The biology behind tree pruning and hedge trimming I read two contradictory arguments which both seem logical to me, related to the tree pruning and hedge trimming:

You should prune/cut trees only outside the growing season, when the tree is "sleeping". In some countries there is even a law forbidding to cut/prune trees within the growing season!
You should trim the hedges only within the growing seasons, when the tree is not sleeping and thus able to heal the cuts.

Which of these two arguments is true and how are they supported by the plant biology?

The difference has to do with the concept of "thinning and heading" and how plants respond to abiotic damage. Thinning refers to the removal of a branch or shoot all the way back to the node which it originated from. This is the primary type of pruning used on trees - either to limit growth or to increase the amount of light permeating to lower branches. Late winter is generally the best time to do this, just before the tree breaks dormancy, since plant pathogens are generally less abundant. By pruning in late winter, this also reduces the amount of time that the wound is exposed before the tree begins active growth.

In contrast, "heading" refers to the partial removal of a branch, usually 1/2 to 1/3 back to the node.  The purpose of heading is to stimulate shoot growth on the remaining branch - hedges being a primary example. Because new shoots and leaves are desired, heading is usually performed at the height of stem growth (in most climates late spring to early summer).

The biologic processes behind this are complex (botanists are just beginning to understand how plant behavior adapts to predation) but in very general terms, plants respond to damage in two ways: by compartmentalizing the wound; and by stimulating growth on the remaining tissue. Many types of woody plants produce latent (or adventitious) buds, which lie dormant within the cambium tissue. Normally these buds are suppressed by auxin hormones produced in the meristem by active shoots. When the meristem is removed (such as through heading the branch), these buds rapidly develop to produce new shoots and leaves. Most species used for hedges are selected because of this ability.

So long story short: thinning is best performed in late winter, when the plant will quickly be able to seal off the damage while limiting the production of unwanted water sprouts and suckers. In contrast, heading is usually done in early summer, when the hedge can vigorously produce new growth and fill out any gaps.

Some resources:

http://extension.wsu.edu/maritimefruit/Pages/PruningBasics.aspx

http://puyallup.wsu.edu/~linda%20chalker-scott/horticultural%20myths_files/Myths/Wound%20sealer.pdf


Can the body always find the right antibodies? If the body produces random antibodies in order to fight a virus, is there a small chance that the specific antibody needed to fight the virus just won't be randomly generated? Even though it is a common virus that normally doesn't kill people?

For example if you have a common cold, is there a small chance that you could die from this just by probability? Whereas someone else won't because they randomly produced the right antibody?

Yes and no. Yes, it's possible that some individuals won't be able to (or happen to) make antibodies to a specific part of a pathogen. But most pathogens are large and complex enough that they have many different targets for antibodies, and it becomes increasingly unlikely that someone won't be able to target any part of the pathogen.

An example is given in Influence of Immune Priming and Egg Adaptation in the Vaccine on Antibody Responses to Circulating A(H1N1)pdm09 Viruses After Influenza Vaccination in Adults. A subset of adults (who were exposed to a particular influenza virus as children) have poor antibody responses to a vaccine to a different strain of influenza virus:

  Significantly reduced antibody reactivity to circulating viruses bearing K163Q was observed only in the USSR/77-primed cohort, whereas significantly lower reactivity caused by egg-adapted Q223R change was detected across all 3 cohorts.

(This is not an argument against vaccination, I feel obliged to point out, because the vaccinated people were still better off than unvaccinated, just not as well protected as they could be.)


Why do antibiotics have a special importance when taking lactulose? “Before taking lactulose, tell your doctor and pharmacist what prescription and nonprescription medications you are taking, especially antacids, antibiotics including neomycin (Mycifradin), and other laxatives.” (Quote from here)

Why do antibiotics have a special importance when taking lactulose?
Why is neomycin (Mycifradin) mentioned separately?

From the Wikipedia article (I'm sure there's a scholarly reference, but I think this is well-known):

  Lactulose works by relieving constipation through a number of different methods. Lactulose is made up of sugar molecules and is partly broken down by the bacteria that live in the lower part of the gut.

So, certain antibiotics affect (and reduce) the intestinal flora (and neomycin especially so, which is I believe the reason why it is mainly used in ointments), leaving the lactulose undigested and not as effective in forcing the body to retain water in the colon, which is the mechanism through which the drug acts.


Identification of UK insect We found this in our UK garden! Any ideas? Not sure if it had/has wings.

It has a segmented tail and 6 legs. It’s about 2 inches/ 8cm long.

That looks like the cast off outer layer of a dragon fly nymph§:

The following resources may be helpful to get a more precise identification:
https://www.fba.org.uk/sites/default/files/EA_specid/ea_specid_mod_8.pdf
https://british-dragonflies.org.uk/odonata/species-and-identification/

§Note: As pointed out by Arthur J. Frost this is actually the exoskeleton left behind when a dragonfly nymph molted and became an adult.


Polymorphism in number of chromosomes? The answer to this question, saying that Down Syndrome - a trisomy of human chromosome 21 - is caused by de novo mutation (rather than resulting from standing variation) made me think about polymorphisms in the number of autosomes (not so much for sex chromosomes because of dosage compensation). The reason for this question is that I would never have thought that an aneuploidy, in theory, could be a segregating trait because of meiotic barriers.

I found evidence of ploidy polymorphisms in plants (especially their hybrids) that occurs when plants with different karyotypes hybridise [see, for example, Vandenhout et al. (1995) and Husband (2014)]. Additionally, I also found that this also applies to some aquatic vertebrates, however, 'fish' are also known for karyotype diversity (see Zhou et al. (2007) and Zhao et al. (2016)).

In rather sharp contrast to that, mammals are (almost) strictly diploid and most mammal species are characterised by fixed chromosome numbers, even though exceptions exist, i.e in mice and other rodents that exhibit intraspecific variation in diploid numbers - these are created by Robertsonian translovations [Graphodatsky et al. (2011)].

However, all of these are diploid and variation always needs to be expressed as a chromosome number of the form $2n$ because of meiosis. The karyotype of a human with trisomie 21 cannot be expressed in that form as this person has $2n +1$ chromosomes. All cases of aneuploidiy in autosomes I am aware of cause disease. My (related) questions now are:

(1) Are there described cases of non-deleterious aneuploidies in autosomes?

Those cannot be segregating in the populations as aneuploidies are not inherited to children, so more importantly:

(2) Are there indirectly segregating aneuploidies in autosomes (i.e. some sort of heritable trisomy that e.g. result from a trisomy followed by chromosomal rearrangement)?

If so, do any of these also exist in mammals, particularly in humans?

Good questions, but you make a claim that isn't necessarily true:

  However, all of these are diploid and variation always needs to be expressed
  as a chromosome number of the form $2n$ because of meiosis. The karyotype of a
  human with trisomy 21 cannot be expressed in that form as this person has
  $2n+1$ chromosomes.

The emphasized text isn't necessarily true - there are certainly more involved ways to describe the karyotype of a given individual or cell line. For instance, take the GM12878 cell line, likely the most well-defined cell line in terms of genetics, epigenetics, and chromatin biology today. It's karyotype is listed as:

  46,XX[23].arr[hg19] 9p13.1(38,787,480-40,911,212)x3

This is a fairly common way of representing changes known as copy number variation, wherein only a small region of a given chromosome is duplicated or deleted. For this cell line, which relatively closely mimics lymphoblastic B cells, the genome is nearly normal (46 chromosomes, XX) with only a small amplification on chromosome 9 (9p13.1(38,787,480-40,911,212)x3). This is a mild example, but smaller copy number variations like this are quite common and can amplify or delete both large chunks or very focal regions of genomes.

But to answer your first question, no, there are no known non-deleterious trisomies in autosomes. Trisomy 13 (Patau's syndrome) and trisomy 18 (Edward's syndrome) children can live to birth, but die within the first few months of life. Unsurprisingly, these chromosomes are also the smallest chromosomes with respect to the number of transcripts that they encode 1. This suggests that the additional amount of genetic material determines the severity of the defects, and this trend also holds true in mice. From a figure caption of the cited paper (which is likely behind a paywall for those without institutional access):

  A correlation between degree of aneuploidy and organismal fitness in humans and >mice. (A) The number of known human transcripts/chromosome in humans. Trisomies >below the line develop to birth. Trisomies above the line are embryonic lethal. Only those chromosomes containing the least amount of transcripts survive birth. (B) In mice, survival of the embryo is inversely correlated with the size of the chromosome that is present in three copies. Linear regression analysis fits the data with an R2 of 0.71.

I was unable to find any examples for your second question. Cancer cells can get very messed up in terms of copy number, but I've never seen anything about heritable aneuploidy.


How many of the four meiotic daughter chromosomes of a homologous pair can be recombinant via crossover? In graphics I've seen, crossing over occurs between the "inner" two chromatids in a side-by-side arrangement of two duplicated chromosomes:

This suggests that only two of the four meiotic daughter chromosomes of a homologous pair can be recombinant via crossingover. Is this true? Or can you have more complex patterns, like the one below, in which all four daughters are recombinant? Does the X-shaped geometry of the doubled chromosomes play a role in models of crossover phenomena?

ps. Sorry if my terminology is strange. I'm a beginner! Experts: Edits to improve clarity welcome!

