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
 
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