divisive ideas rather than the most promising

      Agreed, so cuts down to 10% success rate should be avoided as killing the golden goose of healthy, non-oppressed science

    3. brianmapes 03 Aug 2026
      mechanism design, recognized with the 2007 Nobel Prize, provides the theoretical foundation for understanding how rules shape behavior and outcomes. Mechanism design can be thought of as asking the inverse of traditional economics. Given a desired outcome, what incentives and institutions will produce it?

      "desired behavior and outcomes" is not the essence of healthy "science", as other sections acknowledge

    4. brianmapes 03 Aug 2026
      Betting exclusively on the existing funding model is like building a military composed entirely of infantry, effective for one kind of warfare, inadequate for others.

      um no, all the scales and examples exist in the "existing model"

    5. brianmapes 03 Aug 2026
      Funding at this scale, which has worked well in incubating new technological capabilities, could be extended to basic science as well, where the government is not merely procuring a weapons system, but pursuing scientific advancement for the national interest

      not loving the example-space here, not quite "science"

    6. brianmapes 03 Aug 2026
      Employing postdocs and graduate students remains effective for training the next generation of scientists, but doing so is poorly suited for executing large-scale, mission-driven programs that require continuity, specialization, and long-term institutional memory. Frequent turnover fragments efforts and slows progress. As science funders have noted, no technology company would entrust its core R&D to a workforce composed primarily of temporary trainees, yet this is the standard model in academic research

      Some validity to this partial critique, okay, but perhaps the opposite critique can be leveled at the even larger government-lab model, where specialized long-term cadres might pursue large=vague "missions" perhaps set long ago, usefully shown up and freshened up by an academic with a student sometimes.

    7. brianmapes 03 Aug 2026
      Research shows that when investigators receive longer-horizon support with tolerance for early failure, they produce portfolios with both more hits and more misses, the signature of genuine exploration

      good words

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    whitehouse.gov/science/
  68. www.poetryfoundation.org www.poetryfoundation.org
    won't you celebrate with me by Lucille Clifton
    2
    1. madisonmorton 03 Aug 2026
      born in babylonbabylon Once a great city in Biblical times, see Psalms 137. In contemporary usage, babylon is a place of inequity and oppression.both nonwhite and womanwhat did i see to be except myself?i made it up

      with no true model before her, Clifton chose to live her life in a way that she saw fit. because she was born "nonwhite and woman" she was already damned by society. so what did it matter to society what she "made up" to do with her life?

    2. madisonmorton 03 Aug 2026
      come celebratewith me that everydaysomething has tried to kill meand has failed.

      despite all the odds stacked against her, Clifton still managed to survive. the poem makes no mention of what she has in her life. did she "make it?" did Clifton get the job she always wanted, get that promotion, finish her degree, get married, or live alone; nothing in the poem reveals what should be "celebrated." the poem makes me think about what Clifton is asking us as the readers to celebrate with her. but after reading, i think the message is that living life, against all the odds, is worth the celebration itself.

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    poetryfoundation.org/poems/50974/wont-you-celebrate-with-me
  69. www.crafins.com www.crafins.com
    Von Cicaplast bis Anthelios: Die La-Roche-Posay-Produkte, die Beauty-Fans lieben
    8
    1. Nadine1307 03 Aug 2026
      Erst danach lohnt es sich zu spezialisieren: Effaclar bei zu Unreinheiten neigender Haut, Toleriane bei empfindlicher Haut, Lipikar für sehr trockene Partien am Körper. Wenn du unsicher bist: Leg dir die Gratis-Proben in den Warenkorb, die Douglas ab 10 € Bestellwert dazugibt, und probier die Texturen aus, bevor du dich auf eine Serie festlegst.

      Sobald deine Basispflege steht, kannst du weitere Produkte auswählen. Für unreine Haut gibt es die Effaclar-Serie. Empfindliche Haut profitiert häufig von Toleriane. Bei sehr trockener Haut am Körper eignet sich Lipikar. Wenn du noch unsicher bist, teste am besten die Gratisproben von Douglas ab einem Bestellwert von 10 €. So findest du leichter heraus, welche Pflege zu deiner Haut passt.

    2. Nadine1307 03 Aug 2026
      Er ist der unkomplizierteste Einstieg in die Marke, weil er keine fertige Routine voraussetzt und auf trockenen, beanspruchten Stellen im Gesicht genauso funktioniert wie am Körper.

