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Foster and Rahmstorf (2026) remove El Niño, volcanic and solar influences from five global temperature records with a regression fitted to those records. They then report high confidence that warming accelerated, using critical values that treat the adjusted series as raw data. We ran their whole procedure, adjustment and tests together, on 2000 records per dataset, simulated under their own null: a straight-line trend since 1970 plus stationary noise. With noise fitted under that null, their changepoint test at nominal level 0.05 rejected 0.059 to 0.07 of null records, and the observed statistics had full-pipeline p of 0.0005 to 0.0025 in every record. Their quadratic test fared worse, with full-pipeline p up to 0.054. Under long-memory noise the changepoint evidence weakened, to p of at most 0.04, but held. The acceleration finding rests on the changepoint test.

• Published, Reproduced, Reviewed.Published, Reproduced, Reviewed: A numpy port of Foster and Rahmstorf's 2026 adjustment for El Niño, volcanic and solar influences reproduces their published adjusted NASA, NOAA, HadCRU, Berkeley and ERA5 series to within 0.0001 °C, and the changepoint test of Beaulieu et al. (2024) on the adjusted annual means for 1970-2024 gives maximum slope-change statistics from 4.91 to 6.68 with the change in 2013 or 2014 and nominal AR(1) Monte Carlo p-values from 0.00014 to 0.0033, against 0.041 to 0.19 for the unadjusted series.
• Published, Reproduced, Reviewed.Published, Reproduced, Reviewed: When 2,000 records per dataset are simulated under Foster and Rahmstorf's null hypothesis (a linear trend since 1970, their fitted exogenous terms, and ARMA(1,1) noise fitted under the null) and passed through their whole adjustment and changepoint test, the nominal 5% test rejects 5.9% to 7.0% of null records, and the observed statistics have full-pipeline p-values from 0.0005 to 0.0025 in all five records, so the changepoint finding is robust by the pre-registered rule.
• Published, Reproduced, Reviewed.Published, Reproduced, Reviewed: Under the same full-pipeline null, Foster and Rahmstorf's quadratic test with the ARMA(1,1) correction of Foster and Rahmstorf (2011) rejects 5.8% to 8.0% of null records at nominal 5% on monthly values and 7.2% to 9.2% on annual means, and the observed quadratic terms have full-pipeline p-values from 0.0015 to 0.054 (monthly) and 0.0005 to 0.032 (annual), below 0.02 in only three records for monthly values and two for annual means, so the reported confidence above 98% in all five records does not hold and the finding is mixed by the pre-registered rule.

1 more claim

Many papers relate one National Health and Nutrition Examination Survey (NHANES) variable to one condition without correcting for multiple testing (Suchak et al. (2025)). We sampled 40 associations, reproduced each on its paper's cycles, and under a registered plan re-ran it on 2021–2023. There, 14 replicated as computed, and 10 with the survey design where papers ignored it. Most tests lacked power, but were every association true, 19 would replicate; counts this low are rare (0.047, or 0.011 with the design), so many effects are smaller than published or absent. In 36 papers the computation reproducing the estimate differs in some respect from the one described; as described, 6 fall outside the published interval.

• Published.Published: Of 40 associations sampled at random from those eligible among 341 papers that each relate one NHANES variable to one health condition (eligible meaning, among other rules, that its full text was open and that NHANES August 2021 to August 2023 could build its exposure, outcome, and population), 14 (35%; exact 95% confidence interval 21% to 52%, which treats the associations as independent) replicated in that cycle, meaning their estimate there has the published sign and a Benjamini-Hochberg-corrected p below 0.05, with each analysis computed as its paper's was. Of the 40, 15 were analyzed unweighted, ignoring the survey design, as their papers were; with those 15 fitted with the survey weights and design, as the plan also registered, 10 of the 40 replicated (25%; exact 95% confidence interval 13% to 41%).
• Published.Published: At an unadjusted two-sided alpha of 0.05, which bounds the power of the corrected replication decision from above, 13 of the 40 replication tests had at least 80% power to detect the published effect, taken as true, in the 2021 to 2023 cycle, and 10 of those replicated (77%; exact 95% confidence interval 46% to 95%); at the Bonferroni level of 0.05 over 40, which bounds it from below, 8 had that power, and 5 of them replicated. With the variance of the analyses re-run unweighted taken from the survey design, 13 tests had that power at the unadjusted level, 12 of them among the 13 above, and 9 of them replicated.
• Published.Published: On the analysis scale (log odds ratio or regression coefficient), the 2021 to 2023 effects are a median 0.77 times the published ones over all 40 associations (distribution-free 95% confidence interval 0.32 to 1.05) and 0.91 times (0.32 to 1.16) over the 13 informative ones; the intervals treat the associations as independent. The median is 0.53 over the 15 analyses re-run unweighted and 0.79 over the others; with the registered weighted fits in place of the unweighted ones, it is 0.85 (0.35 to 1.08).