There can be and often is more than one crossover per chromosome in meiosis, but how many crossovers occur can depend on the species, sex, age, environment, and which particular chromosome is involved1,2,3. For example, humans typically show 2-3 crossovers per chromosome, but females often show higher recombination rates than males.

However, the structure you drew seems unlikely due to a phenomenon known as crossover interference, which suppresses the occurrence of closely spaced crossovers4,5. See also this historical introduction from Nature.

In Drosophila melanogaster, males do not make any crossovers6. In contrast, females show an average of around 1.2 crossovers per chromosome7. This means that most tetrads have just one crossover, but some will have more and this second crossover can occur between any pair of chromatids. Thus, there can be from two to four  recombinant chromosomes, but most commonly there will be two.

(Note that this last reference (7) is a 2018 review article on this subject and could be a good place for you to start learning more once you've mastered the basics of this subject — figure 1 in particular seems directly relevant to your question.)

References:

Alberts B, Johnson A, Lewis J, et al. Molecular Biology of the Cell. 4th edition. New York: Garland Science; 2002. Meiosis. Available from: https://www.ncbi.nlm.nih.gov/books/NBK26840/
Fledel-Alon, A., Wilson, D. J., Broman, K., Wen, X., Ober, C., Coop, G., & Przeworski, M. (2009). Broad-scale recombination patterns underlying proper disjunction in humans. PLoS genetics, 5(9).
Wang, Z., Shen, B., Jiang, J., Li, J., & Ma, L. (2016). Effect of sex, age and genetics on crossover interference in cattle. Scientific reports, 6, 37698.
Berchowitz, L. E., & Copenhaver, G. P. (2010). Genetic interference: don't stand so close to me. Current genomics, 11(2), 91-102.
Otto, S. P., & Payseur, B. A. (2019). Crossover Interference: Shedding Light on the Evolution of Recombination. Annual review of genetics, 53, 19-44.
John, A., Vinayan, K., & Varghese, J. (2016). Achiasmy: male fruit flies are not ready to mix. Frontiers in cell and developmental biology, 4, 75.
Hughes, S. E., Miller, D. E., Miller, A. L., & Hawley, R. S. (2018). Female meiosis: synapsis, recombination, and segregation in Drosophila melanogaster. Genetics, 208(3), 875-908.


What is this pollinator's name? What is the name of this bee pollinating a lemon tree?
Area: south-central Europe

I'm not an entomologist, but it seems to me that this bee is a Xylocopa, or a carpenter Bee:

Xylocopa iris

If this is, in fact, a Xylocopa, narrowing it down to the species level will be very difficult, since the Genus has more than 500 species. You could start with one of the most common carpenter bees in Europe, Xylocopa violacea:

Xylocopa violacea

However, I believe that this may be in fact Xylocopa violacea because of the antennae: you can see a little orange stripe next to the tip of the antenna in the bee of your photo, just like in the bee of the photo above.


Are there dextral/sinistral higher animals? For example, almost every dog I've met in my life (more than 20 subjects) uses their right paw touching one while asking for attention. Can it be used as a criterion for calling them dextral? If not, what?

However, I realize that even those dogs who live in the street might get influenced by dextral people:

  There is no domestic animal which has so radically altered its whole
  way of living, indeed its whole sphere of interests, that has become
  domestic in so true a sense as the dog (Konrad Lorenz)

Is there any research about it?

Handedness has been studied in several different species of toads. As basal tetrapods, the authors argue that these taxa are unlikely to be influenced by human hand dominance and are thus a better model for studying the evolution of handedness.

Bisazza et al. (1997) studied "pawedness" in Bufo bufo, B. viridis, and B. marinus in wild-caught animals by determining which forelimb was used to remove a piece of paper from the animals' snout or a balloon placed over its head.

The results were mixed. B. bufo preferred the right forelimb in both tests, but B. viridis and B. marinus did not. B. marinus did preferentially turn its head left in another experiment, using the right forelimb for support.

A subsequent study by Malashichev and Nikitina (2002) showed that Bombina viridis is "lefthanded," while Bombina bombina is "ambidextrous."

So based on these studies, lateralization appears to have a long evolutionary history.


Which of this 2 affirmations is more close to the explanation of evolution? I am almost secure that this affirmation aren't exactly true but I want to know which of these statements is more near to a description of how evolution works:

The evolution has an exactly target and always progress to it, each generation the childs are more close to make complete a certain task, that is beacuse evolution is like "directional".
For example: The task is be 10cm taller. Each generation the race become 1mm taller up to complete the task.
The evoultion is random but the specie (or natual selection) try to reach a target, each generation has random traits but only benefical traits tends to "survive" and get offpring.
For example: In order to survive the task is be 10cm taller. Some childs are half cm taller and other childs are half cm smaller, the last ones die naturally and only the taller ones survive enough to get offspring.

The second is marginally better because it mentions randomness and emphasizes differential survivorship, but the parts about "trying to reach a target" and specifying a particular "task" are misleading at best. I would rewrite the statement as follows (I have edited for grammar, spelling and style as well, but emphasize more substantive deviations with strikeout for omitted parts and boldface for added parts). The substantive edits change the meaning of the statement significantly: most evolutionary biologists would be very uncomfortable with the second statement as written above (setting aside any grammatical issues).

  Evolution is has a random component but the species (or natural selection) tries to reach a target, may result in directional change: each generation has some random variation in traits but only individuals with beneficial traits tends to  are more likely to survive and produce offspring. For example, In order to survive the task is be 10cm taller. taller individuals survive better than smaller ones.  Some offspring are a half cm taller and other children are a half cm smaller; the latter die naturally and only the taller ones survive long enough to produce offspring.

I would probably say "offspring" rather than "children" in a technical context.

Note also that this emphasizes evolution by natural selection; broadly speaking, there are many non-adaptive processes (vicariance, drift ...) that also lead to evolution (change in gene frequencies between generations).


Why do chickens continuously lay unfertilized eggs? As per subject: why do chickens continuously lay eggs even if they are not fertilized?

Is this sort of behaviour found in other species of birds (or other egg-laying animals), or only in chickens? Is it natural, or domestic chickens have been specifically bred for it?

If it's natural, what kind of sense does it make to divert energies and nutrients to continuous lay unfertilized eggs which have no purpose other than being possibly eaten by someone else? How could such a wasteful reproductive behaviour have evolved? Even if it has been specifically selected for in breeding, it still seems to make very little sense in the first place.

Chickens are domesticated Red Jungle Fowl. In the wild, Red Jungle Fowl live in flocks with one rooster for every few hens (where "few" is probably less than five in the wild, though in zoos flocks may be larger and have a higher rooster:hen ratio).  Since one rooster can fertilize many hens, in the wild virtually all eggs will be fertilized.  Since jungle fowl, of course, lay far fewer eggs than domestic chickens, the cost of the extremely rare unfertilized egg will be low.

In principle, there could be a molecular mechanism that checked for evidence of fertilization before allowing an egg to be laid, but of course such a mechanism would have its own costs, and would almost never actually be useful.


Did my wildlife camera take pictures of coyotes? A wildlife camera took these photographs of these animals. These are the only pictures my camera collected of them. This picture was taken in the central interior of British Columbia, Canada. The distance from the camera to the subject is a few meters, and the height of the camera off the ground was probably about 50 cm.

I think they're too small to be wolves, and they don't appear to be any of the dogs I've seen in the area. My intuition strongly points to them being coyotes based on pictures, videos, and occassionally seeing them in the light of day. However, I'm hoping that someone can explain why my intuition is right, if it is right.

The small coniferous tree beside the road (left of center) is about 50 cm tall.

Short Answer

Yes, these are likely coyotes.

 Long Answer

Your options of dog-like carnivores (i.e., Canidae) in BC include the following:

Coyote (Canis latrans)
Grey wolf

British Columbia Wolf (C. lupus columbianus)1,2
Northwestern wolf (C. lupus occidentalis)1,2

Domestic dog (C. lupus familiaris)

Siberian husky
Utonagan
Tamaskan
Alaskan malamute
Northern Inuit dog
Saarloos wolfdog
Shikoku
others...

Red fox (Vulpes vulpes)

Let's start ruling out the unlikely options:

[I'm not trying to be comprehensive, but rather just pointing out the easiest evidence we can see]

Dogs: Many of these might look wolf or coyote like, but it is very unlikely that any of these domestic breeds would be forming wild packs (as is indicated by your image containing multiple specimens). (In fact, it's unlikely you'll even see half of those breeds in BC to begin with!). I'll leave it to you to peruse the links I provided if you insist on examining and comparing their anatomies/morphologies to your specimens.
Fox: Although the largest of the true foxes, this is still a relatively small canine; they typically are less than 20 inches high and 35 inches long [source]. Without some measure of scale, we can't be sure, but your specimens certainly look larger than that relative to the tree in the background. More definitely, however, is that V. vulpes has a tail that is typically half or more of its own body length. The tail also rests nearly to the ground. The length of tail on your specimens do not match either of these length characteristics. Further, the very bushy, white-tipped tail of the fox is not represented by your specimens' only-somewhat bushy, dark-tipped tails. Red fox are also typically solitary hunters (source; unlike your shot of multiple specimens).

