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On average fees are lower in Canada than in the US, but it is not exclusively due to how the system is financed. There are other differences that may not be universal, such as that in Canada there are often no tuition waivers for graduate students in natural sciences, whereas it is fairly common in the US. However, both are partially subsidized and both are massively higher than in countries where the costs are entirely or mostly met with public funds.

As others have mentioned, wealth and privilege are fundamentally different measures. Privilege is a relative assessment, if there is not disparity, there is no privilege. Wealth, on the other hand is an absolute measure. The education system in Canada and US seems to be more similar to me than you realize (coming from a third system). Public universities are also subsidized in the US and most of the tuition is actually carried by the states/provinces. You can find truly subsidized systems in e.g. Germany where you basically attend university for maybe 100-300 Euros, which typically also includes a public transit ticket. And here the question would be what the tie-breaker should be? Typically being a legacy student had the highest benefit, but also simply living in a good school district (as those boost your scores). Likewise being well-off or simply being in an area where you have access to extra-curricular activities increase your chances. What admission officers do is actually looking into personal backgrounds and folks with high scores but coming from traditionally underprivileged schools get a leg up. That to me sounds like evening the playing field as you mentioned before. What they do not do as some folks think is to bluntly boost folks based on race or ethnicity. Another common twist is to claim that folks actually discriminate against whites or Asians (using them as the well-known model immigrant argument). However, the actually implementation of these measures is that race-based limitations are lessened- to a degree. Universities are actually not allowed to specifically address structural racism (and again, if there are confusion about what that means I am happy to discuss this in another thread). In the US at least there is a ruling that universities are allowed to use a broad range of factors (but never race per se) in order to fulfil certain goals, such as increase diversity on campus, which has many benefits (and having led research groups and taught students in low- as well as high diversity system has made me a believer). As iNow has mentioned, the way we measure is inherently flawed and measures such as affirmative actions are imperfect measure to address at least some issues, but they have been grossly mischaracterized. It often neglects the structural issues we have by asserting that the way we rank our students without use of affirmative action is objective or (even worse) "normal" but it ignores the history of it and how folks with influence constructed our education system and the way we evaluate academic potential. It is interesting, for example that legacy and athletics (which both happen to be major reason for white student admissions) are not terribly controversial, whereas ethnic background as part of individual histories is. As a real example that I heard, two persons with similar scores, but one coming from a well-off family, with an alumnus parent. Another, resettled as a refugee child, struggling with the English during middle school but working their arse off to graduate top of their class. Sure you can abstract the whole story to a degree where you eliminate things like race or their country of origin. But to me that actually sounds more like the type of sanitary political correctness that some folks like to complain about so much. That is actually not true. Asian Americans were less beneficiaries of affirmative action, but rather they profited by having certain barriers removed that were in place. Of note, the majority of Asian Americans still support affirmative actions for underrepresented minorities, but they are not part of that group (as a whole). This is a whole different can of worms, as often Asians are viewed as a monolithic group but actually exhibit massive disparities within (the largest among all ethnic groups, IIRC). But as the group as a whole is comparatively small they are often leveraged for these types of discussions, whether they like it or not. In fact recent legal challenges against affirmative action have been using Asian Americans as an example why it is unfair (though again, it appears that Asian community is not quite on board with that). It is also a bit interesting to me that the whole admission process is viewed as if anything other than white is a result of affirmative action. It is kind of based on the assumption that white is the accepted norm and anything else is kind of an ancillary process. But this, again, is yet another can, but closely related to the structural issues mentioned before.

Yes, chromosomes are much more dynamic than initially assumed. Perhaps you are thinking exclusive about the condensed chromosomes (the typical "X" structure you see in karyotyping). However, it is actually the uncondensed chrosomes (which are more diffuse and less striking in microscopic images) when they are active (i.e. being transcribed) and how the chromosome organizes itself is dependent on many proteins (including but not exclusively by histones) controls which parts are accessible, for example.

