the study said that the 5 patients with VITT that they looked at had the IGLV3-21 * 02 polymorphism, but it's a fallacy to say that means that you can't get clotting without it
Glp and G9a are ubiquitous as they are import epigenetic regulators (histone methyltransferases). Sounds difficult to work on, and hard to supplement if they play an important role in many cell types
TRP channels were first cloned over 20 years ago, and are indeed medically relevant for nociception and pain. The piezos are equally relevant; knockouts are embryonically lethal, and the function of mechanosenstation in somatosenation and in general continue to be elucidated. For instance, it was only a few years that they were identified as being required for the baroreceptor reflex.
As an example, Douglas Bates, the author of R's lme4 excellent package for generalized linear mixed-effects models, has switched to julia to develop MixedModels.jl. The julia version is already excellent, and has many improvements over lme4.
This paper is the first structure of any odorant receptor-ligand interaction. There's currently no equivalent structure for mammalian odorant receptors to validate the docking theory, but it's likely correct.
Not really. GPCRs amplify signals at each step via their second messenger cascade. These channels form homotetramers whose structure differs greatly from the canonical seven transmembrane domain structure of GPCRs. So this study is important since there were no studies indicating how odorants bind and activate odorant receptors. However, it is unlikely that the mechanisms in insects odorant receptors will directly apply to those of mammalian odorant receptors. In contrast, mammalian odor receptors will work much more like those of other class A GPCRs like the β-adrenergic receptor, of which there are numerous structures interacting with ligands and in various configurations, and which was the basis of the work that won the nobel prize in 2012.
This is truly a landmark study. This is the first structure of any odorant receptor. It is, however, one from an insect, so the structure is not homologous to mammalian olfactory receptors, which are a large family of G-protein-coupled receptors.
The Code Breaker by Walter Isaacson is a recent biography of Jennifer Doudna, who won the Nobel Prize for her pioneering work on CRISPR, that you might enjoy
I don't follow. What's stunning about it? Doesn't it just mean that there is little evolutionary pressure or selection on the olfactory receptor genes? Not sure what the discovery is, or its significance.
RNA uses uracil/uridine rather than thymine, but uridine is actually quite immunogenic. That's what has prevented people from using mRNA as a therapy until recently, when the founders of BioNTech figured out that they could use pseudouridine (abbreviated as Ψ) instead. See [1] for more information.
I have no idea why you think that there were no studies in April. A quick search shows that's wrong. There were initial reports in March, followed by many peer-reviewed studies that started coming out in April, which were then followed by studies with more objective measures (rather than retrospective self-reports) and larger sample sizes.
Yes, there were a lot of reports back in March about the loss of smell as a frequent and specific symptom for COVID-19. I'm not sure why this article acts like it's a new thing. And, yes, patients recovering from the loss of smell (hyposmia or anosmia) can often have smell distortions and disturbances (known as parosmias and phantosmias).
There were many papers that came out over 4 months ago with more people and other approaches, all with similar conclusion [1-3]. Not sure why this paper is getting a lot of press.