I know what you're thinking: "duh, get to the wolves vs coyotes already!!"

See here for a guide to differentiating wolves, coyotes, and dogs

British Columbia Wolf (C. lupus columbianus): According to Goldman (1941)3 and here, this subspecies of wolf is large with a dark (black with some cinnamon brown color) coat. No mention of a light ventral region is mentioned, which is apparent even in your night-camera shots!
Northwestern wolf (C. lupus occidentalis):

Their color does not rule them out -- This wolf subspecies is quite variable in color and can range from all dark, to mottled grey to all white. (see here for visual comparison of some wolf colorations).
This is potentially the largest of wolf subspecies (27-36+ inches tall at shoulder [source] and 4.5 - 7 feet long (nose to tail tip)! [source:i, ii). Your specimen's do not look this large, but they could be juveniles. It would be great to get a height estimate of that plant in your picture or diameter estimate of that tree...
This site suggests that the average pack size is 6-12 wolves, which is significantly more than showed up on your camera (though, obviously this could be coincidence and not a definitive way to rule out this wolf).

This leaves the coyote:

Size: Between the size of the fox and grey wolf: 21-24 inches at shoulder; 3.5 - 4.5 feet long (nose to tail tip) [source].
Color: Gray (or reddish brown), often grizzled, often with whitish/paler throat, chest, and/or belly. Black patches may be seen on the tips of tails on on feet. [[sources: Bekoff (1977)4 and CDFW].
Anatomy/morphology: Bekoff (1977)4 and CDFW compare coyotes to wolves. The snouts are thinner with smaller nose pad on coyote vs wolf, and a coyote's ears are taller and more pointed. Your images, unfortunately, don't really allow us to differentiate adequately.
Behavior: typically less social than wolves and will rarely travel in groups larger than their immediate family. Even still, they often keep their distance and practice more asynchronous activity. However, coyotes are most often observed as lone individuals or in pairs (especially during breeding season)4. This matches your camera's image.

Coyotes are most active in the early evening, but their activity can be variable. Many coyote have become quite nocturnal (especially near humans), but they are known to also be sporadically active throughout the day and showing peaks of activity at dawn and dusk. [sources: Bekoff (1977)4 and Wikipedia. Wolves, though, are also active during evening and night...

Summary

So, based on the the few number of individuals, coloration, and perceived relative size of your specimens, it seems most likely that these are coyote. If you can get us estimates of height and diameter of the foliage in the background, this could be stated more definitively.

You could always go back to the site and photograph and compare the tracks, too (try starting here and here to compare)....

...

Though of course, it could always be a "coywolf" (also see here) :p.

 Citations

 1. Nowak, R. M. (1995). Another look at wolf taxonomy. In Carbyn, L. N.; Fritts, S. H.; D. R. Seip (eds.). Ecology and conservation of wolves in a changing world: proceedings of the second North American symposium on wolves. Edmonton, Canada: Canadian Circumpolar Institute, University of Alberta. pp. 375–397. [see map on p 376 here]

 2. Goldman, E. A. (1941). Three new Wolves from North America. Proceedings of the Biological Society of Washington. 54: 109–113. [See HERE for a map]

 3. Goldman, E.A. (1941). Three new wolves from North America. Proc. Biol. Soc. Wash, 54: 109-13. [available here]

 4. Bekoff, M. (1977). The coyote Canis latrans. Mammal. Spec, 79:1-9.[see here]


Are descriptive statistics sometimes more useful than tests of significance? How does the biology community currently feel with regards to publishing descriptive and effect size statistics rather than significance stats?  Almost every journal article I read in the cell biology field almost always reports things like P values and stats tests to report statistical significance, but should effect sizes be more important to a biologist?  Do we even care if something is statistically significant if the effect size is negligible?  Rather than crunch for significance, could one get away with showing things like confidence intervals, eta^2, Cohen's d, and r values instead over P values?  P values tell you the odds that if you assume the null hypothesis is true, then the observation you're making are only 5%(assuming of course P<0.05).  However, this can lead to the logical fallacy as noted by Aristotle--theory A predicts that changing X will cause Y.  An experimenter thus performs experiments to manipulate X and sees changes in Y, therefore he/she concludes theory A is supported, which is however completely wrong.  Theories B, C, D, E....... could all also predict that X changes Y and may even be better at it.  Even if you conclude that your findings "support" theory A, it's still weak because you haven't ruled out all of the other possibilities.

So in order to avoid statistical significance relative to null hypothesis that has all sorts of pitfalls, can one just use descriptive and effect size statistics just as effectively, if not more so?

I'm not a statistician, but I think the comments have got it right.  There is never a reason to omit P values, statistical power or some other measure that you have done something that is not a random outcome.

For the sake of reference lets define the terms you reference:
Eta squared is a ratio of the variances of two sets of measurements
Cohen's d is a measure of the difference between two means.
R value or Pearson Correlation describes the linearity of two numbers, usually one of them being a measurement and the second being an experimental variable.

These numbers as you say are descriptive, but they could be created by throwing coins and writing them up.  With small numbers of measurements, and a large enough range of possibilities, its possible to get terribly large numbers here.

Biology, medicine, social science and economics are really susceptible to this.  You go into the field and measure butterfly wings or do surveys of people's opinions, or try to guess who is going to win the election and its quite expensive to do more measurements.

If you are measuring something hard to determine because accuracy is important such as a close election race or that is really complicated such as which genes convey a susceptibility to type 2 diabetes (a problem which remains unsolved because so many genes play a role) you need large numbers of responses.  Yet each study that comes out gets some answer, but if you want to believe it these numbers should convince no one in most cases.

Microarray data and RNASeq data analysis for instance often suffer from this problem.  The measurements are all statistically significant but each one costs hundreds or even thousands of dollars.  Most experiments do a minimal three measurements to understand the variance in each measurement and then do 2 to 8 actual measurements.  That's not going to so revealing when working with a system with thousands of genes in it. one bad sample with slightly different culture conditions can ruin the experiment.

Our butterfly biologist may measure 100 butterflies and stop when the P values are 0.05 or 0.001 - its a lot of work camping out and setting nets.  The truth is that 5% is a number that can happen at random a lot.  Even a 0.1% error will happen in one in ten such experiments.  In thousands of experiments published that means that 10% of them have a mistake.  Not so great.

It gets worse though - not only significance, but bias needs consideration.  Because biologists and most other scientists don't understand statistics, the assumptions that we use when we calculate a P value are often inappropriate and don't give honest estimates of the chance that this is a random phenomenon.

If good looking result is chosen specifically to show to prove the point or some data are thrown out because they simply don't look good, or if a hypothesis is chosen in a biased way simply to fit an unreliable set of data.

Or the statistical assumptions of the calculation might simply be so inappropriate that to really cite them is an out and out lie. An everyday example of this is to do a BLAST search.  The E-value calculations, if read as a P value would be wrong, even though they are mathematically correct - two strings that show a 10% identity will have a small E value - 10^-8 for instance, but this is only the chance two strings of these lengths will have so many letters in common.  Anyone who plays with BLAST will quickly throw out anything that has less than 30% identity unless they are desperate, even though the E-values are infinitesimal.

John Ioannidis has made this subject his focus and has published widely on this topic.  A good place to start is his commentary "Why Most Published Research Findings Are False".

  There is increasing concern that most current published research findings are false. The probability that a research claim is true may depend on study power and bias, the number of other studies on the same question, and, importantly, the ratio of true to no relationships among the relationships probed in each scientific field. In this framework, a research finding is less likely to be true when the studies conducted in a field are smaller; when effect sizes are smaller; when there is a greater number and lesser preselection of tested relationships; where there is greater flexibility in designs, definitions, outcomes, and analytical modes; when there is greater financial and other interest and prejudice; and when more teams are involved in a scientific field in chase of statistical significance. Simulations show that for most study designs and settings, it is more likely for a research claim to be false than true. Moreover, for many current scientific fields, claimed research findings may often be simply accurate measures of the prevailing bias. In this essay, I discuss the implications of these problems for the conduct and interpretation of research.


Does spinal cord have pain receptors? I understand that the brain itself does not have pain receptors, so when the brain is damaged or cut, there is no experience of pain. For example, surgeons can operate on the brain while a patient is awake without causing pain.

How about the spinal cord? Are there pain receptors in the spinal cord? Will damaging the cord itself cause a feeling of pain?

tl;dr
Like the brain, the receptors commonly called 'pain' receptors aren't in the spinal cord itself, but they are present in the meninges around the cord, and damage to the cord can be perceived as pain in particular because it can increase activity in the pathways carrying 'pain' information to the brain.
Details
Nociceptors, often called pain receptors, are peripheral structures that sense and transmit noxious stimuli to the central nervous system. The cell bodies of afferents from these receptors are found in the dorsal root or trigeminal ganglion. The receptor structures themselves (the afferent terminal of these neurons) are not found in the parenchyma of any central structure, though they do innervate the meninges of both the brain and spinal cord. Despite the lack of peripheral receptors of nociception, damage to the spinal cord is often associated with increased activity in the tracts that carry nociceptive information.
This may be beyond the question you're asking, but I would note that the IASP defines pain as:

a sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.

