CharonY

It would be incredibly inefficient and almost impossible to control the dosage. Typically anything larger is provided intravenously. That is why insulin (~5.8 kDa) pills are not available, for example (but there seems to be some work on it).

Well, there is a lot that can go wrong and without looking at the raw data or precisely revising protocols it is tricky to see whether there is something off with the protocol. That being said, Y2H has been shown to create massive amounts of false positives, if conduct large meta- and/or validation studies. However, typically under controlled conditions it is not as bad as what you described.

Well, the displayed biological knowledge is as limited as the mathematical, so at least there is some consistency here.

Typically with immobilized thrombin you will have less or no residual thrombin. In some cases digests seem to be less efficient (though not reproducibly so).

There is also immobilized thrombin that is covalently bound which saves a step over most biotin-thrombin protocols.

Your lecturer is referring to small molecules which are completely different beasts than proteins (most likely organohalogens or similar bioaccumulative compounds). Typically, proteins will be digested heavily by proteases (or bacterial actions) during the passage. Even if they don't, they have to be taken up actively by intestinal cells (where further degradation may occur). That is a rather rare event, but it is quite possible.

If immobilized thrombin or affinity columns are too pricey I guess you are limited to whatever separation method you have at hand (as new columns are not cheap either). Without knowing your target protein it is tricky to say but at least in theory reversed phase or ion exchange prep HPLC should do the trick. Even if inactive I would try to avoid additional contaminants in crystallization experiments as much as possible. Also, I typically check purity of overexpression purificaitions via LCMS as sometimes stuff stick to the column and get co-purified, which can be a problem if the desired proteins is not very highly expressed,

Change in genetics are are what causes inheritable morphological changes. OP specifically mentioned wings. In a number (if not most) of species the evolution is speculative, hence the insistence on immediate positive selection is unfounded. Most known elements, however, point to outgrowths of wings from a variety of structures (such as gills or arms) and not some completely novel, additional structures.

That is not typically how things happen. Mutations are typically neutral or sometimes detrimental, beneficial ones are very rare. For example, mutations in enzymes tend to happen in duplicated genes as they would not be selected against (or, as you put it, add overhead). The cost of duplication is, as a whole often not very high (i.e. only weak or no selection). For example, in organisms with bipedalism, changes in the arm strength is probably not associated with a high cost. Over time changes may accumulate that significantly change its structure from the precursor.

While that is partially true for wings as the intermediates are still functional appendages, it should be noted that changes do not need to be beneficial themselves. As long as they are not heavily selected against, they may persist and even spread throughout a population either by chance (e.g. drift) or by co-selection, for example.

That does not seem to be the case, if we assume that the panels are the weak point:

As others have noted elsewhere, this assessment is incorrect. It has to be recognized first that the war council was in charge of military affairs and the emperor basically had the sway only after the cabinet became evenly split after the second bomb and the Soviet attack. Even before the bombs dropped Japan was looking at terms to surrender, though the efforts started probably only in spring 1945, with the Soviets being instrumental as mediator. What happened then in detail is somewhat shrouded in mystery and obfuscation as there are few detailed records about who advocated what within the cabinet, which opens things up to one-sided interpretation. But even before that it is clear that Japan was far from an unified voice. Tomoshige tried to assassinate the then prime minister Hideki Tojo in order to set up a new cabinet under Prince Higashikuni and immediately sue for peace via Moscow (Summer 1944). Shigenori Togo (Minister of Foreign Affairs 1945) was a proponent of the Potsdam, whereas Korechika Anami (Minister of War) and Yoshijiro Umezo (Chief of Army) were opposed. The specific position of Prime minister Suzuki are more ambivalent. However, (and as usual for historic analyses) it is almost impossible to find an answer to what if scenarios (would they have surrendered without atomic strikes? Would they have surrendered if the Soviets had not attacked? Would they have surrendered if the Allies had promised to leave the Emperor untouched?) . As such any declarations with certainty to such speculations are unfounded.

There is no (Pacey et al. Hum Reprod. 2014) or only weak evidence for that:

It is used in low concentrations and it is readily converted to ethylmercury in the body, which is eliminated fairly quickly. There are efforts to replace thiomersal, especially for infants, though. However, in absence of alternatives the risk is far lower than that of infections and is very safe for adults (occupational Hg exposure in industry can be higher, for example).

ScienceDirect is not a journal, but a platform launced by Elsevier. You have to look at individual journals and their policies/costs. They vary to a very large extent.

I do not think that 10 mins would be enough to describe and list all the steps that you propose. I think you are getting lost in details that do not really help to understand the physiological relevance of the processes. Rather, I suggest that you describe in more rougher terms where the intermediates branch off into the respective pathways. It makes a lot of sense if you specifically check out the branches from TCA (as well as the role of glutamate).

it is a term that is mostly borne in social sciences in the 19th century following the assumption of a linear progression of society as proposed by Tylor, Morgan, Bachofen or Frazer. So technically it probably should be more discussed in the context of social Darwinism (another historic social science entity). Not that many creationists are careful in making these distinctions. With regards to Evolution, to me the Futuyma is a pretty good go-to-read. From there it would be a question of how much depth and which aspects would be of most interest to you.

Basically what Phi said. In the early days i.e. (19th century) evolutionism was used but it also entailed elements that are clearly not true (i.e. assumption of progressive improvement). As such it was ultimately dropped by the developing scientific community. It has been somewhat revived recently, typically by deniers.

