CharonY
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None of that would work based on our understanding of basic microbiology. First, genetically engineered organisms are usually not terribly competitive. Also there are many different reservoirs of resistant bacteria and it is virtually impossible to replace them with sensitive strains. Take wastewater, for example, a huge reservoir of resistant bugs. There is no physical means to replace that biota with something artificial, other than sterilizing the everything, put the new strains in. And even then, unless everything is kept perfectly sterile, as long as there is selective pressure, selective bugs will become dominant again. In other surface it amounts to the same issue, there is generally no way to simply stabilize an artificial microbiota. And as hypervalent mentioned, the moment antibiotics in play, the selection favours the rise of antibiotic bacteria again.
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! Moderator Note Just a gentle reminder that the topic are statute of limitations. I suggest to frame the discussion within the framework of a justice or legal system rather than the fulfillment of desires and/or revenge fantasies. If that notion is to be further discussed we may want to split the topic.
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AFAIK psychopathy as a personality disorder is not a proper diagnosis and is more a collection of traits, many of which overlap with other disorders. As such, it is not really suitable for a clinical diagnosis, much less treatment.
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! Moderator Note We do not provide medical advice here. The best you can do is to consult with specialized MDs on the matter.
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I have not listened to the talk (and it would help to post the name of the presenter; Lisa Feldman Barrett), but what you posit is not mutually exclusive. It would only mean that emotional responses are not universal, but dependent on learned contexts. What Barrett proposes differently to other theories is that emotions do not arise from dedicated pathways but constructs emotions on the fly. In other words, it is an interpretation of the brain of your current state. At least I think that was roughly the gist of the theory. It essentially shifts the mechanism from something basic to a higher function. The main challenge here, is (as almost always) that this higher functions still need a mechanism which such a higher level theory does not provide (or at least from my limited understanding). The power, however is that it provides some explanation why some behavioural therapies work in emotional disorders. I.e. if folks understand their bodily feeling associated to, say, anxiety, it allows them to deconstruct the elements and try to disassociate themselves from going deeper into that emotion. I suspect within this theory, medication help not because they target anxiety, but because they change the bodily feeling and lifts one out of the context of it. What other research have shown, however, is that certain disorders might actually have biomarkers that distinguishes affected individuals, which could point to some underlying mechanisms (though as usual in this type of research, variability is very high and it is uncertain how reliable those markers are). As a whole, I think the interpretation that emotion is not real is not an accurate representation of the theory. It is more accurate to say that the proponents suspect a higher function activity connected to emotion. Also I will note that most science is not in the business of proving things, outside of mathematics.
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I will preface this by stating that I do not think we have an entomologist as a member here. So unfortunately you may not get an in-depth answer regarding the methodologies used in that field. However, I can answer in a more general aspect with regard to the use of maths in biology but first: Seeking knowledge never makes you seem like an idiot (in fact, the opposite, i.e. stating assumptions as facts is much more likely to do that). In biology mathematics is generally used as a (often superficial) tool. I.e. often there is not a lot of in-depth knowledge on the maths itself (with specialized exceptions). More commonly folks apply certain mathematical methods for a defined set of applications (such as simple correlation studies, hypothesis testing and so on). That being said, it is not necessarily a good situation as many researchers really boost their research by applying or even developing new models to gain better insights using their data. In the field of entomology I could envision that DNA-based work may become more common for a variety of questions and in that area there are quite a few established mathematical models in use. I will also say that not having expertise in something does not qualify you from gaining the required knowledge. Obviously the goal is to gain enough knowledge to rival a mathematician, but rather getting enough to bolster the biological work. And as a matter of fact, you will gain necessary skills as you start working in a given area. Considering that there is nothing magical to mathematics, there is really no reason why that should limit your ambitions.
