Cognitive Bias in Forensic Pathology Decisions was published today by Journal of Forensic Sciences

From the abstract “We examined all death certificates issued during a 10-year period in the State of Nevada in the United States for children under the age of six.” /2
We also conducted an experiment with 133 forensic pathologists in which we tested whether knowledge of irrelevant non-medical information that should have no bearing on fo- rensic pathologists’ decisions influenced their manner of death determinations. /3
The dataset of death certificates indicated that forensic pathologists were more likely to rule "homicide" rather than "accident" for deaths of Black children relative to White children. /4
“Participants read a vignette describing a not straightforward or simple case in which a 3.5-year-old child was presented to an ED with diminished vital signs and who died shortly after arrival. /5
In the vignette, the caretaker described finding the toddler unresponsive on the floor of a living room. Postmortem examination determined that the toddler had a skull fracture and subarachnoid hemorrhage of the brain. /6
By random assignment, each pathologist read one of two vi- gnettes, which were identical apart from two pieces of information: some were told that the child was African-American and that the care- taker was the mother's boyfriend /7
whereas the other pathologists were told that that child was White and that the caretaker was the child's grandmother. To be consistent with typical medical information, the race of the child was stated, but the race of the caretaker was not explicitly stated. /8
In the Black condition, pathologists were about 5 times more likely to rule the death as a "homicide" rather than an "accident" (35.4% vs. 6.2%), but in the White condition, the results were the opposite: /9
A dataset of death certificates in NV revealed that Black children, relative to White children, were more often judged as victims of homicides rather than accidents. /10
The experimental data, along with the death certificate data, taken together, show that even highly trained professional scientists can be biased in their decisions. /11

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An interesting thing about carp is that they can go into anoxic hibernation and switch to an anaerobic metabolism based on converting glycogen to ethanol.

The waste ethanol is diffused out the gills

https://t.co/V3D1umHf04

Carp can switch over to an anaerobic metabolism and quietly exhale booze until the situation gets better.

They basically evolved the same metabolic pathway as yeast, independently.

In theory, if you spent a few thousand years breeding carp for it, you could use them to make booze.

They'd be enormous, almost entirely glycogen deposits with a fish added as an afterthought.

The really interesting thing about anaerobic carp, is that they can go 4-5 months without oxygen by relying on liver glycogen.

You, a human, have only about 100 grams of glycogen in your liver, about 400 more grams in your skeletal muscles. Call it 500 grams total.

In humans, glycogen is also burned for energy. This is where the marathon runner's bonk comes from: you only have about 2,000 calories worth, and running a marathon burns those 2,000 calories.
https://t.co/hXlo8qgkD0
Look like that they got a classical case of PCR Cross-Contamination.
They had 2 fabricated samples (SRX9714436 and SRX9714921) on the same PCR run. Alongside with Lung07. They did not perform metagenomic sequencing on the “feces” and they did not get


A positive oral or anal swab from anywhere in their sampling. Feces came from anus and if these were positive the anal swabs must also be positive. Clearly it got there after the NA have been extracted and were from the very low-level degraded RNA which were mutagenized from

The Taq.
https://t.co/yKXCgiT29w to see SRX9714921 and SRX9714436.
Human+Mouse in the positive SRA, human in both of them. Seeing human+mouse in identical proportions across 3 different sequencers (PRJNA573298, A22, SEX9714436) are pretty straight indication that the originals

Were already contaminated with Human and mouse from the very beginning, and that this contamination is due to dishonesty in the sample handling process which prescribe a spiking of samples in ACE2-HEK293T/A549, VERO E6 and Human lung xenograft mouse.

The “lineages” they claimed to have found aren’t mutational lineages at all—all the mutations they see on these sequences were unique to that specific sequence, and are the result of RNA degradation and from the Taq polymerase errors accumulated from the nested PCR process

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