The terms can be used in a number of contexts. For example if you are talking exclusively about large scale changes (say, in paleoecological context) it is clear that you are talking about e.g. clades or other larger groups rather than, say small molecular changes within a population. Microevolution is then used to delineate the opposite situation (e.g. talking about allele variation in a single population). I.e. a common use is to delineate changes that above or below the species level or equivalent. Obviously the boundaries are (as the species concept in self) not strictly defined. It is just sometimes a convenient term to establish context. Also, there are sometimes uses that are not typical (especially in blogs but sometimes also in poorly written highschool textbooks). Note that evolutionism is never used in the scientific community.

Considering that he said Russia (instead of Soviet Union) and the topic I was assuming we are talking contemporary concepts of conservatism. As you know, there have been large historic shifts on what could be considered conservative ideals.

I am not so sure about the overall benefits, especially if they are not freely available. That being said there is a distinct disconnect between our knowledge of how harmful certain food is and how we react to them. Probably the biggest killer that we routinely ingest is sugar. It is directly responsible for a vast chunk of health care spending and leads to deadly diseases. At the same time it is very addictive and as such is found almost everywhere to sell products. While there is rising awareness of it, it seems to me that there is much more incentive to speculate of potential risks of adding additional protein(s) into crops than what we are doing to ourselves on a routine basis.It is good and well to be on the outlook of risks, but ignoring well recognized and existing ones in favor of potential ones for which we have found not evidence yet. And heck, I know a bunch of people who would be delighted to find adverse health effects, as these findings could make an academic career. Ecological risks are probably the likeliest source. But seriously, modern (and even ancient) agriculture has already changed the shape of food variety and often mutated without actually knowing how DNA was changed. And we are complacent about it, because it makes food cheaper for us. In many ways, GMOs are just distraction so that we do not have to think about the food issues we already have.

The need to distinguish the various sub-types is also a criticism on the paper you cited. In a commentary Mileshkin et al (R Coll Radiol, 2015) criticized that Morgen et al. used all diagnosed adults as baseline, which includes groups for which chemo is not indicated.

I think in Suzuki's case activism may have overtaken the scientific part (note this is based from some articles I saw that were basically handwaving without evidence). With regard to microRNAs, that part is actually still disputed. There is some evidence that part of the finding could be based on residual contamination which is more common in next generation sequencing than initially believed. As a sidenote, of course there are many aspects we do not understand yet. But there are many other things we produce and expose ourselves to (endocrine disruptors for starters) that are potentially a much higher risk, whereas GMOs mostly consist of stuff that we ingest, anyway. But obviously this sounds much more scary. Compare it with the perceived risk of cell phones, for example. There have been concerns early on that close proximity to cell phones and cell phone towers could lead to health issues. Subsequent studies (similar to GMOs) were negative (though I believe there was at least one that was inconclusive). However there was still some resistance against cellphones and wifi due to that, until it became too convenient to have one. Since then hardly anyone thinks twice of using one while pregnant or carrying it close to one's testicles. I guess if something is just convenient enough we will not ask to much of potential effects, which just shows how screwed up our ability to do proper risk assessment is.

As hypervalent said, you should confine yourself to specific types of cancers. From there, you need to find actual studies (or reviews) in the scientific literature. Also you will have to define success rate a bit. E.g. in terms 5-year survival, remission, etc. Also, one need to define alternative treatments carefully as the latter can be very diverse and may have benefits as supplementary treatment. Likewise, there a lot of variations in in the implementation (e.g. how patients are monitored during treatment, how many intervention strategies are actually available) and their usefulness for different groups in the population (e.g. young vs older persons). If people are biased it is easy to skew results by comparing the worst case scenario from one with the best case in the other. For sake of discussion let us start with Hodgkin lymphoma. Generally, with modern treatment methods, the 5 year survival rate is generally reported to be around 80% (higher for early stages). Before that, treatment typically was limited to surgery and radiation which resulted in a 5y survival of less than 30% (G. T. Pack and D. W. Molander, Cancer Research 1966). The survival dropped sharply beyond stage I. Similar data can be found for most treatable cancer forms and it is clear that the rate have increased with the development of new and improved therapies, far exceeding an increase of 2% over spontaneous remissions or early-generation therapies. Unfortunately, you will find much less data on alternative methods used exclusively for treatment (most likely as untreated. Most uses are complementary to alleviate symptoms. That is a general theme you will find as most form of cancers are serious enough that it will be hard to find a large study group to partake in unproven natural healing or similar treatments. As such there will be a lot more anecdotes than data sets. That being said, the NIH had set up a whole study section devoted to exploring alternative treatments, but I have yet to see a study that claims superiority to traditional treatment options.

Soft tissue is generally anything that is not bone or other highly calcified structure. That being said the question is actually not quite trivial to answer. It depends highly on what you need to see and the amount of fine structure which is present. For example looking at bone marrow tumors MRI is as good or better than CT. Same is generally true for tumors in soft tissue. However, if you want to look at fractures, CT allows you to see them better. Same is true for calcific deposits. Thus, often when fractures or other injuries are suspected CTs may be ordered over MRI. On the other hand, metanalyses showed that MRI was superior for diagnostics of liver lesions (Lee et al. Radiology 2015). Except for the cases where one is clearly superior to the other, the expertise of the readiologist will also play an important role. So both instruments have their respective value and are to a degree complimentary to each other.