CharonY

That is not as clear. There is a yield gap between what is called organic agriculture and conventional farming (estimated ca. 20% on the high end) but studies looking into crop rotation indicate that the difference can be <10% (Ponisio et al. Proc. Roy. Soc. B 2015).

I do not know how conserved they are, but if they are not, PCR based amplification/identification may not work out. What is often done to find enzymes with desired functions is to isolate protein fractions, test them for desired activity and then sub-fractionate those until you get a decently pure sample to analyze further.

That and the fact that he is more into publishing than research are warning signs. It should be noted that he apparently did work in a bioinformatics core facility, but he is not an active researcher and clearly has an agenda. Ask yourself, why do reputable media not report on it?

It is indeed only a limited binding site, which is called an eptitope (and as a side note, while most common, antigens are not all proteins). There a range of options to identify epitopes, depending on what you start off with and what you want to figure out. They range from 3D analysis of high-resolution imaging of co-crystallized antigen-antibody complexes (which provides structural information but is costly and difficult and sometimes impossible to perform) to genetic methods. You will find more under the umbrella of epitope mapping.

While I do not like to use of one disease to make another seem more harmless (it ain't a zero sum game). You should know that there are plenty of serious diseases endemic to the US. Seasonal flu is a big killer every year despite vaccinations and just because it is new it does not mean that existing measures are failing nor that there is a significant increase in overall risk. If you really want to be afraid, think about AB resistant bacteria.

Bacterial survival and propagation is hugely different from virus (esp as latter cannot multiply outside host cells). The virus in question is propagated facilitating direct transmission. It affects different organs in different ways. Treatment options are vastly different. So the comparison would make as much sense as any other two random infectious diseases.

Novel ones or similar to known ones?

Yersinia is a bacterium, not a virus. Whole different ballgame.

Well, most biological actions on the cellular level involve the actions of proteins on one level or or another so that is not very useful for the understanding of the actual mechanism.

It is really unclear what OP wants. If the goal is e.g. to identify enzymes with certain activity the standard procedure would be to test protein fractions for said activity followed by deeper characterization of these fractions, for example. If testing for absence or presence of certain enzymes DNA-based studies would generally make more sense.

There have been studies suggesting that stress may alter lipid metabolism, but as often, mechanisms are unclear. Similarly observations were made with exercise stress, but the effects are also somewhat complicated and not simply a matter of up and down. At minimum, it depends on the duration and type (exercise tends to stabilize or reduce, long-term stress associated with increase in cortisol, the opposite). While many are like that (though most studies ask for filling out daily diaries/questionnaires and not just general recalls), there are also some with controlled diets. But rather obviously they tend to be short term. But even then it would be virtually impossible to limit and control all other life events that may influence metabolism. And even if you could, there is a good chance that you are creating a highly artificial environment which will limit our ability infer biological mechanisms. I am not entirely sure how that would work, even ignoring the current hypotheses, there is only evidence for local accumulation of cholesterol and since most of it is eventually enveloped in the tissue I am not entirely sure how that could raise overall cholesterol levels. As a side note, I am not sure whether you were joking, but the ability to volunteer for medical experiments has obviously virtually no impact on incarceration rates.

Sequencing using next-gen method is relatively affordable, but assembly can be tricky. And without a related genome as scaffold it is unlikely to close. You can still search for ORFs in an incomplete genome, but at some point you would have to ask yourself whether it would be worth the money and effort. I.e. what is the actual research question? If the goal is to identify a protein with a specific function it seems like a rather useless endeavour to sequence the genome.

From what I have read, a significant part of the delay was caused by the bureaucratic structure of the Chinese system. I.e. before committing to official announcements and rather extreme measures (which simply could not happen in Western countries). The reporting system is multi-layered, and effects have to be confirmed bottom up, as well as top-down. But each layer has a different reporting authority. For example local authorities can only provide the actual numbers of infections, but they did not had the capabilities to test. The Chinese CDC can confirm cases and share with national and provincial health authorities. However, the CCDC has no reporting authority to the public. So getting the whole picture is, at best, cumbersome. In addition it appears that there was a screw-up on the local level who did not provide continuous information to the CCDC which may have led the higher authorities to see it as more containable as it was. And of course as a whole the Chinese system likes to err on the side of secrecy and stability. So there is an inherent inefficiency in the authoritarian system, which also facilitates (if not encourages) deception. But yes, as for OP, there is no indication of any wrongdoing from the WHO.

I think you misunderstood my post (which had a typo, I meant de novo sequencing, not de novo synthesis). De novo sequencing in protein sciences refers to sequencing an isolated protein via fragmentation in the MS. From there, at least in principle, you can deduce the amino acid sequence and use that sequences for further analyses. It does not refer to DNA sequencing.

You can use mass spectrometry, but as I mentioned before, without genomic information it will be difficult to identify all but the most conserved proteins. De novo sequencing is a possibility in which you use MS to try to deduce the AA sequence. But that is often tricky and often does not work well straight from complex mixtures. One could try to run a 2D-gel and try to isolate enough of a particular protein of interest but it is not really something that would work well in high-throughput.

SDS-PAGE only separates, but alone does not identify what proteins you separated. You need to combine with a targeted approach such as Western blot, but that requires a suitable antibody and knowledge what you are looking for. Mass spectrometry is also theoretically possible, but without genome data you will have to rely on closely related species or need to conduct de novo sequencing which is not that great most of the time.