I am not sure what you mean in terms of structural modification. Do you mean chromosomal structure and dynamics? That part is a whole research direction, but the challenge there of course is that it is not amenable to many analytical techniques. The reason being that if you isolate the chromosome to actually look at it, you are disrupting its native configuration. And observing the dynamics as well as its consequences in vivo is extremely challenging to say the least. However, there are studies on it, mostly by using clever experiments to disrupt or change chromsomal tertiary structure (e.g. by deleting or modifying proteins involved in it) but obviously that is not something that could be solved by sequencing. Likewise looking DNA methylation pattern is possible, but again, it is not done by simple sequencing, and looking their impact on gene expression requires yet another technique (say, transcriptomic measurements). Even then the translation into cell physiological impact is difficult and you also have to consider that an adult organism has many, many different cell types each with different methylation patterns and each with different consequences. There is a considerable amount of data out there looking into many aspects ranging from developmental biology stress responses. An open question such as this cannot be easily answered as there are so many sub-specializations. To given an idea you could start looking in one older study who has basically started to make maps of cells during differentiation (Meissner et al., Nature 2008 454, 766-770), provided you can access via a library. If not you could look up open databases that have stored methylation patterns. While it is not my area of specialization it is my understanding that folks have gone away a bit to just do the mapping because ultimately it did not lead to massive insights. The work now tends to more targeted in order to figure out functional consequences, which takes way more time.

I think mostly because it is really vague and unclear in which direction you are going with this. One possible way to interpret is that there are differential epigenetic changes (such as DNA modifications) that happen at different rates and in different patterns depending on the cell line. And there are also different chromosomal re-arrangements (structurally and otherwise) depending on cell line, differentiation and so on. There is of course also the interaction of the nucleus with different signaling molecules affecting gene expression and so on. Or you might refer to the specific mechanisms when the haploid genomes fuse in the zygote, which is more of a developmental question. I should also add that we are a small community and if you have highly specific and/or niche questions, there is a good chances that we do not have anyone with that specific expertise able to answer questions off the top of their head.

Yeah, it is odd that they accidentally injected some with half the planned dose, which is a weird thing to happen in a trial.

Yes and no. For the most part no or at least it is not as easy. Generally speaking your blood proteome correlates with your current condition, but it is fairly dynamic. I.e. it changes during the day, depends on how much you eat or drink, whether you are stressed or not and so on. There are certain proteins that start increasing if there are damages, but they are not always specific (e.g. certain inflammation markers) and those that are more specific tend to be markers that are associated with serious injury (with e.g. cause the leakage of those proteins into the bloodstream). And even then it is often necessary to combine several protein biomarkers and/or other biomarkers (e.g. creatinine levels and other indicators) in order to make a proper diagnosis. Disease that are much less well defined, such as many of those you have listed generally only display generic markers such increased inflammation. The reason for that is pretty clear. Injury and inflammation, regardless of origin, tend to affect similar pathways and it is unclear where there is a simple yes/no response. More likely we see quantitative differences. However, they could depend a lot on the individual (i.e. individual may have different healthy baselines) making them not trivial to use clinically. There are efforts to identify and build biomarker panels (i.e. groups of proteins) that together might diagnose issues typically using proteomic techniques, but success rates have been low with some successes. Also, there are non-protein biomarker candidates, such as DNA modifications in the case of colon cancer. Finally, once there is a candidate in actual clinical use typically protein levels are measured via ELISA, as those are the most robust to handle. For discovery, mass spectrometry is typically used.

It is often difficult to predict how the immune system reacts and how (and whether) it generates long-lasting immunity. In this particular case I cannot tell you what happened, but it is common that the reaction of the immune system have weird, non-linear relationship. Which is why statements like "strengthening the immune system" are tricky as it consists of feed back loops on many levels involving many different cell types. There are cases where initial strong responses are not building up memory, for example, which might be the case here. However, it must also be noted that it could be an issue of small numbers, as the half-dosage group effectively splits the total cohort. So it could also be a statistical fluke at that point. I should also add that there is not just one immune response, the immune system fundamentally has different elements, and typically when we talk about vaccinations we look at the adaptive response. However, the innate immunity also plays a role and interacts with adaptive responses. And even more complicated, in vertebrates now also something similar to innate memory has been discovered (often called trained immunity).

It is a brilliant way to dismantle this type of oversight. Use media to make folks ignore those accounts (now easier than ever) and then do whatever you want. Time-tested technique of autocrats.

The AstraZeneca vaccine seems to be working, too. They had 131 infections. However, they tested two dose regimens, with one (halved first dose and standard second dose) seemingly being more effective (90% vs 62%).

At this point it is pure fantasy. You might as well imagine some random sci-fi method and give it a cool name.

No we cannot do that, either. We take it from another cell.