Pain is probably best understood less as a sense that nicely maps the external environment to a conscious representation of that environment, and more as an emotional need state, like hunger. Many different receptor structures and nerves can transmit a signal that can eventually be interpreted as pain, and in fact pain can be experienced without any physical peripheral input at all (as the IASP definition attests). This is one of the reasons nociceptors are typically not called pain receptors by people who treat or study pain.


How can GMO contaminate biologic plants? Let consider two use cases :

I am the only farmer within a 200km radius. I first grow GMO plants. A few cycles later I decide to grow bio plants, so I uproot all of the GMO plants and plant fresh new bio plants.
I am surrounded with GMO plantations and I decide to grow bio plants.

In both cases, can we consider the plantation as bio or was it contaminated and how?

First let me say this: I am no gardener. Every plant that enters my home or yard dies a slow death of neglect. I do have some experience trying to remove weeds from other non-weeds, and there is a practical aspect of "uproot every GMO plant" that I think may be impossible, but this is speculation. Let's get into a literature review.

A frequently cited paper is Dröge, M., Pühler, A. & Selbitschka, W. Horizontal gene transfer as a biosafety issue: A natural phenomenon of public concern. Journal of Biotechnology 64, 75–90 (1998). Table 3 contains the most relevant information about horizontal gene transfer between plants.

In situation number 1, consider that the rhizosphere (the area of soil around the root of a plant) is constantly populated with bacteria. These bacteria are shown to sometimes transfer genetic material to and from the plant, through the roots. Unless you somehow sterilize the soil after uprooting your previous crop, consider everything you plant in that field possibly contaminated.

Situation 2 is less clear, but Monsanto does sue farmers found to be using their seeds without a contract, and many farmers say this is because of cross-pollination. I think you should assume that your field will soon be contaminated.


What is the advantage of circular genomes for bacteria and linear genomes for other organisms? Bacterial are a great group of organisms. They have circular genomes and never went toward linear genomes while other organisms show the opposite strategy and don't have circular genomes (disregarding their cytoplasmic genome). Why they have followed these different strategies?

You can package linear genomes much more efficiently than circular genomes, and bacteria simply don't require the information density to be prosperous.

To be a bit more specific, it's the torque strain put on the double-helix while it's being wound that makes the difference. Linear genomes can be wound around Histones, and these Histones can be further formed into more complex and dense patterns so that the DNA of a linear genome is condensed to a mere fraction of the size it was before. The high density allows cell division to occur much, much easier than it would otherwise happen in Eukaryotic cells.

Circular genomes cannot get rid of the torque stresses like linear genomes can. To attempt a similar packaging scheme as Eukaryotic cells would result in the DNA breaking apart at some point before you reached a high level of information density.

I'll look through my BioChem books again to find a reference later on, but hopefully you should have a solid idea of "why" from the above. For now you can do a little thought experiment: Think of all the ways you can wind a single piece of string or thread around things to make it as dense as possible. Then think of all the ways you can try to achieve the same density with a rubber band without breaking it. The string should win out in both the ease at which you can manipulate it, and the level of density you can achieve.


Are nucleotides at the ends of DNA stripped on aging? I had the following understanding (now after reading a popular science article seeming wrong understanding):

DNA in (regular) cells (in human and some other organisms) are protected by telomers. Telomeres are shortened at each division. When telomeres reach zero size, nucleotides of the ends of DNA become "stripped" so that the DNA shortens a little. The shortened DNA does is not fully functional. This leads to aging of the organism.

But in a popular science article I've read that telomeres however shortened seem not to reach zero length. So the DNA nucleotides at the ends of DNA are never stripped. However shortening telomeres leads to the cell to become not divisible or even death of the cell.

So two related questions:

Are coding/regulatory nucleotides (not just telomeres) at the ends of the DNA ever stripped as a result of aging?
If they are not stripped and so the DNA itself is not damaged, how shortening telomeres may lead to aging? That is how aging can be caused by just shortening telomeres which however do not reach zero length?

The Stanford article that you read is correct, in the sense that telomeres do not need to be completely removed by cell division before deleterious effects occur and cells start undergoing senescence.

This Nature article describes an experiment in which the minimum length of telomeres (beyond which chromosomal fusion occurs) was determined:

  The critical telomere length was 12.8 repeats (of six base pairs)
  long, they found — any shorter and the chromosomes began to fuse
  together at their ends (R. Capper et al. Genes Dev.
  doi:10.1101/gad.439107; 2007). Baird suggests that without
  sufficiently long telomere caps, the cell may perceive the chromosome
  ends as broken strands of DNA and attempt to piece them together.

Therefore, we can conclude that while it is not impossible for non-telomeric nucleotides to be stripped from chromosomal ends, this generally does not happen, since cellular defense mechanisms such as non-homologous end joining (NHEJ) and microhomology-mediated end joining (MMEJ) would activate before that point, and start joining chromosomal ends together. This would then lead to issues during mitosis, which would likely halt further cell divisions.


How do PrP mutations lead to prion disease? My understanding is:

The PrP gene in human cells is expressed as both PrP-c (normal protein) and  PrP-sc (prion disease protein). This happens post transcriptionally, that is, the normal and the diseased protein are not distinguished based on genetic mutations, rather they are synthesized based on the same gene, but differ in their tertiary structures, which makes their functions also different.

If the amino acid sequence of both proteins is the same (same gene), then what determines whether the synthesized protein will take the disease-causing tertiary structure or the normal one? Is it due to post-translational modifications?

And finally (I apologize for advance for multiple questions): how do prions, which are void of nucleic acids (being proteins), integrate into the genome of a newly infected host by reverse translation, and become a familial disease?

If the amino acid sequence of both proteins is the same,
  what determines whether the synthesized protein will take the
  disease-causing tertiary structure or the normal one?

PrP-C and PrP-Sc do indeed have the same primary structure. However, they differ in secondary and tertiary structure. The protein can take more than one shape (conformation), where the likely conformation spaces taken by the protein are due to chemical and physical interactions. Many proteins can change their shape, often this is not well understood in detail. However, we know that the conformational space of some proteins allows for several, stable conformations of a single protein; the factors which stabilize it in a conformation or cause it to switch are difficult to understand in vivo.

PrP-Sc tends to accumulate in compact, protease-resistant aggregates. Circular dichroism shows that normal PrPC had 43% alpha helical and 3% beta sheet content, whereas PrPSc was only 30% alpha helix and 43% beta sheet. Although the exact 3D structure of PrPSc is not known, it has a higher proportion of β-sheet structure in place of the normal α-helix structure. The end of each fiber acts as a template onto which free protein molecules may attach, allowing the fiber to grow.

Prion proteins therefore propagate accumulation of more and more prion proteins.

  Is it due to post-translational modifications?

No.

  How do prions, which are void of nucleic acids,
  integrate into the genome of a newly infected host by reverse
  translation, and become a familial disease?

They do not enter the genome through reverse translation. The DNA sequence itself is mutated and the mutation drifts across generations for as long as it is being passed on through the germline.


what is the princlple of using DMS (Dimethylsulphate) for structural analysis of rRNA? I want to check the secondary structure of rRNA (PTC) in a particular position by using DMS footprinting. I have deleted the modified nucleotide (m5c) which is present in the PTC and it helps in the ribosomal structural stability. I am interested to know after the deletion of the modified nucleotide.

I am using DMS treated RNA with primer extension. I don't understand the basic principle of DMS reacting on RNA. can you please explain me.

I used this article for reference:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2701642/

Here is a good explanation of the theory and chemistry behind DMS footprinting, from chapter 11 of Probing RNA structure within living cells :

  In vivo chemical probing assay using dimethyl sulfate (DMS). (A) DMS methylates the N1 atom of adenosines and the N3 atom of cytosines. Both of these positions are located on the Watson–Crick face of the respective nucleotides. (B) Scheme of a structured RNA interacting with a protein ligand to exemplify residues accessible to DMS modification. (C) Mapping the modified positions by reverse transcription. The enzyme terminates the extension due to steric hindrance by the bulky methyl group at the Watson–Crick face of A and Cs. (D) The pool of cDNAs is separated on a standard denaturing gel. A and C denote the sequencing lanes, which are essential to map the modified positions. In addition, an RT control, which is prepared from RNA extracted from untreated cells, is essential to determine any natural stops of the RT (lane -). Comparison of the RT control lane with the cDNA pool created from DMS-modified RNA (lane +) reveals sites of modification. Note that the band resulting from a DMS modification migrates one nucleotide faster than the corresponding band in the sequencing lane, because the ddNTP is incorporated into the nascent cDNA, while the methyl group results in a stop one residue prior to the modification.

My take -- DMS adds a methyl group at the hydrogen-bonding face of exposed A and C bases. As and Cs protected by either proteins or base-pairing interactions are not methylated.  Methylated bases inhibit reverse transcriptase, resulting in a truncated DNA product that can be visualized on a gel.  Comparison to an untreated control allows for inference of which As and Cs of the RNA sequence are exposed and which are protected, from which the native RNA conformation can be inferred (or the possibilities greatly constrained).