12 more claims

An observational atlas linked GLP-1 receptor agonists to dozens of outcomes beyond glucose, weight and the heart. We pooled the serious adverse events that 234 placebo-controlled trials, with 161309 participants, posted to ClinicalTrials.gov, coded blind to the results under a registered plan. Reports of serious bacterial infection (ratio 0.88, confidence interval 0.83 to 0.93) and pneumonia (0.87) were less frequent on the drugs, as were pneumonia counted in people and death. The reductions held under random effects, with any trial left out, if infection terms overlapped within participants as all serious events do in each comparison, and in trials not coded as recording only on treatment. Of the atlas's associations with enough events to test, the trials found three in its direction with no difference from it detected, contradicted none, and left most inconclusive, among them every neurological and psychiatric one; its large hazard of drug-induced pancreatitis concerns a subtype the trials don't separate.

• Published, Reproduced.Published, Reproduced: Of the 539 interventional studies of GLP-1 receptor agonists with results on ClinicalTrials.gov on 2026-10-12, 234 randomized trials compare a GLP-1 receptor agonist with placebo, in 257 comparisons with 161,309 participants in their adverse-event tables (93,765 on the drugs and 67,544 on placebo). In them, reports of serious gallbladder and biliary disease, counting a participant once for each of the outcome's terms they had, are more frequent on the drugs (Mantel-Haenszel ratio 1.38, 95% CI 1.21 to 1.57), and so are reports of serious nausea and vomiting (2.02, 1.52 to 2.68), as the trials' own publications and the drugs' labels lead one to expect.
• Published, Reproduced.Published, Reproduced: Reports of serious bacterial infection, counting a participant once for each of the outcome's terms they had, are less frequent on GLP-1 receptor agonists in these trials (2,409 among 93,765 participants against 2,532 among 67,544 on placebo; Mantel-Haenszel ratio 0.88, 95% CI 0.83 to 0.93, q < 0.001), and so are reports of serious pneumonia (1,442 against 1,568; 0.87, 0.81 to 0.93, q = 0.0020); both stay significant under random effects and with any single trial left out. Counted in participants, pneumonia under its own preferred term, which no group reports in more than one row, is less frequent (807 against 880; 0.86, 0.79 to 0.95). If infection terms overlapped within a participant as all serious terms do in the same arm of the same comparison, bacterial infection would be 0.89 (0.82 to 0.97).
• Published, Reproduced.Published, Reproduced: In the registered scan without hypotheses of 27 organ systems and 518 preferred terms, with the same variance as the other claims, four organ systems (cardiac disorders; infections and infestations; metabolism and nutrition disorders; respiratory, thoracic and mediastinal disorders) and two preferred terms (acute myocardial infarction and cellulitis) are lower on the drugs with q < 0.05 in a random half of the trials and p < 0.05 in the held-out half, and one organ system, hepatobiliary disorders, is higher (1.36 in the first half, 1.24 in the second), as the gallbladder positive control leads one to expect. Among those lower are serious infection reports as a whole (0.88 and 0.89) and cellulitis (0.64 and 0.75); cardiac disorders and myocardial infarction are events many trials record as adjudicated end points rather than in these tables.

