Miscellaneous Research Thread

An apsect that has been there in plain sight, ( even without ASD diagnosis) that Bath have ignored for years, and simply made kids worse with sleep hygiene.
Previous issues with Bath include kids aligning reponses with what they thought was desired to gain school accommodations and avoid FII . There's a limit to how robust any (subjective) data is.
 
Yes, there is nothing the least bit surprising about this. Something similar was found by Walter Freeman for olfaction a very long time ago.

And it does not go against neuroscience at all. We understand that a lot of neurons are tuned to higher level inferences/responses. They have to be to give us higher level concepts, like "I am in the same place". These neurons will fire in a context dependent manner and that includes an accumulation of recent experiences. A cell that was used for one sort of inference a week ago might be used for a different inference after having to wander through mazes for a week.

This does not seem to be randomness they are talking about, but drift in responsiveness. Randomness used to be accepted as a key factor in cell firing and synaptic vesicle release. Christof Koch has fairly recently come to the conclusion that a lot of what was thought to be random is just a reflection of shifts in artefacts relating to crude experiments on cells being activated in a non-physiological way.
 
This paper is from February, but I thought it of potential interest given how frequently questionnaires like HADS are used in ME/CFS patient cohorts -

Selecting a depression measure for research: A critical examination of five common self-report scales

"Content and structural validity were deemed ‘inadequate’ or ‘doubtful’ for the BDI, PHQ-9, and HADS. Adequacy of criterion and construct validity varied across measures. HADS received ‘doubtful’ or ‘inadequate’ ratings across all properties. All but the PROMIS-D received ‘doubtful’ ratings for internal consistency. The CES-D and PROMIS-D received the highest cross-cultural validity ratings. Continued use of depression measures that lack theoretical grounding, robust psychometrics, or equivalence across diverse populations should be reconsidered."
 
I think there is more than enough to make a formal "deconditioning is clearly not a factor here, and neither is lack of motivation" paper that settles the stupid argument once and for all. Hell some of the psychobehavioralists actually acknowledge it, although only to excuse the failures of their own trials. How is this even somehow controversial?!

Same with cortisol, frankly. There is nothing there, and all of it is simply because of the damn "stress hormone" nonsense. Decades lost on pure nonsense.
 
This is completely random.
However, for some reason the fact that guinea pigs that are tortured with compressed audio need more than 7 days to recover back to 50% won’t leave me alone.
Of course, any chance that this has anything connection to PEM is likely close to 0%.


Overcompressed sound, a new auditory risk and a window on new pathophysiological mechanisms, 2024, Dos Santos et al

Dos Santos, T.; Hugonnet, C.; Avan, P.

Abstract​

Exposure to loud sound during leisure time is identified as a significant risk factor for hearing by health authorities worldwide.
The current standard that defines unsafe exposure rests on the equal-energy hypothesis, according to which the maximum recommended exposure is a tradeoff between level and daily exposure duration, a satisfactory recipe except for strongly non-Gaussian intense sounds such as gunshots.

Nowadays, sound broadcast by music and videoconference streaming services makes extensive use of numerical dynamic range compression.
By filling in millisecond-long valleys in the signal to prevent competing noise from masking, it pulls sound-level statistics away from a Gaussian distribution, the framework where the equal-energy hypothesis emerged.

Auditory effects of a single 4 hour exposure to the same music were compared in two samples of guinea pigs exposed either to its original or overcompressed version played at the same average level of 102 dBA allowed by French regulations.
Apart from a temporary shift of otoacoustic emissions at the lowest two frequencies 2 and 3 kHz, music exposure had no detectable cochlear effect, as monitored at 1, 2 and 7 days post-exposure.

Conversely, middle-ear muscle strength behaved differentially as the group exposed to original music had fully recovered one day after exposure whereas the group exposed to overcompressed music remained stuck to about 50% of baseline even after 7 days.
Subsamples were then re-exposed to the same music as the first time and sacrificed for density measurements of inner-hair-cell synapses. No difference in synaptic density was found compared to unexposed controls with either type of music.
The present results show that the same music piece, harmless when played in its original version, induces a protracted deficit of one auditory neural pathway when overcompressed at the same level. The induced disorder does not seem to involve inner-hair cell synapses.

PDF | Web | DOI | Proceedings of the 10th Convention of the European Acoustics Association Forum Acusticum 2023
 
Distinct genetic architecture in the tails of complex traits
Souaiaia, T; Wu, H M; Ori, A P S; Choi, S W; Hoggart, C J; O’Reilly, P F

Complex traits are highly polygenic, with heritability explained by many hundreds of common variants of small effect together with rare variants of large effect1. Yet how this genetic architecture varies along the trait continuum has been underexplored, as has the role of natural selection in shaping this variation.