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It is not helpful that you conflate biota with pathogens. The fact that certain pathogens may be acquired along the way does not invalidate the fact that your biota is not just a simple accumulation of bacteria, but an ecosystem that is developed within you. Increasing immune responses and inflammation is very, very bad idea, as a) they result in damages to your body and b) can disrupt a healthy biota, which allows certain pathogens to settle more effectively. Folks with certain syndromes that result in bowel inflammation are at higher risk being affected by opportunistic pathogens for example. With regard to infant colonization, while the biota generally establishes post-birth, the important bit is that succesful colonization (e.g. in conjunction with lactation) first with Bifidobacterium followed by transition after weaning is an important aspect of healthy development. In other words, not each exposure suddenly changes the microbiome, it settles depending on a variety endogeneous and exegenous factors (including diet and lifestyle). Early disruptions either in the mother or in the child are linked to alterations in the immunoprofile and have also been associated with certain adverse health effects. For the most part we are constantly beset with rather nasty bacteria. But the fact that you have got an intact biota protects you from that. What you also need to understand is that in order for the adaptive immune system to work you need balance. Overabundance due to health issues, can result in rather severe diseases (such as autoimmune disorders). There is evidence that the interaction of the immune system with the microbiota assist in this balancing act. Note that some pathogens, including food borne ones, actually overstimulate host immune response in order to infect their hosts. One route is to use inflammation to suppress the beneficial biota and thereby allowing the pathogen to outcompete them. The normal flora is only restore once the inflammation subsides. In other words, deliberately disrupting your immune system outside of highly specific cases, is a horrible, horrible idea.
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Well, the lit discusses a variety of pumping mechanisms and possible flaws in the models , but since they are not within my realm of expertise I am not really able to speculate much about that. It does get very technical very quickly and perhaps someone else with more background in geology and/or biogeochemistry could add something here. Just another nitpick, the word is "wandern" . There is also "waten" which translates to "wade" which probably are derived from the same Latin source. I feel that is an important discussion in itself. With your permission I would like to split that off in a new thread and talk about that a bit.
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Well, there will be folks voting for mayonnaise, because it is more relatable. Spoiled or not.
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The basic issue with your premise is that we actually do not accumulate pathogens. Rather there is a certain equilibrium in our biota between harmless, opportunstic harmful and actual pathogens. If you are healthy, the latter are in a controlled level, resulting in no disease. There is literally no way to cleanse yourself of your biota in a healthy way. What you are specifically thinking about are a subset of pathogens and parasites that are persistent but often stay dormant (Toxoplasma gondii is an eukaryotic example, another well known prokaryotic one is Mycobacterium tuberculosis). Treating those requires aggressive measures and typically only works when they are actually active (and are usually pretty harmful to the patients, too). There is simply no way to keep bacteria out, nor is it a good idea (past typical hygiene). Washing raw products before consumption is not a bad idea, but trying to get rid of the normal biota on your skin is. Destroying your normal skin composition allows other bacteria to settle, which can cause to all kind of problems (not sure whether tea oil is potent enough to actually do anything, though). The best defense is a) keeping away from infection sources and b) maintain a healthy biota which helps outcompeting pathogens.
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Fair enough, though it is part of a larger movement to discredit science (i.e. that folks are just doing bandwagon science), which is an ongoing and rather disruptive trend and (IMO) needs at least to be noted when encountered. It also poses the dangers of the "both sides" discussion which as beset science in all kind of subjects, ranging from evolution to vaccination. It simply has no place here. Now then: A key to the Tarim basin seems to be salinity, which increased CO2 uptake by the water with dissolution of soil carbonate and subsequent storage. So at least for that particular system it may be somewhat explainable, though from what I can see (with limited expertise) is that it is a hypothetical at this point.. However, there is a body of literature out there indicating that carbon sink rates are found to be rather high in certain arid and semi-arid regions. So far, there does not seem to be a consensus on possible mechanisms, which include the applicability of certain techniques to desert systems. In other words, it is not entirely clear. Also to nitpick, vadose is not a German word. AFAIK it is derived from the Latin vadosus/a/um (shallow). It is probably also related to the Latin word vadere (wandering).
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While I have not provided any negative reps, I want to clarify that there is no easy route to grant money. No proposal will be funded based on the topic alone. They all require rigorous review. The only "easier" route is if the PI in question has a strong reputation, as their suggestions to perform research will have more weight than a newcomer. I.e. regardless of the topic, the methodology has to be sound. You cannot just put cancer or global warming on your grant and expect money rolling in. Moreover, the actual research once conducted will also undergo review, a system that is entirely independent of funding mechanisms. To suggest that there is an easy way to get funded and publish in a mainstream journal is laughable. Well, there are actually examples of something like that happening, but they were cases connected Koch industries who bankrolled researches to find evidence against global warming.