      Sounds more natural:

      Der Cicaplast Baume B5+ ist ein guter Einstieg, wenn du La Roche-Posay zum ersten Mal ausprobieren möchtest. Du kannst ihn sowohl für trockene und beanspruchte Haut im Gesicht als auch am Körper verwenden.

    3. Nadine1307 03 Aug 2026
      Kurz zusammengefasst: Der Cicaplast Baume B5+ ist der beste Einstieg, das Anthelios Invisible Fluid der stärkste Alltagskauf, und für empfindliche Haut führt an der Toleriane Sensitive Creme wenig vorbei.

      Too long sentence. Sounds very unnatural. Better:

      Wenn du zum ersten Mal ein Produkt von La Roche-Posay ausprobieren möchtest, würde ich mit dem Cicaplast Baume B5+ beginnen. Für den täglichen Sonnenschutz eignet sich das Anthelios Invisible Fluid. Bei empfindlicher Haut ist die Toleriane Sensitive Creme eine gute Wahl.

    4. Nadine1307 03 Aug 2026
      Manche Haut reagiert auf so ziemlich alles. Für die ist die Toleriane Sensitive Creme gemacht: Ceramide, Glycerin, Thermalwasser, keine Duftstoffe, sonst nicht viel. Genau diese Unaufgeregtheit ist der Punkt. 2.323 Bewertungen ergeben im Schnitt 4,7 von 5 Sternen.

      Sounds too much like AI. Better:

      Empfindliche Haut braucht oft nicht viele Inhaltsstoffe, sondern die richtigen. Die Toleriane Sensitive Creme setzt auf Ceramide, Glycerin und Thermalwasser. Auf Duftstoffe verzichtet La Roche-Posay bewusst. Das kommt auch bei vielen Anwendern gut an. Bei 2.323 Bewertungen erreicht die Creme durchschnittlich 4,7 von 5 Sternen

    5. Nadine1307 03 Aug 2026
      Das Anthelios Invisible Fluid UVMune 400 mit LSF 50+ ist der La-Roche-Posay-Sonnenschutz, der es tatsächlich in tägliche Gesichtsroutinen schafft.

      Very hard to read. Better:

      Das Anthelios Invisible Fluid UVMune 400 mit LSF 50+ gehört für viele zur täglichen Gesichtspflege. Die leichte Textur lässt sich gut auftragen und eignet sich deshalb auch für den Alltag.

    6. Nadine1307 03 Aug 2026
      Neben dem Cicaplast Baume B5+ gibt es vier La-Roche-Posay-Produkte, bei denen sich der Kauf aus meiner Sicht am ehesten rechnet, sortiert nach dem Hauttyp, für den sie gemacht sind. Alle vier führt Douglas im selben Markenshop.

      Very difficult to read, sounds like AI. Better:

      Neben dem Cicaplast Baume B5+ gibt es noch weitere Produkte von La Roche-Posay, die ich gerne empfehle. Je nach Hauttyp können andere Pflegeprodukte besser zu deinen Bedürfnissen passen. Die folgenden vier gehören für mich zu den besten und sind alle im La-Roche-Posay-Markenshop bei Douglas erhältlich.

    8. Nadine1307 03 Aug 2026
      Interessanter als die Herkunft ist aber, wo die Marke inzwischen steht: Was jahrelang hinter dem Apothekentresen lag, ist heute fester Bestandteil des Beauty-Regals.

      Same here. Better:

      Früher war La Roche-Posay vor allem aus der Apotheke bekannt. Heute ist die Marke für viele ein fester Bestandteil ihrer Hautpflegeroutine.

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    crafins.com/p/DG-V01-jolie/
  70. www.poetryfoundation.org www.poetryfoundation.org
    poem in praise of menstruation by Lucille Clifton | Poetry Foundation
    2
    1. madisonmorton 03 Aug 2026
      there is a river more faithful than this

      describing menstruation as a river is not only an artistic point, but also an extremely accurate one. women are able to bear children, bringing life into the world. menstruation reminds us of what our wombs could have carried each month. in some mythologies, rivers and water sources are highly regarded because of their correlation to life and sustenance, similar to the functionings of a womans body.

    2. madisonmorton 03 Aug 2026
      if there is a river more beautiful than this

      here, clifton is reimagining the process of menstruation as a beautiful one. for so long, women have been made to feel ashamed of the most natural process our bodies go through.by calling it beautiful, society can develop a better sentiment around menstruation.

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    poetryfoundation.org/poems/54584/poem-in-praise-of-menstruation