6 more claims

Whether antidepressants raise suicidal behaviour in adults is disputed: the FDA's pooled trials found no increase past young adulthood, and re-analyses of approval data on newer drugs found more suicide attempts. We tested this in the serious adverse events placebo-controlled trials posted to ClinicalTrials.gov, under a registered plan. This version corrects the first, which counted a participant listed under two of an outcome's terms twice. With the posted tables and the trials' public reports, serious suicidal behaviour affected 43 adults on antidepressants and 17 to 18 on placebo (risk ratio 1.86 to 1.96): nominally significant, but at the least favourable count not after the registered correction for two endpoints. Without the trials the re-analyses also used, the excess is similar but less certain. Pediatric trials showed more serious suicidality on antidepressants, as the FDA found. These data lean toward more suicidal behaviour in adults but cannot establish it.

• Published, Reproduced.Published, Reproduced: Of the 932 interventional studies naming an antidepressant with results posted on ClinicalTrials.gov on 2026-10-13, 393 randomized trials compare an antidepressant with placebo in 413 comparisons with 99,730 participants at risk in their adverse-event tables. In the 306 adult trials that randomized participants from the start (71,643 participants), nausea is more frequent on antidepressants in the 207 comparisons whose non-serious tables list it (57,580 participants; Mantel-Haenszel risk ratio 2.08, 95% CI 1.98 to 2.18), as these drugs' known side effects predict.
• Published, Reproduced.Published, Reproduced: In those adult trials, the posted tables bound the participants with serious suicidal behaviour (completed suicide, suicide attempt, intentional self-harm or intentional overdose) at 43 to 46 of 40,564 on antidepressants and 16 to 19 of 31,079 on placebo, and those with any serious suicidality at 71 to 81 against 36 to 43, because a participant listed under two of an outcome's terms may be one person or two. Across every count the tables allow, the Mantel-Haenszel risk ratio is 1.76 to 2.20 for serious suicidal behaviour (p 0.0097 to 0.0502) and 1.29 to 1.73 for any serious suicidality (p 0.0078 to 0.20). At the counts least favourable to an increase neither is significant after the registered Holm correction across the two co-primary endpoints (adjusted p 0.10 and 0.20); at the most favourable both are (0.016 and 0.016).
• Published, Reproduced.Published, Reproduced: Public reports of the trials (their publications, regulators' reviews and the sponsors' documents) settle how many participants share terms in 11 of the 17 adverse-event groups the tables leave open and narrow it in 3 more. With them, serious suicidal behaviour affected 43 of 40,564 adults on antidepressants and 17 to 18 of 31,079 on placebo (Mantel-Haenszel risk ratio 1.86 to 1.96; p 0.025 to 0.036), and any serious suicidality 72 to 77 against 40 to 41 (1.38 to 1.51; p 0.041 to 0.12). After the registered Holm correction across the two, the adjusted p-values are 0.071 and 0.12 at the counts least favourable to an increase and 0.0496 for both at the most favourable.

6 more claims

Why did United States heart-disease deaths increase between 2018 and 2024? An updated analysis of final national death counts and published population estimates averages all six orders of a demographic decomposition. Known-age deaths increase by 28135. Population size contributes 25981.4 deaths, age composition 26512.2, and age-specific rates -24358.5. Demographic contributions outweigh the negative rate contribution. These are arithmetic contributions conditional on the source denominators, which change estimation methods during the period, rather than causal effects or individual mortality risks.

• Published, Reproduced, Reviewed.Published, Reproduced, Reviewed: In the bundled CDC WONDER D158 final snapshot for United States residents with known age, 2018-2024 heart-disease deaths increase by 28,135. Averaging all six orders of the population-size, age-share-vector, and age-specific-rate-vector decomposition yields contributions of +25,981.4, +26,512.2, and -24,358.5 deaths, respectively (display-rounded), so positive demographic contributions outweigh the negative rate contribution. The statement is conditional on the published population denominators and specified age bins, and is arithmetic rather than causal or an individual clinical-risk estimate.