Why do we feel tired if we sleep excessively? When we eat, finally we feel full. I know which mechanism causes the sensation of being full. But when we sleep excessively we often still want more sleep. Why does this happen? Is there a mechanism underlying this?

Studies have proven somewhat the opposite of what you're asking

For example a study from 2004 - "The impact of extended sleep on daytime alertness, vigilance, and mood" found that,

  Average daily POMS vigor and fatigue scores also improved during the sleep extension period

And thus concluded

  Extended sleep leads to substantial improvements in daytime alertness, reaction time, and mood.

Whilst an older study from '73 -"Performance and Mood Following Variations in the Length and Timing of Sleep" found that,

  Neither sleep duration, nor any other sleep parameter consistently correlated with the performance or mood measures.

The study does go on to state however,

  Therefore, it seems reasonable to assume that the detrimental effects of acute changes in the length and/or timing of sleep were not directly related to any specific changes in the length or electrophysiological patterns of sleep, but to as yet unknown physiological changes resulting from the disruption of an established circadian rhythm of the sleep and wakefulness.

This perhaps suggests that the question which should be asked should not be why does oversleeping makes us feel tired, but why does the disruption of normal sleeping patterns make us feel tired?


Can single-cell organisms have through-holes? (Are donut-cells a thing?) I've watched a YouTube video about microorganisms, which featured a shot (below) of a single-cell organism, that looked like it had several through-holes in its body. Somehow I have a pretty steady mental image of a single-cell organisms being basically blobs: a sphere, an ellipse, a branching tree-like structure, all seem like plausible single-cell creature shapes to me, but something like a donut just doesn't. Is my intuition wrong and this is just a normal thing cells do? If so, how do those holes form? And if not, why does this shot look like a cell with holes?

I thought that those holes might be just me wrongly interpreting the image. One idea was that this might be a result of the cell's complex 3D structure being projected on a 2D screen, but the movement of particles inside of the cell (which you can see in the video) seems to support the "cell with holes" interpretation. The other one, that was suggested in YouTube comments, is that those "holes" might be vacuoles inside of the cell. It seems that for that to be true, the image would have to be more like an MRI scan, revealing only a "slice" of the cell. But you can see some of 3D structure there, so it doesn't seem right either.

Yeah, holes seem to happen in leptomyxa:

L[eptomyxa] reticulata is an edaphic protozoan and a predator of bacteria and amoebae. [...] The plasmodium is very polymorphic; its size varies between 50 .mu.m and 1 cm. It generally spreads in the form of a very thin transparent protoplasmic layer. It may have the shape of a full blade, sometimes perforated with holes, or of a network; the pseudopodial zones with active locomotion present a typical fan-shaped contour.

There are some hi-res images from other sources showing the same

Image source: http://penard.de/Amoebozoa/Tubulinea/Leptomyxida/
It seems that what happens is that branches "merge back" after touching "at the tips" leaving holes in such organisms, but that's just speculation on my behalf. I haven't (yet) found a source discussing the dynamics of how these holes get formed.
And a couple more images from  a different source--a broader review of leptomyxidae.

[Above] Light microscopy of Leptomyxa arborea n. sp. and L. variabilis n. sp. (by S.
Geisen and C. Burberg) on the plastic bottom of a Petri dish (Phaco). A-F: Leptomyxa arborea,
various shapes and specimens of different size. G-M: Leptomyxa variabilis, various shapes of
trophozoites (G-K and M); cysts (L-M). Arrows indicate the most pronounced bunches of
adhesive filaments; arrowheads indicate pore like structures in cysts. Scale bar is 100 μm in A-E
50 μm in F-K and 25 μm in L-M.

[Above] Isolate of Leptomyxa sp. (by morphology of trophozoite indistinguishable from
L. reticulata) observed in the sample from Valamo Island, North-West Russia (by A.Smirnov).
A: usual appearance of a trophozoite. B-D: subsequent stages of contraction of the cell on the
object slide under the bright light beam. Figure D shows pseudopodia very similar to those or
Rhizamoeba; polypodial cell like this one can move relatively rapidly for some distance.
Molecualar data from this strain were not obtained. Scale bar is 50 μm.

By the way, the "branches" are more or less "legs"/"limbs" used in locomotion; but also this species is multinucleate:

Leptomyxa reticulata is the type species of the genus Leptomyxa. It is a
multinucleate, expanded organism with plasmodia-like organization of its ramose body,
possessing a simple life cycle [...] Moving amoebae usually form adhesive uroidal filaments along the posterior end of the body or an uroidal structure consisting of a pack(s) of such filaments (the latter often is seen when the locomotive cell adopts a shape of
an irregular ramose triangle, with the base directed anteriorly).

A more diagrammatic explanation:

Main morphological traits of leptomyxid amoebae. A-E: Leptomyxa cf. reticulata
(Valamo Island strain by AS). A: expanded, plasmodium-like ramose cell, slowly moving on the
substrate. This is the “textbook” appearance of Leptomyxa. B – more compact, faster moving and
actively feeding cell. C: Disturbed cell showing compact lobose pseudopodia. Leptomyxa accepts
shapes like this under certain influence (light, temperature, etc. in order to relocate rapidly). D:
solitary cyst with double wall. E: several cysts covered with the shared outer cyst wall (D-E are
drawn based on photos by Pussard and Pons 1976a)

(So yes, creepin' amoeba with holes and "limbs"!)
A more interesting question at this point is whether there are any (naturally occurring) single-nucleus examples of "cells with holes".


How long can you keep sheep eyes in formaldehyde before dissecting? We're preparing for an experiment in our classroom and my teaching partner and I are at different points in the unit.  I am concerned that the experiment will be less successful because of the freshness of the eyes.  How long can they eyes be stored in the fridge before they have to be dissected and is freezing them an option?

Formaldehyde is a preservative, and is used to prevent decay. As long as the tissue is completely perfused (and there shouldn't be any issues with eyes that I'm aware of) it can be kept essentially forever. Have fun!


Dynamic instability of microtubule Why is it said that , warmth facilitates assembly and cold facilitates disassembly of microtubule?
But till now what I  had learnt is that as temperature increases so the kinetic energy of molecules increases so does the order decreases.
So what is the reason behind the above phenomenon?

In the paper "Phase diagram of microtubules" Fygenson, 1994. it's evident that with increasing temperature the length of the aggregates is growing. But it of course depends on other additional parameteres like concentration and I assume the type of the protein - alpha and beta-tubulin.


Is it possible to condition the body to reduce bruising? I do combat sports, and in these sports there are a lot of hits that can cause bruising.

I've found that, over time, physical conditioning can reduce and/or eliminate the bruising to the point where even after hard impacts, there is no residual bruising.

However, I was under the impression that it is not possible to "condition" for reduced bruising since bruising is the result of ruptured capillaries, and you can't condition to not rupture blood vessels.

Can someone offer an explanation to why, with conditioning, it is possible to reduce/eliminate bruising?

Bruises are a type of hematoma of tissue in which capillaries and sometimes venules are damaged by trauma, allowing blood to seep, hemorrhage, or extravasate into the surrounding interstitial tissues (reference).  From what I read there seems to be two reasons why you notice a reduction in bruising.

The first would be because there is a deadening of nerve cells where they get used to the pain and eventually less sensitive. There could also be the development of some scar tissue from the bruising which has irregularly developed nerve endings leading to lesser stimulation. (reference 1 and reference 2)

The second reason could be because you yourself get stronger. The Wolff's law states that:

  Bone in a healthy person or animal will adapt to the loads under which
  it is placed.1 If loading on a particular bone increases, the bone
  will remodel itself over time to become stronger to resist that sort
  of loading.2 The internal architecture of the trabeculae undergoes
  adaptive changes, followed by secondary changes to the external
  cortical portion of the bone,3 perhaps becoming thicker as a result (reference).

So, repeated stress on the bones of your face/hands should be make them stronger. I don't think your body can adapt to heal faster in an area from repeated bruising as most likely scar tissue will develop from repeated stress on the skin. You can however improve your nutrition and diet to help your body heal better (reference).


Is this formula for calulating the energy requirements of pets applicable to all animals? This website gives the formula: 70M3/4 = Resting Energy Requirement for pets in calories/day, where M is the mass in kilograms. Is this formula correct and accurate, and will it work for rabbits, mice, and guinea pigs?

No, I would not use this formula for rodents. The "3/4-law" is usually used only for mammals with a mass of m>10 kg and was derived by Kleiber from limited empirical data sets.
For mammals with a bodymass below 10 kg the prefered exponent seems to be 2/3 which was derived from the relationship of volume and surface of the body and heat energy as the main source of metabolic rate. See here.

Either way this are only approximate calculations I would not trust too much as exceptions occure frequently and also the age and/or physical state can make a difference.