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There is quite a bit work out there focusing on stable isotope work, but not specifically regarding carbon sinking (though one might find some with some digging). A good way to check whether there are updates on a given topic is to look at papers which have cited a study in question. Much of the papers are discussing the role of deserts and semi-arid regions for carbon sinking rather than the Tarim Basin specifically (e.g. Schlesinger Global Change Biology 2016). And this sounds like someone making assumptions without putting any thoughts into it. They obviously described their methodology in their paper.
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It is true that it is important assess the net cost of production and distribution. For example a study (Weber and Mathews, Environ. Sci. Technol. 2008, 42, 3508–3513) has shown that on average transportation only accounts for 11% of the total carbon footprint. I.e. the vast majority of emission happens during production itself. From that, it appears the type of food is more important than distribution and storage.
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That's a good point. The total cost (production, emission, persistence in the environment, degradation time etc.) should be considered. I assume that it is going to be somewhat complicated, though. I am thinking that some bioplastics can be very well degraded if they are collected and composted properly. But that would require an infrastructure with its own cost, too.
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That is a bit tricky, though. There is no industry standard as to what is really considered compostable, and accordingly there are biopolymers who theoretically degrade, but only under optimal conditions. In landfill or other unfavourable conditions they may persist for almost as long as regular plastics. 3D printers often use PLA. While it is obtained from renewable resources, it degrades slowly under unfavourable conditions. If properly composted (i.e. right mix of bacteria and high temp) it works fine. But again, in landfill or ocean it will persist quite a while.
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Here is a good analysis of what has happened. Essentially she made inroads with a lot of groups she had problems before (conservatives/non-college educated/African Americans).
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At this point I suspect that Trump thinks that he is still in a reality TV-show and he is building up to a season finale. Probably with the hope that there will be sequel, otherwise he is only in for the ratings (and personal enrichment).
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Yes, often replication studies, or studies building up on the study in question could verify or invalidate the prior study. Alternatively, a statistician might spot issues in the data analysis that reviewers may have missed. There is none as such as data analysis is always dependent on the type of data. What is possible is to conduct meta-analysis (i.e. incorporating data from other studies) and look at the stability of the outcome. You mean running different statistical tests on the same data set to find one that indicates statistical significance ? This is often called data dredging , and while it is not outright fraud, it indicates poor understanding statistical analyses and also the data set. Essentially one runs afoul of multiple hypothesis testing issues.
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Do you mean "quantum"? Yes there is a field in biology, generally in the field of molecular biology . Prominent examples include photoactivation of biomolecules, or modelling of electron transfers as a series of tunneling processes as well as DNA dynamics.
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Yes, but that would mean laws are being reformed because they have a race-based effect and as such are not a race-blind measure. That is actually also potentially difficult as there are studies out there indicating that black felons are getting higher sentences for the same crimes as their white counterparts. I think the impact of minimum sentencing laws are less because of the law itself, but because of its connection with a) the difference in sentencing due to the type of drug, which as noted has a skewed race effect, and b) the higher likelihood to convict black addicts and dealers compared to white counterparts. In other words, an effective reform package would have to take a closer look into which laws are unevenly or unfairly applied and remedy those. While one might argue that it is kind race blind in the end, it would require a race-conscious approach to spot those issues in the first place.
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In the 2014 paper it appears that they claim an increase in the ventilatory response whereas respiratory rate change was not significant. I am no animal physiologist, so I am wondering what are the expected values? I would have assumed that there is a significant change in the respiratory rate so I am wondering what the actual consequences of ventilatory responses alone would be. From a quick look I also failed to detect the baseline values of genta-treated mice so I wonder whether there was a baseline shift.
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I'd have to read the papers a bit more carefully, but after an initial screen it seems to me that the response is not driven primarily by CO2 sensing, but rather that hypoxia-hypercarbia somehow results in depolarization which then triggers movement. What they primarily show is that injuries prevent these responses. To reconciliate these findings with existing lit on the dive reflex I would be wondering (because this is not my area of expertise) what the usual measures are used to assess the reflex vs the measures the authors used in their study. I.e. how does the arousal response that was tested by Allen et al. to the dive reflex? It may very well be that different aspects are tested and hence, the numbers do not add up to a whole.