Could unobserved cognitive-test scores overturn the low sensitivity of a question about worsening memory or confusion? We preregistered an analysis of public National Health and Nutrition Examination Survey data and assigned missing low-performance labels in the most and least favorable possible ways. Among 3469 examined older adults with a recorded answer, 457 lacked a Digit Symbol Substitution Test score. Observed-score sensitivity was 24.15%. Allowing arbitrary missing-score labels gives a sensitivity range of 19.27% to 33.78%; the upper endpoint has a confidence interval from 30.75% to 36.82%. Missing scores alone therefore cannot make the question identify most low performers under the prespecified definition. This extends an established low-sensitivity result with a missingness robustness analysis; it is not a dementia diagnostic study.

• Published, Reproduced, Reviewed.Published, Reproduced, Reviewed: Among examined NHANES 2011–2014 adults aged 60 or older with recorded MCQ084 responses, unrestricted low-performance labels for missing DSST scores at the fixed cutoff of 40 yield survey-weighted SCD sensitivity bounds of 0.192660 to 0.337814, with a 95% confidence interval of 0.307465–0.368164 for the upper endpoint, below 0.5.

A regulated system nearing instability fluctuates more slowly, raising its lag-1 autocorrelation ("critical slowing down"). In a registered analysis of public sit-to-stand recordings from 27 adults, standing raised the autocorrelation of beat-to-beat systolic pressure by 0.0431 (CI 0.0066 to 0.0761). The rise was not larger with diabetes (probability of a larger rise 0.505, CI 0.2802 to 0.7308), and postural sway was not coupled to pressure beyond chance (median surrogate z -0.028). Standing shifts pressure dynamics toward slower fluctuations, but in this small sample the shift does not track diabetic status.

• Published, Reproduced, Reviewed.Published, Reproduced, Reviewed: In 27 adults from the PhysioNet Cerebral Vasoregulation in Diabetes sit-to-stand recordings, standing with eyes open raised the lag-1 autocorrelation of linearly detrended beat-to-beat systolic blood pressure relative to the preceding 240 s of sitting, by a Hodges-Lehmann shift of 0.043 (bootstrap 95% CI 0.007 to 0.076), with 19 of 27 participants rising (one-sided Wilcoxon signed-rank p = 0.012; Holm-adjusted across two primary tests p = 0.025).
• Published, Reproduced, Reviewed.Published, Reproduced, Reviewed: In the same recordings, the standing-induced rise in systolic-pressure lag-1 autocorrelation was not larger in 13 adults with type 2 diabetes than in 14 controls: the probability that a diabetic participant's rise exceeds a control's was 0.505 (bootstrap 95% CI 0.28 to 0.73; one-sided Mann-Whitney p = 0.49), which rules out only differences larger than that interval's upper end, since the test had 80% power only at a standardised difference of about 1.0.
• Published, Reproduced, Reviewed.Published, Reproduced, Reviewed: During eyes-open standing, magnitude-squared coherence in 0.05-0.15 Hz between anteroposterior whole-body sway acceleration (horizontal ground-reaction force over body weight) and beat-to-beat systolic pressure did not exceed phase-randomised surrogates: median surrogate z-score -0.03 across 26 participants, 2 of whom exceeded 1.645 (one-sided Wilcoxon signed-rank p = 0.54).

Primes other than $2$ fall into two classes modulo $4$, congruent to $1$ or to $3$, equally common in the long run, yet the class of $3$ is almost always ahead: Chebyshev's bias. Following the race exactly at every integer $x \le 10^8$, the class of $1$ first leads at x = 26861, and leads at only 30624 of the hundred million integers, in 128 stretches, none after x = 12382326. Weighting each $x$ by $1/x$, the class of $1$ leads on a share 0.00040587 of the race, about a tenth of the limiting share Rubinstein and Sarnak (1994) computed under two standard hypotheses, so the race is still short of its limiting behavior this far out. Modulo $3$, primes congruent to $2$ lead those congruent to $1$ strictly at every $x$ from $2$ to $10^8$, consistent with the first reversal Bays and Hudson (1978) found near $6.1 \times 10^{11}$.