What part, roughly, of the carbon in a plant comes from the soil? As opposed to the atmosphere? C4 plants contain a slightly higher percentage of carbon-13 than C3 plants. Is this because of carbon obtained from the soil or the atmosphere?
I have read that plants using different chemical pathways, such as millet and wheat, incorporate distinctive proportions of stable carbon isotopes from the SOIL.
Do C4 plants need more carbon-13, or does that process just happen to result in accumulation of more carbon-13?

Only a small fraction of plant carbon is soil-derived: e.g. from Majlesi et al 2019:

although the majority of plant C was obtained from atmosphere by photosynthesis, a significant portion (up to 3–5%) of C in plant roots was derived from old soil"

(in an experiment with Scots pine and reed canary grass).
As laid out by this review of C4 photosynthesis, the primary reason for differential isotopic make-up of C3 and C4 plants is that the biochemical pathways they use fractionate isotopes differently — not because the plants' requirements are different.

Because of the very different
affinities of Rubisco and PEP
carboxylase for CO$_2$ , C$_3$ and C$_4$ plants
differ in the carbon isotopes that they
assimilate. While most atmospheric
CO$_2$is made up of ${}^{12}$C, a small fraction
includes ${}^{13}$C. Rubisco has a fairly high
$K_m$ and hence low affinity for CO$_2$, and preferentially fixes ${}^{12}$C. The ratio of ${}^{13}$C
to ${}^{12}$C ($\delta^{13}$C) in a C$_3$ plant is thus much
lower than the ratio in the atmosphere;
the carbon in structural and storage
carbohydrates contains much less
${}^{13}$C. PEP carboxylase has a lower
$K_m$ for CO$_2$ than Rubisco and hence
a higher affinity; as a consequence it
discriminates much less against ${}^{13}$C
than Rubisco does, so that the $\delta^{13}$C
is appreciably closer to atmospheric.

Majlesi, Soroush, Jukka Juutilainen, Anne Kasurinen, Promise Mpamah, Tatiana Trubnikova, Markku Oinonen, Pertti Martikainen, and Christina Biasi. “Uptake of Soil-Derived Carbon into Plants: Implications for Disposal of Nuclear Waste.” Environmental Science & Technology 53, no. 8 (April 16, 2019): 4198–4205. https://doi.org/10.1021/acs.est.8b06089.


Is there any independent non-DNA based information system in the cell The information in protein is not neccessarily independent of the genome as the information of amino-acid sequence comes directly from the  genome. The process of post-translational modification may be another candidate but the main players in this process are proteins so its not clear whether this process is totally determined by genome (total DNA-based information) or some portion of it comes from a different source.
Obviously the external world is a source of information but I am interested in internal sources.

According to the comments, the question is about inheritance systems of cells. The "mainstream" information storage and inheritance system is of course DNA (and RNA in some cases). However, there are additional and parallel inheritance systems even within a single cell (not to mention in multicellular organisms). These form a subset of epigenetic inheritance methods and - as expected - are less precise than the information copying mechanisms of polynucleotide replication (in eukaryotes) and certainly more limited in the amount of information that can stably maintained throughout generations. This was explored in detail by Eva Jablonka and Marion Lamb (among others) in a few books and many papers:

Jablonka, E. & Lamb, M. J. 1995. Epigenetic inheritance and evolution: The Lamarckian dimension. Oxford University Press, 346 pp.
Jablonka, E. & Lamb, M. J. 2006. Evolution in four dimensions: Genetic, Epigenetic, Behavioral, and Symbolic Variation in the History of Life. MIT Press, 472 pp.
Jablonka, E. & Szathmáry, E. 1995 The evolution of information storage and heredity. Trends in Ecology and Evolution, 10, pp. 206-211.
Maynard Smith, J. 1990 Models of a dual inheritance system. Journal
of Theoretical Biology, 143, p. 41-53.

  “An epigenetic ineritance system (EIS) is a system that enables a
  particular functional state or structural element to be transmitted
  from one cell generation to the next, even when the stimulus that
  originally induced it is no longer present. In other words, EISs are
  the systems that enable the transmission of various phenotypic
  expressions of the genetic information in an individual.” (Jablonka & Lamb 1995, p. 80.)

Epigenetic inheritance methods include the following systems that could in theory code for information that is potentially inherited from parent to daughter. The list is far from being exhaustive.

DNA methylation: a methyl group added to a gene's promoter represses its transcription. Methylation is heritable: when DNA replicates, methylation carries over. There are other chromatin-marking methods that are inherited.
Steady-state inheritance system: "the inheritance of functional states through self-sustaining metabolic networks, maintained by positive feedback." (Jablonka & Szathmáry 1995 TREE) The cytoplasm itself is also inherited by the daughter cells, but any information "stored" in the cytoplasm cannot effectively be "replicated" from cell to cell.
Structural inheritance system: 3D structures of the cell provide the template for similar structures to assemble, e.g. "transmission of cytoskeletal organization and of cortical organization" (Jablonka & Szathmáry 1995 TREE).
Symbionts and parasites (bacteria, viruses, plasmids, etc.) that can replicate within the cell (so that when the host divides, both daughter lineages receive the partner). Note, however, that if the parasite is too virulent then it is expected that horizontal transfer is more emphasized than vertical "inheritance".
Prion proteins. Prions are proteins that may exist in several distinct conformations, and at least one of these conformations is capable of replication by forcing its alternate conformation (and therefore alternate function) on the normal physiological form of the protein (both having the same amino-acid sequence). See Shorter, J. & Lindquist, S. 2005. Prions as adaptive conduits of memory and inheritance. Nature Reviews Genetics 6, p. 435–450.
...


Herbivorous plants that consume falling leaves I've just seen a report about specialized herbivorous plants which build special traps to catch falling leaves from trees above them.

The only thing, which I'm missing is the correct name of this plant. Do you have any idea what plant(s) could this be?

Many plants do this, with varying degrees of specialization - for some it is perhaps incidental, others have evolved this strategy to gain nutrients (often water as well). You are probably thinking of bromeliads, a diverse group of plants in which many species have specialized leaves that form cups at the base to collect water and litter. These structures, a type of phytotelmata, have similarities to some carnivorous plant traps.

These tank bromeliads are able to efficiently absorb nutrients from animal or plant matter which falls into the tank:

  Considerable absorbed nitrogen is mobilized in the rosette center. Tested bromeliads appear to be well equipped to utilize minerals and organic nitrogen originating from tank-impounded plant and animal debris as nutrients.

This litter catching habit occurs in other lithophytic and epiphytic plants, i.e. those which don't grow in soil, because it allows them to capture nutrients when growing on rocks or trees. Examples include the staghorns/elkhorns and basket ferns:

  They form a characteristic 'basket' that collect litter and organic debris, hence the common name. The collected debris decompose into humus, providing the plants with nutrients it would otherwise not have received from being suspended above the ground.


Effect of HIV on T-cells When HIV infects macrophages, it doesn't kill or destroy them immediately, but once it infects T-cells, they're destroyed. Why is that? As in why does it destroy T-cells and not macrophages or other cells.

  This process does not destroy the macrophages.
  Unlike macrophages, helper T cells are destroyed.

From this article:

  Researchers found that when the virus productively infects the few permissive CD4 T cells present, death occurs through apoptosis mediated by an enzyme called caspase-3. But when HIV abortively infects nonpermissive CD4 T cells, death occurs by pyroptosis, which depends on the activation of caspase-1. It turns out that the vast majority—roughly 95 percent—of CD4 T cell death in lymphoid tissues is driven by caspase-1-mediated pyroptosis.

When it comes to macrophages, however:

  macrophages are much more resistant to cytopathic effects of lentiviral replication than for example activated CD4+ T cells [23, 24, 25], and HIV-1 has evolved sophisticated mechanisms to prolong the life span of infected macrophages [24, 26]. Especially long-lived macrophages may therefore harbor the virus for long time periods, thus constituting HIV-1 reservoirs and posing a major obstacle to virus eradication from infected individuals.

Source


Species identification. Is this a leech? The pictured creature, shown at the bottom of a glass, was attached to a friend’s child after he was swimming in the Ottawa River today. It stretches out to roughly an inch in length but in this “resting pose” was around half that length. Below is a shot of the mark left behind:

It looks like a leech to me, but I thought I’d ask the Internet.

Yes this is a leech. It appears to be a species in the family Glossiphoniidae, or the freshwater jawless leeches. This family of leeches is relatively flattened with a poorly defined anterior sucker.
According to The Canadian Encyclopedia, there are about 45 species of leeches found in or around Canada.
Langer et al. (2018)1 provide a more limited selection of Glossiphoniidae leeches they ascribed to Ontario. Of the ones they list, yours most looks like a specimen from the genus Placobdella.
See, for example, this image of Placobdella phalera from de Carle et al. (2017)2 found in Ontario, Canada:

 Source: Figure 1, de Carle et al. (2017)

1  Langer, S.V., Vezsenyi, K.A., De Carle, D., Beresford, D.V. and Kvist, S., 2017. Leeches (Annelida: Hirudinea) from the far north of Ontario: distribution, diversity, and diagnostics. Canadian Journal of Zoology, 96(2), pp.141-152.
2  de Carle, D., Oceguera-Figueroa, A., Tessler, M., Siddall, M.E. and Kvist, S., 2017. Phylogenetic analysis of Placobdella (Hirudinea: Rhynchobdellida: Glossiphoniidae) with consideration of COI variation. Molecular phylogenetics and evolution, 114, pp.234-248.