Proving a negative is quite difficult, though, and I'd argue that in the absence of any supporting evidence it should not be considered a likely alternative hypothesis to an animal origin. Was there a study eliminating bats? I thought that most just do not believe snakes to be a likely candidate (and the study supporting snakes was a bit shaky, mostly based on codon usage IIRC), at least compared to mammals or birds.

That is not what splicing means. I assume you mean to clone luciferase gene into a crop. Well for starters you could look at the thermodynamics and estimate how much energy is released and also note that most of it is released as light. Then contrast it with other exothermic reactions that normally occur and figure out whether it would put a dent into the heat budget (hint: nope). But I would direct you to read up on thermogenic plants.

First of all, the FDA has approved several ketamine-based treatments including the IV drips. They are expensive because, well first you have to lay a drip and second, due to the massive side effects you need medical personnel at hand (which makes it expensive). Recently, a ketamine-based nasal spray has been approved, but you still need medical supervision to use it. So that is rather a bad example for your case. While blaming the FDA is very popular, it is really not the limiting factor. Just to provide some numbers, trials for FDA approval average to about $19 million. The average cost for developing a new drug is roughly 2-3 $ billion, i.e. FDA approval is just a small fraction of the overall cost. Looking at overall expenditures, marketing takes up about the same amount as research (depending on company and product it can be much more or less), again dwarfing the FDA-related costs. So no, if companies do not develop something it is because it is not financially viable it is certainly not due to the FDA. Moreover, it still does not limit public research institutes. Edit, I accidentally crossposted with Strange, but since I feel that my post is addressing a common talking point, I am going to let it stand, unless there are objections.

Regulation of basal metabolism is fairly complex and from what I have seen also poorly understood. In addition, most nutritional studies do not provide mechanistic insights. Roughly speaking, there are factors that, depending on the study, might indicate changes in metabolic rates, but the relationship remain complex. Changes in body mass, for example can change metabolic rate, as well as calorie restriction. The latter is connected to an effect you might be thinking about, called postprandial thermogenesis which reflects the short-term increase of metabolic rate related with the type of food composition (highest if high in protein, lowest if high on fats). However, the actual net effect is difficult to assess because it is also dependent on the amount as well as the precise type of metabolite ingested, as well as a whole range of characteristics of the subjects (e.g. age, exercise, nutritional status etc.). So while we know that the basal metabolism shifts depending on food composition, the overall net effect on weight is going to be highly dependent on the individual with quite some contradicting results in the lit.

Also, the FDA does not regulate medical research, i.e. they do not have the means to stop someone from publishing data suggesting efficacy of drugs. Likewise, pharmaceuticals cannot do that either. The only means is to actually finance research themselves and also have a agreement with the researcher to not publish the results. Often that does not fly as most researchers want/need to publish. But pharmaceutical companies are free to do their own research and not publish it. But at the same time it does not limit the abilities of university or other researchers to pursue it independently. The strongest means to interfere which we have seen in cases of tobacco, nutritional and climate change research is to finance researchers to create studies that sow doubt about certain links they do not want (e.g. tobacco and cancer, sugar intake and obesity, CO2 and climate change), as well as create PR and lobbying campaigns (see the Koch brothers). So one could create a political climate where certain types of research are more or less difficult (but note that not too long ago the NIH has funded a section dedicated to things like alternative medicine with rather disappointing results). However, if you are talking about actively influencing and suppressing research communities the short answer is: no.

Most universities have researcher profiles though which you can go in order to ask for a position. In addition, most researchers advertise open positions on their personal home pages. That being said, if you are not local, a cold call (or rather email) without a compelling write-up and CV will probably go unanswered. We got tons of requests for graduate student positions and it is difficult to commit someone just based on paperwork (i.e. without having seen them in the lab or without recommendation of someone that you trust).

Well, probably doesn't help that Arizona Beverage Company is in New York. I am pretty sure it is an allegory of sorts for something. But then, maybe not.

So there is actually some interesting data out there trying to look at this issue. One big problem is that body weight is a composite result of many different factors. In addition, high calorie intake can often be associated with a variety of other lifestyle factors that may affect health outcome differently. For example, folks following a low carbon diet have been shown to decrease body weight, but LDL and HDL-cholesterol levels were elevated. In retrospective studies certain folks with high body weight, low exercise and high carbon diet often (but not always consistently) showed higher cholesterol levels. Some studies suggest a stronger association in youths, as obesity there indicates presence of higher levels of risk factors.

That is what I meant with dietary cholesterol vs de novo synthesized cholesterol. As mentioned there is some data suggesting modulation of de novo synthesis, but the connection is unclear. There is more data out there suggesting that lifestyle changes (such as exercise) as well as diet (but, as mentioned, not necessarily related to cholesterol intake) can alter cholesterol levels, but I am unaware of the fact that most of these effects are transient, perhaps you could point me towards the lit? Effects on diet on health are notoriously difficult to establish. That is partially why I said that metabolism cannot be solely dependent on genetics. In addition to the availability of metabolites and its precursors, such as signaling pathways that react to a large number of other external and internal cues play a role (e.g. along the steroid axis you mentioned). Stress, lack of sleep, physical exercise (or lack thereof) etc. can significantly alter metabolism on many levels. As such I consider the previous claim that all is just genetic to be an extraordinary claim.