• Published, Reproduced, Reviewed.Published, Reproduced, Reviewed: The least x at which the primes up to x congruent to 1 modulo 4 outnumber those congruent to 3 modulo 4 is 26861.
• Published, Reproduced, Reviewed.Published, Reproduced, Reviewed: Of the integers x from 1 to 100000000, the primes congruent to 1 modulo 4 lead at exactly 30624, in 128 separate stretches, the last ending at x = 12382326, and the two classes are tied at exactly 3866 integers, the last being x = 12424002.
• Published, Reproduced, Reviewed.Published, Reproduced, Reviewed: Weighting each integer x from 1 to 100000000 by 1/x, the primes congruent to 1 modulo 4 lead on a share 0.00040587 of the race, about a tenth of the limiting share of about 0.0041 implied by Rubinstein and Sarnak's logarithmic density of 0.9959 for the other side.

2 more claims

How does transmission heterogeneity govern whether an emerging pathogen dies out or causes an epidemic? In negative binomial branching processes at reproduction number 2.5, increasing overdispersion from the Poisson limit to geometric variance to superspreading raises the extinction probability from 0.107355 to 0.4 to 0.860685. Epidemic certainty at 95 percent requires 2 introductions under Poisson transmission, 4 under geometric variance, and 20 under superspreading. Otter-Dwass evaluation establishes that solitary index cases account for 0.721943 extinction probability, or 83.88 percent of extinctions. Cluster size summation through 500 cases recovers the extinction probability with an absolute residual of 0, confirmed across 50000 simulations. Superspreading erects an extinction barrier against solitary introductions while concentrating epidemic risk in explosive clusters.

• Published, Reproduced, Reviewed.Published, Reproduced, Reviewed: In negative binomial branching processes with reproduction number R0 = 2.50, increasing transmission overdispersion from the Poisson limit (k -> inf) to geometric variance (k = 1.00) to SARS-like superspreading (k = 0.10) increases the single-case extinction probability from 0.107355 to 0.400000 to 0.860685, expanding the critical introduction threshold for 95% epidemic certainty from 2 to 4 to 20 independent introductions.
• Published, Reproduced, Reviewed.Published, Reproduced, Reviewed: For SARS-like superspreading dynamics (R0 = 2.50, k = 0.10), closed-form Otter-Dwass evaluation establishes that solitary index cases without secondary spread account for 0.721943 extinction probability (83.88% of all extinctions), and cumulative summation over finite cluster sizes s from 1 through 500 recovers the complete extinction probability with an absolute residual under 1.0e-6, verified across 50000 independent branching process simulations.

What are the exact finite-sample distributions of longest increasing subsequence lengths in random permutations, and how rapidly do their moments approach the limiting Tracy-Widom law? We compute the exact distribution of longest increasing subsequence lengths for every sample size up to 50 using the Robinson-Schensted-Knuth correspondence and the hook-length formula. At the largest sample size, the exact expected length is 11.309389 with variance 1.94134, corresponding to a normalized centered mean of -1.475863 and normalized variance of 0.526961. Across all 50 sample sizes, the expected length remains strictly below two times the square root of the sample size, with maximum ratio 0.799695. Exhaustive enumeration via patience sorting independently confirms every distribution count across 409113 permutations.

• Published, Reproduced, Reviewed.Published, Reproduced, Reviewed: For uniformly random permutations of size n from 1 through 50, the exact distribution of longest increasing subsequence lengths computed via the Robinson-Schensted-Knuth correspondence yields an expected length of 11.309389 at n=50, with all expected lengths strictly bounded below 2*sqrt(n).
• Published, Reproduced, Reviewed.Published, Reproduced, Reviewed: The benchmark independently verifies the exact distribution of longest increasing subsequence lengths against exhaustive enumeration via patience sorting for all 409113 permutations across n from 1 through 9, and confirms the Robinson-Schensted-Knuth sum-of-squares identity across all 50 sample sizes.

Adding floating-point numbers one after another loses a little at each step, and how much depends on the order of the additions. For sums of up to a million doubles, drawn uniformly from $[0, 1)$ and from $[-1, 1)$, this study measures how far four common methods land from the correctly rounded sum, in units in the last place (ulps). Adding left to right, the error averages 196.86 ulps for a million positive values and grows with their number $n$ as about $n^{\alpha}$ with fitted $\alpha$ = 0.545, close to the square root that independent rounding errors predict. Pairwise summation stays within 2 ulps at every length. Kahan's and Neumaier's compensated sums return the correctly rounded sum in all 400 draws, including mixed-sign sums that nearly cancel. Every value is reproducible exactly, on any machine and Python version.