How long does a tan last? How long do melanocytes and melanosomes continue to protect DNA after UV exposure? Basically, if skin is tanned, then over the next month it is shed, will melanocytes continue to produce high levels of melanin to keep the new skin tanned without requiring more UV exposure? The cells react by producing more melanin after exposure but will they continue to do this in new skin cells?

The tanning response to UV occurs in two phases:

The immediate response begins at exposure to UV-A, reaches a max at 1-2 hours, and fades between 3 and 24 hours.
This article speculates that this is due to the redistribution of melanosomes rather than additional melanin production.
The delayed response is more durable, occurring by repeated exposure to UV-B, as well as as UV-A and visible light. "It is a gradual process in which the skin starts darkening 48–72 h after irradiation, reaches a maximum ∼3 wk after exposure, and the skin does not return to its original melanin content until ∼8–10 months later."
This source says this is due to additional melanocytes, melanosomes, and more melanin, in general.

Both processes are influenced by genetic factors.

Source for the initial points, which also contains interesting details on the enzymes involved in these processes.


Are we naturally born right or left handed or ambidextrous? Most of you here will be right or left handed. A few might be ambidextrous. But were we born that way?

I'm wondering if everyone was born ambidextrous, but as they grew up became more dependent on one hand, and that hand after more use now has stronger muscles, bones etc. Or were we naturally born with one hand stronger than the other?

I've heard somewhere that it has something to do with the brain, and which side which hemisphere is on. Not sure the validity of this statement. It's also been pointed out that chimps and apes show handedness, so this probably not just a human thing.

So, are we naturally born right or left handed? Or are we all born ambidextrous and does left or right handedness develops later?

tl;dr

Yes!

Is handedness determined before birth?

Without thinking of whether handedness is genetically or environmentally defined (see below), is handedness decided before birth?

Hepper et al. 1991 and DeVries et al. 2001 show that handedness can be inferred from from fetal position and hand usage. Typically, looking at what thumb is used for sucking is good indication of handedness.

Is handedness heritable?

The question

  [A]re we naturally born right or left handed?

can sometimes be understood as

  Is handedness genetically determined?

or in more concrete terms as

  Is handedness heritable in humans?

If it is not obvious to you that this is your question, then you probably don't understand the concept of heritability! Then you should have a look at Why is a heritability coefficient not an index of how “genetic” something is? first and then come back here to read the results.

There have been a large number of studies on the question, unfortunately most of them were very small studies with small sample size. Medland et al. 2008 is pretty large scale twin study which report a heritability of 0.24.

In other words, yes handedness is heritable. To be more accurate, 24% of the total variance in handedness is explain by additive genetic variance. Yet again in other words.

The cooperation-competition hypothesis

On the evolution of the handedness in he human population you might want to hear about the cooperation-competition hypothesis. For that, you should have a look at this TED-ed video. As you watch this video, you'll probably be interested in reading the wikipedia article on frequency-dependent selection.

Thanks to @Mockingbird for pointing out to this video.


Growing E. coli at room temperature? If I were to do a blue/white selection of transformed E. coli on LB agar ampicillin plates at room temperature (23⁰C) for about 2 days and 18 hours, will I run into the issue of satellite colonies or any other issues?

Since b/w screening is a means to  selection, you want maximum selection pressure. This will be obtained by incorporating all optimal conditions. The many enzymes of the lac operon are going to function best at their optimal temp.

Why would you do this? If it is because you can't go in the next day it's better to do it when you're available. You're only going to doubt your results when you get them.


Is there a double helix RNA? I wonder what is its function and if it can be the genetic material for a living organism. If not, why?

Yes, double-stranded, helical RNA exists. It can occur naturally, a famous example would be Rotavirus, as well as synthetically in the lab.

Please note, however, that viruses strictly speaking do not qualify as a living organism.

References:

RNA double helix structure identified using synchrotron - McGill University

Double-stranded RNA viruses - Wikipedia

Rotavirus - Wikipedia


Why aren't circadian rhythms exactly 24 hours long? Most organisms exhibit circadian rhythms that have a periodicity of about, but not exactly 24 hours. Why is this? And to what extent can variation in periodicity in circadian rhythms among the individuals of the same species (if a variation does indeed exist) influence the level of competition they face in acquiring resources?

Biological/organic systems are notorious for imprecision, making a perfect 24-hour cycle practically impossible - nevermind the fact that "hours" are a purely artificial concept that humans invented to help make sense of time.

The simplest "close-enough" way to measure days that doesn't require an implanted clock microchip or heavy computing power is to detect extreme changes in light or temperature associated with transition between day and night.

An extra argument against hard-locking to a 24-hour cycle: Adaptability and migration. If every life form is locked to a strict 24-hour cycle with fixed time slots for sunset and sunrise, this limits migratory adaptation since different regions have different sunset/sunrise and day lengths at different times of the year. Timing a wake-up and sunrise and sleep at sunset (or the reverse among nocturnal species) generally works across most of the planet no matter the season (the only exception being the niche case of a solstice at the poles, for example http://www.slate.com/blogs/bad_astronomy/2016/06/22/why_does_the_sun_never_set_at_the_north_pole_in_the_summer.html )

There's also some evidence that days on Earth are getting longer ( see
https://www.space.com/40802-earth-days-longer-moon-movement.html )


What does x in "Miscanthus × giganteus" name stand for? I came across a species name that contains "x" in its name, namely Miscanthus × giganteus. What does this symbol stand for and is it commonly used in taxonomic nomenclature?

It means that the plant is a hybrid. Having it in the middle means that it is between species of the same genus, else the × (it's not the letter x but the multiplication symbol ×) would have been in front.

It is very commonly used in taxonomic nomenclature, namely every time you have a hybrid. This means you'll usually see it with plants, as animals very rarely interbreed.

Wikipedia says that your plant is a hybrid from Miscanthus sinensis and Miscanthus sacchariflorus. It is an easy place to look up most hybrids you might encounter.


What is a good miniprep protocol for the class room? I'm trying to find a good protocol for plasmid minipreps and I'm looking at 3 preps I've found:

Using phenol/chloroform

extract with phenol:chloroform:isoamylalcohol,
isopropanol precipitation, 12,000g spin down,
rinse with cold 70% ethanol.

Using lysozyme

lyse with lysozyme,
remove pellet,
isopropanol precipitation,
wash with cold 80% ethanol.

Using alkaline lysis

open cells with 80% glucose in EDTA buffer,
add SDS and NaOH,
pellet protein/membrane with acetic acid/acetate,
ispropanol precipitation,
wash with cold 70% ethanol.

They all differ in how to break open the cells and separate plasmids from the rest of the cell -- quite a bit.  Can anyone help me figure out which protocol is best here?

The protocol I used in my genetics lab course was alkaline lysis followed by ethanol precipitation similar to this one.  Nothing terribly toxic or requiring a fume hood (at least at the small volumes used).

The more practical, reliable method is to use a miniprep kit (usually spin columns) from one of several suppliers (Qiagen, Promega, Bio-Rad, etc.) which are fairly affordable at $1-2 per prep.


Do SSRIs downregulate or upregulate the 5-HT3 receptor? What effect do SSRIs have on the expression of the ligand-gated ion channel, the 5-HT3 receptor?

There are five subunits to this receptor (5-HT3), which are encoded by the genes HTR3(A-D) and differentially expressed depending on cell location in the (human) body. In contrast to the information in the previous answer, my first source actually has shown HTR3A to be most highly expressed in the CNS. The others are almost exclusively found in cells of the gut.

My second source reveals that the 5-HT3A receptors are up-regulated (show increased expression) on the cell surface in the presence of agonists and antagonists to the receptor. So, if an agent was increasing the amount of 5-HT (serotonin, an agonist) outside the cell, as would an SSRI, the expression of the receptor subunit-encoding genes would be expected to increase.

Niesler, B., Frank, B., Kapeller, J. & Rappold, G. A. Cloning, physical mapping and expression analysis of the human 5-HT3 serotonin receptor-like genes HTR3C, HTR3D and HTR3E. Gene 310, 101–111 (2003).
Morton, R. A., Baptista-Hon, D. T., Hales, T. G. & Lovinger, D. M. Agonist- and antagonist-induced up-regulation of surface 5-HT3 A receptors. Br. J. Pharmacol. 172, 4066–4077 (2015).


What are the buoyancy control mechanisms of Chambered nautilus? I'm currently working on an underwater robot and was hoping to use the principle used by the nautilus for buoyancy control. So how do the Chambered nautilus control its buoyancy?

The various species of nautilus use a combination of active transport of salts and passive diffusion of water for buoyancy (Denton and Gilpin-Brown 1966, Ward 1979, Greenwald et al. 1980). The chambers are filled with seawater. Salts from the seawater in the chambers is removed by a structure called the siphuncular epithelium. This process makes the chambered water hypotonic, meaning it has lower solute concentration relative to the animal. The hypotonic water then diffuses from the chambers into the blood, creating air pockets in the chambers. Greenwald and Ward (2010) have a recent summary of what is known about nautilus buoyancy, if you want to know more.