Are you thinking that we have some means to detect genetic relationship? Generally speaking- no. There a few indicators of attractions that imply that folks tend to search genetic diverse partners based on smell (which seems to correlate with genetic differences- most likely major histocompatibility complex). But as everything in biology, it is not a firm mechanism. Obviously it depends a lot on with whom you grow up with. If you are used to certain folks (and presumably their smell) you associate them with family. This is what we also observe to various degrees in a range of animals. We use familiarity cues to build relationships rather than by solely by detecting genetic divergence. As a whole I am confused why cartoons are used to ask these types of questions, it seems a bit circumspect whereas it would be much easier to discuss whether and how precise humans are able to detect genetic relatives, for example.

The issue is when some archers are allowed to move and others are not.

! Moderator Note You have been asked not to post this mysticism in the mainstream science section.

That is what I am going for. The issue is not whether it has proteolytic activities, it is more whether and when it would actual have an health benefit. I have not seen any reports that suggest it being used in folks with digestive issues and from there it is difficult to assume that it would have benefits in folks that do not have digestive issues. And if it is now known to have benefits, it is unlikely that there is an optimal ratio to be found.

I was more wondering whether you have got any sources indicating whether bromelain has digestive benefits without other indications? It is difficult to figure out a quantity if it we cannot establish under which condition it would be beneficial in the first place. Conversely, are there studies indicating benefits to treat digestive disorders?

Why do you think one needs to take it?

I have not watched the video, but Ct values do not differ between countries. They are the result of the qPCR. What you might mean is where the cut-off for a negative test is. I suspect there may be different recommendations but most use a cut-off around 35. There is not a huge variation and since typically the runs are further validated there is little reason to assume that difference between countries are due to different testing. In fact, there is good evidence that there is a much stronger correlation with measures taken (or not). There are some folks who want to use it more diagnostically. E.g. using Ct values (which correspond to different concentration of isolated viral RNA) to determine viral load. However, that is not trivial as each step starting from sample collection introduces significant variation. Moreover, you would need to use internal standards to make sure that the values can be compared. That takes time as leaves room for error, which is why it is not often done. Specifically, China had one of the most stringent responses, including isolating every positive case. While one might question the precise numbers, there are no indication for major outbreaks and in some cases they started testing the whole city when outbreaks were detected. These measures are known to massively reduce infections. The US we know that they have a scattered response and the President actively encourage folks in engaging in dangerous activities. And so the number rise, as expected. India has actually a lot of infections and deaths (second only to the US). But they have a massive population and relative to the population they have tested much less than the US. I am not familiar enough with the responses in India to comment on their policy. But the numbers and trend definitely do not look great. I think there was a heavily criticized lockdown which has slowed cases a bit, but again, I would need to do more reading on India.

RuBisCO is used in C4 plants. The trick is that it is a two-step process where a C4 body from Pep carboxylase is moved to deeper tissue where RuBisCO is better protected from oxygen. There, the C4 body is decarboxylated to release CO2 which is then used by RuBisCo.

You can enucleate a eukaryotic cell and put a new nucleus in. We cannot build cells.

I doubt it. It is more that before the trials mRNA vaccine candidates so far had low immunogenicity and it the approach was considered to have a low success rate. The technology was around for some time, but it was not considered to be that competitive to traditional approaches. That is also why the drugs were developed by somewhat smaller companies, which have been working on drugs since 2005/2013, respectively, rather than being adopted by the big pharmas. Especially in the middle of an outbreak you would want a vaccine that creates strong immediate responses rather than multiple dosages, which is likely another incentive to go the traditional route. Considering that up until now no mRNA vaccines had been approved it is a high-risk scenario where the vaccine might have failed for a number of reasons. On top, there is still the issue that we won't have any long-term data on mRNA vaccines. It is really because out of despair and necessity where mRNA vaccines have been propelled to prominence. And in the end, it is crucial to have a range of methods available as we won't have the time to gather sufficient data. Despite promising phase 3 results, we have no guarantee that it will play out the same way in the broader population.

It is actually still in a trial with around 60k people. I do not think that they have released results yet. One interesting bit about this one is that it is developed using traditional approaches and looking at the paper it also seems to have a faster immune response.

They still need to go phase III, though.

Lime and garlic salt works really well, if you have something to bind it together. Like in a sauce, rather than just seasoning. Often the tomato delivers enough acidity though a sprinkle of light vinegar or citrus can brighten it up. Or you can make it denser with aceto balsamico.