I've noticed some things running slower too, but I wasn't sure if my computer was getting older. As for the interface/asthetic, it's pretty terrible in every regard.
It's just very conversational. If you are comfortable with stats and just need a reference it can be obnoxious. I think I went through the first edition in my PhD and it was better than a stats course. But when I want a quick reference for something it is to much reading to get to the point. It might be more well organized now though.
As an MD/PhD I wish all MD researchers read this book. Heck, I wish all neuro researchers read it. If you are already established in in stats and math and your interest is just another math book to casually read or reference, this is a bad choice
Usually we test against best current treatment and not just always against placebo. If something clearly improves outcomes for a patient, it's unethical to not give them a treatment so that you can test your new intervention against a placebo.
Stress increases cortisol and cortisol for a long time wrecks the immune system. There are a lot of other things that effect cortisol levels, but it's at least on very plausible pathway for some getting sick more easily.
Article says this has been done other places already. Has this specifically been campaign ads or does it also involve things that are considered politically motivated messaging? For example, is there danger of vaccination PSAs getting banned because some politicians say bizarre things about them?
There are all kinds of presentations for seizures. Ones in the frontal lobe are particularly hard to catch based on external presentation. If one is suspected of having seizures they will get a continuously monitored EEG where times associated where the seizure like state is monitored electrically. Sometimes it's a really weird presentation of a seizure or sometimes it's psychogenic. Either way it's good to have these people get some help I'd it keeps happening.
1. Blood brain barrier and CSF should be separate for all but tiny molecules. It's why CT angiograms are able to visualize distinct vessels. So it is pretty hard to directly interact with this sort of thing in vivo
2. A good chunk of the neuro community have been operating under the assumption that some of those mouse model findings are mechanisms in humans too. Since we couldn't easily prove it, people used a bunch of next best tools with fancy imaging that demonstrated it was very likely. On top of furter proof, this sort of study allows us to begin pinpointing exactly how close our next best tools are at estimating in vivo processes without opening up the head.
I wish I could, but in addition to this happening over a decade ago, he changed his lab's focus afterwards. He went into neurotransmitter research in skin since it has some overlapping embryological origins with the brain.
I had a neuroscience professor in undergrad who did a bunch of experiments where the only variables were things like the material of the cage, bedding, feeder, etc. He systematically tested variations in each separately. Outcomes varied in mice no matter what was changed. I would love to tell you what outcomes he measured, but it convinced me not to go into mice research so it's all just a distant memory.
On the other hand, I've worked with people since then who have their own mice studies going on. We are always learning new ways to improve the situation. It's just not a very impressive front page so it goes unnoticed by those not into mice research methods.
As in it has a higher inter rater reliability. The statistical term of reliability that is used when describing the likelihood to reproduce a measure under similar conditions.
Asperger's was not reliably diagnosable between healthcare workers trained to diagnose it. In other words, a diagnosis of Asperger's in someone's medical chart was not a reliable way of knowing if they had Asperger's.
It can be helpful to get a diagnosis of autism for kids in public school. Kids end up needing additional one on one time and resources are limited. Those with the biggest problems are the first to be approved for these resources, and a formal diagnosis makes it easier to get that approval.
Autism can be reliably diagnosed at 2.5 years of age, so we probably aren't looking at a strong cultural bias in in how kids are presenting with autism. These models using data from countries where the healthcare systems provides support for appropriate screening and testing further minimizing bias due to culture. In other words, one would not expect these models to be overfit to phenotypically distinct representations of autism as a result of culture.
Variations in brain plasticity have been suspected of playing a role in autism for a long time. Brain plasticity may vary by region, throughout development, and at a molecular level. If population dependent variations in plasticity are indeed responsible for the lack of model generalizability, then the next step would be to do as I previously suggested. That is, identify where the many genome wide variations converge on biomarkers driving differences in plasticity.
I'm not convinced the result is as important here as the methods. Separating language from complex cognition when evaluating individuals is difficult. But many of the people I've met in neuroscience that study language and cognitive processes do not hold the opinion that one is absolutely reliant on the other in all cases. It may have been a strong argument a while ago, but everytime I've seen a presentation on this relationship it's been to emphasize the influence culture and language inevitably have on how we think about things. I'm sure some people believe that one cannot have complex thoughts without language, but most people in speech neuro I've met in language processing research find the idea ridiculous enough they wouldn't bother spending a few years on that kind of project just to disapprove a theory.
On the other hand, further understanding how to engage complex cognitive processes in nonverbal individuals is extremely useful and difficult to accomplish.
It's important to note that models that use genome wide association analysis have demonstrated extremely high predictive value across large cohorts sharing geography but are very poor when applied on a geographically distinct population. This suggests that although autism has a strong association with genetics, neurophysiology unique to autism develops in the context of highly complex genetic associations that are likely subject genetic drift across population and time.
When we have a a few genes of interest that are important in screening for a rare disease we accept that novel variants will continue to be identified throughout the years as more people are screened. Autism as a prevalence of 1-3%. I don't remember the exact number but I think something like 30% of autism diagnoses are believed to be secondary to fairly severe but distinct genetic syndromes. So when we talk about a subgroup of autism without clear etiology we are looking at a fraction of 70% of 3% of the population. We're approaching rare disease territory when we talk about subgroups within autism. A rare disease with a highly complex genetic association across the genome that is subject to genetic drift is not a good candidate for genetic screening.
All that being said, studies like this may provide valuable insight into what microbiology is being influenced, even if we can't reliably predict which variants are responsible. Id love to see future investigations relate genetics to biomarkers instead of behavioral tests in autism.
The problem was that a diagnosis of Asperger's was unreliable and therefore useless. We definitely need to identify individuals within the diagnosis of autism spectrum disorder that can reliably be identified and benefit from specific interventions. However, Asperger's did not provide that.