• Published, Reproduced, Reviewed.Published, Reproduced, Reviewed: Adding 1000000 doubles drawn uniformly from [0, 1) from left to right lands a mean of 196.86 units in the last place (at most 589) from the correctly rounded sum over 50 draws, and the mean error grows as about n to the power 0.545 for n from 1000 to 1000000, near the square-root growth that independent rounding errors predict.
• Published, Reproduced, Reviewed.Published, Reproduced, Reviewed: Pairwise summation of the same positive draws stays within 2 units in the last place of the correctly rounded sum in all 200 draws for n from 1000 to 1000000, with a mean error of 0.4 units at n = 1000000.
• Published, Reproduced, Reviewed.Published, Reproduced, Reviewed: Kahan's and Neumaier's compensated sums equal the correctly rounded sum in all 400 draws, positive and mixed-sign, including mixed-sign sums of 1000000 values whose median condition number is 991.

1 more claim

Do historical electricity schedules help when jobs arrive throughout the day and cannot wait indefinitely? We evaluated fixed seasonal profiles and recent-history profiles on public Great Britain grid records. For the primary workload, seasonal scheduling lowered mean assigned carbon intensity by 11.24% in 2024 and 12.01% in 2025 relative to immediate execution. Yet 17.61% and 15.55% of jobs received higher intensity. Recent-minus-seasonal mean differences were -0.21 and -0.07 g CO2/kWh. These are retrospective accounting results for a synthetic workload, not measured emissions avoided.

• Published, Reproduced, Reviewed.Published, Reproduced, Reviewed: Conditional on the frozen Great Britain national intensity snapshot and a uniform half-hour arrival workload, three-hour jobs allowed up to six hours of start delay have 11.24% and 12.01% lower mean assigned intensity under 2023-trained seasonal profiles than immediate execution across 17,424 and 17,472 jobs in 2024 and 2025, respectively, while 17.61% and 15.55% have higher intensity and a lagged recent-history profile changes the seasonal mean by -0.21 and -0.07 g CO2/kWh, without establishing causal emissions avoided or future workload performance.

Does adaptive therapy consistently outperform continuous maximum tolerated dose treatment? Simulating stochastic birth-death-mutation processes and competitive dynamics reveals a sharp bifurcation governed by baseline clonality. Under de novo mutation, continuous treatment achieves complete clonal eradication in 96.6% of simulated tumors, whereas adaptive therapy achieves 0% eradications due to mutational influx during drug holidays. Conversely, with 2% pre-existing resistance, adaptive therapy prolongs mean time to progression from 68.6 days to 74.8 days while reducing cumulative drug exposure by 18.1%. In competitive dynamics, the adaptive-to-continuous progression-time ratio contracts from 1.11 under a 20% fitness cost to 1.09 under neutral resistance. Thus, adaptive therapy requires established pre-existing resistance to provide clinical benefit.

• Published, Reproduced, Reviewed.Published, Reproduced, Reviewed: In the presence of 2.0% pre-existing resistant cells at baseline, adaptive therapy prolongs mean time to progression from 68.6 days to 74.8 days while reducing cumulative drug exposure by 18.1% compared to continuous therapy.
• Published, Reproduced, Reviewed.Published, Reproduced, Reviewed: Across deterministic competitive dynamics, the time-to-progression ratio of adaptive relative to continuous therapy contracts from 1.11 at a resistant fitness cost of 0.20 to 1.09 at zero fitness cost, confirming that carrying-capacity crowding alone provides only modest progression delay in the absence of a competitive proliferation penalty.
• Published, Reproduced.Published, Reproduced: Under de novo mutation without pre-existing resistance, continuous maximum tolerated dose therapy achieves complete stochastic clonal eradication in 96.6% of simulated tumors, whereas adaptive therapy achieves 0.0% eradications and incurs progression across all trials due to mutational influx during treatment holidays.