Here we developed an approach based on polygenic risk scores that reveals widespread departures from common-variant architecture in one or both of the tails of 74 quantitative traits. These observations were replicated across ancestries, cohorts and repeated measures and using an alternative family-based approach2.

Incorporating rare variants identified from sequence data resulted in marked reductions in these deviations, suggesting that rare alleles of large effect are key drivers of trait-tail architecture. Forward simulations showed that stabilizing selection could generate the observed patterns, whereas modelling reproductive success provided empirical support for the role of selection.

These findings show that although complex traits are polygenic in the population at large, they have a distinct and less polygenic architecture in their tails due to selection. This has implications for rare-variant discovery and complex trait and disease prediction.

Web | DOI | PDF | Nature | Open Access

Together, these findings provide robust support for our overarching hypothesis: namely, that selective pressures on many complex traits have led to distinct concentrations of high-effect rare alleles in their tails. Therefore, although complex traits are broadly polygenic in the population, they often become oligogenic in one or both of their tails, depending on selective pressures on the trait.
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Relevant to SequenceME.
 
reeserichardson.blog

How much of Thermo Fisher’s antibody data has been manipulated?

We’ve documented more than 450 instances of apparent data manipulation in Thermo’s catalog
reeserichardson.blog reeserichardson.blog

How much of Thermo Fisher’s antibody data has been manipulated?​

[ TL;DR: As of 3 June 2026, we have identified more than 450 images bearing signs of manipulation in verification data advertised by Thermo Fisher Scientific in its online primary antibodies catalog (+1 by Abcam). See the full repository of problematic images, curated by myself and Sholto David, here:

Zenodo – Problematic images in vendor antibody verification data

You are welcome to contribute new findings at this Google form.

This blog post was original posted on 28 May 2026 and has not been edited to update counts since that date. There is an update covering Thermo Fisher’s response at the bottom of this post. ]
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Discussion on Hacker News.
 
… The authors suggest that multimodal rehabilitation was associated with a significant reduction in depressive symptoms, while improvements in fatigue were restricted to PCS patients without depressive symptoms. The intervention thus reduced fatigue only in a minority of the cohort [… While we red this article with great interest […] we believe that the authors’ interpretation of their findings and the conclusions drawn warrant reconsideration
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Data from our group [2], as well as findings from earlier studies in the field [3–5], consistently demonstrate significant improvements in fatigue among PCS patients during rehabilitation, as assessed by various validated instruments including the Multidimensional Fatigue Inventory [2], Modified Fatigue Impact Scale [3], Chalder Fatigue Scale [4], and Fatigue Severity Scale [4, 5].
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While fatigue undisputedly represents a core symptom of PCS and a central therapeutic target [6], its overlap with depressive symptoms requires careful differentiation as depressive symptoms may contribute substantially to the chronification and overall symptom burden of PCS. The reported mean PHQ-9 score of 22.15 ± 5.34 reflects a generally high level of depressive symptom severity within the analyzed cohort and approximately 70% of the cohort were classified as depressed based on PHQ-2 criteria.
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The reported hospitalization rate during acute infection of 10.6% […] However, the overall rate suggests that the majority of patients were not severely affected during the acute infection phase […] As recently published [2] and consistent with general observations from our rehabilitation center, depressive patients exhibited higher baseline fatigue scores than non-depressed patients. However, both subgroups demonstrated significant improvements during rehabilitation, followed by a re-increase in fatigue and depressive symptoms at 6-month follow-up.
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Hmm, why would that be?

Differences between our findings and those reported by Kuperschmitt et al. [1] may partly be explained by variations in measurement instruments, patient characteristics, and rehabilitation settings. Nevertheless, we believe that the title “Depression, but not fatigue, improves as part of multimodal post-COVID rehabilitation”, along with broader conclusions suggesting that PCS patients, independent of symptom spectrum and indication for rehabilitation, do not experience any improvement in fatigue, may overstate the evidence presented.
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Fatigue remains a central and clinically dominant symptom of PCS across rehabilitation settings, and its complex interaction with affective and somatic dimensions should be interpreted with caution, particularly in light of the marked heterogeneity of long/post-COVID phenotypes. A careful assessment and stratification of patients followed by individualized rehabilitation approaches including constant monitoring of symptom changes and patient reported outcome measures may be key to successful treatment strategies.
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Huh. And I thought hypervigilance was very bad and a foundational cause and association of abnormal illness beliefs.
 
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