The diffusion of water in  is not a rapid process. The maximum ascent and descent rate of Nautilus from depths appears to be about 3.0 m m$^1$ (Dunstan et al. 2011).  This does not seem like an efficient process or rate of depth change for an underwater robot.

Literature Cited

Denton, E.J. and J.B. Gilpin-Brown. 1966. On the buoyancy of the peraly nautilus. Journal of the Marine Biological Association of the United Kingdown 3: 726-759.

Dunstan, A.J., et al. 2011. Vertical distribution and migration patterns of Nautilus pompilius. PLoS ONE 6: e16311. doi:10.1371/journal.pone.0016311

Greenwald, L., et al. 1980. Cameral liquid transport and buoyancy control in the chambered nautilus (Nautilus macromphalus). Nature 286 55-56.

Greenwald, L. and P.D. Ward. 2010. Buoyancy in NAutilus. Topics in Geobiology 6: 547-560.

Ward, P.D. 1979. Cameral liquid in Nautilus and ammontites. Paleobiology 5: 40-49.


The mystery of coconut tree Could anyone please explain to me, why the nail which is nailed in a coconut tree is not raised from ground level, when the tree is growing up?

First it needs to be said that coconut trees are not true trees, but palms, whose trunks are made of stems which grow in a cross woven pattern.

That being said - its true for any plant that no plant grows from the bottom up.  If you make a mark on any plant that mark will not rise much as the plant grows.

Plants grow from buds at the end of their stems.  As the plant grows taller  its because the tissue adds from the ends of its branches/stems.

In this illustration you can see the terminal bud, which is where the plant is growing up and also out into branches.  The palm is more like a bundle of grass stems, so the terminal bud is not obvious, but the leading edge of the grass will grow here.

A tightly wound core of stems in the crown of the palm, called the Heart of Palm is where the palm grows (see "growth point" in picture below).  It is also a terminal bud, but it is not as exposed and is not as obvious.

(figure from The Food and Agriculture Organization of the UN, fao.org)


How is an RT-PCR representative of the RNA contents in a cell? For example, we first collect all the RNA contents from a mammalian cell line. Say, for instance, we collect 80 uL of RNA with a concentration of 150 ng/uL. Next, to make cDNA, we take 1,000 ng of the RNA. However, this 1,000 ng is a completely random sampling of the total RNA we had. How is that random sample of RNA representative of the RNA contents originally in our cells?

It isn’t really clear exactly what the questioner is asking, but…

...one way of thinking about this is to ask how likely is it that a low-abundance RNA will be absent from the sample taken from the preparation of RNA. This would make the sample non-representative at the qualitative level.

The question states that 12,000 ng of RNA is isolated. Since nothing else is specified I assume this is total RNA. A rough estimate of total RNA per eukaryotic cell is 20 pg.

This means that the preparation came from 6 x 105 cells. (I’m assuming 100% yield, but this won’t really affect the conclusion.)

Now assume that a low-abundance mRNA is present at 10 copies per cell. The total RNA preparation therefore contains 6 x 106 copies of that low-abundance mRNA.

We take a sample of 1,000 ng from the total 12,000 ng. In other words we take 1/12th of the preparation of RNA. If that RNA preparation contains 106 copies of the low abundance mRNA how likely is it that we happen to take a sample which contains no copies of that low abundance mRNA? Here my maths fails me, but intuitively I say that the probability is very very small.

Now, if there are 1,000 different low-abundance mRNAs in the cell the probability of missing each of them is very very small, but the overall probability of missing one of them is 1000 x very very small, so maybe very small.

I'll continue thinking about how to calculate the value of very very small, but if anyone wants to help out - thanks in advance!


Why don't all bacteria have F-plasmids by now? Some bacteria can undergo gene transfer by conjugation. Conjugation is a form of horizontal gene transfer, meaning from one (unrelated) bacterium to another (in contrast to vertical gene transfer, which is from predecessor bacterial cell to successor (daughter) cells). Conjugation is initiated when one bacterium has an F-plasmid (Fertility plasmid) and forms an F-pilus, connecting the F+ bacterium with an F- bacterium, initiating transfer of the F-plasmid.

Why is it that during evolution not all bacteria have acquired this F-plasmid?

Conjugation occurs between cells of the same species too. For this to occur cell have to be close to each other. Now, if you have an isolated population of bacteria that never gets in contact with an F+ bacteria then this population would stay F-. Also not all conjugation events are successful, mechanical perturbations can disrupt the pilus through which genetic material is transferred.
This old article can give you good details:
THE ORIGIN OF BACTERIAL SPECIES - GENETIC RECOMBINATION AND FACTORS LIMITING
IT BETWEEN BACTERIAL POPULATIONS ARNOLD by W.RAVIN

  F+ shares, however, an important property of bacteriophage: after infection
  it behaves as though it were an addition to the bacterial genome. As an addition, it can furthermore exist in one of two forms: in one form, it
  is an unintegrated part of the bacterial genome, and may be  replicated either more or less rapidly than the "chromosomal" or linked genes (being
  infectious or lost through dilution, respectively); in its other form, it
  is integrated in the sense that its replication is coordinated with the
  replication of the host's genes, as though attached to them. In this latter form, found in Hfr bacteria, the F+ factor is incapable of infecting other bacteria (while permitting conjugation with them) and also prevents
  superinfection of its host bacterium by a nonintegrated F+ factor.

Taken from the linked paper. So you can see that are situations where conjugation occurs yet the F- won't become F+.

Also :

  What is particularly interesting about the F+ factor is the fact that there
  seem to be a number of different  kinds. An F+ factor making a bacterium
  fertile with some  F- cultures does not necessarily  make it capable  of conjugating with others (49).

So not every F+ cell can conjugate with another F- cell.


What will happen if a poisonous snake bites itself? I wonder if in general snakes are immune to their own venom. I would like to know studies or references about times snakes bit themselves and got sick or the contrary.

“The conventional wisdom is that they have circulating antibodies in
  their blood,” says Stephen Mackessy, Ph.D., a Professor of Biological
  Sciences at the University of Northern Colorado and an expert in
  venomous snakes. “This would protect them from their own venom, as
  well of venom from another snake in their own species.”

  Hypothetically, if a speckled rattlesnake bit another speckled
  rattlesnake, the immunity they’ve built from being exposed to low
  levels of their own venom—kept in glands behind their eyes and
  secreted when they bite—would protect them from a fatal wound. (Even
  though the glands are closed, they still contain blood vessels that
  allow the venom to circulate in their system, causing mild exposure,
  Mackessy says.) But a speckled rattlesnake that meets up with a cobra
  might have a different day entirely.

So in the case snake were to bite itself it wouldn't suffer as much from the poison compared to the actual bite it self-inflicted.


Water soluble molecules I believe I may have misunderstood water solubility this entire time.

I assumed that water soluble meant that it would literally dissolve in water. It would break down into atoms. A sugar molecule would break its bonds and become something else...

However I must be mistaken because I'm reading about why DNA is spiral shaped and it says that it is to keep the hydrophobic bases inside the spiral to protect them from the water, but keeping the hydrophilic phosphate and sugar molecules on the outside.
I would assume that because these molecules are hydrophilic they would disassociate from each other but this has to be incorrect. What am I misunderstanding about water solubility and what would happen if the bases were exposed to water?

This question really belongs at Chemistry.SE, but I'll give you a quick answer. A substance is soluble in water when its solid form (such as a sugar cube) completely dissolves in water to become a sugar solution. The sugar molecules themselves are unaffected, essentially - instead of all being bound to one another in a crystal, they are now floating around in the water. The proof is in the taste - solid sugar and sugar solutions taste pretty much the same. If the sugar had been broken down into component hydrogen, oxygen, and carbon, it would taste much different!

On the other hand, hydrolysis is what happens when water actually participates in a chemical reaction to break one or more molecular bonds within a certain molecule, breaking it down to two new molecules (or one molecule and an atom, or whatever). While sugar can be hydrolyzed, it requires either very high heat, or the presence of a catalyst such as an enzyme.


Why is the 4.4 kb band barely visible in this HindIII digest of lambda DNA? Why is the 4.4 kb band barely visible?

Also, what is the mass (ng) of DNA in band X if lane S contains 250 ng of digested lambda phage DNA?

First of all, the 4.4 kb HindIII band is derived from the right end of λ DNA, so during storage it anneals to the 23.1 kb left arm fragment via λ's 12 bp cohesive ends. You can solve this problem by preheating the markers to 65°C for a few minutes then cooling rapidly (i.e. on ice).

In a stained gel the intensity of a band is proportional to the amount of DNA in that band. This is why the heavier bands are more intense. The fragment X in lane 2 is similar in intensity to the 0.5 kb λ fragment so DNA content of the two bands is similar.

The amount of DNA in the 0.5 kb band is 250 ng *(0.5/48.5) where 48.5 is the size of wild-type λ DNA. I'll leave it for you to complete the calculation.


What is called the "area size that an animal usually lives in"? What is called the "area size that an animal usually lives in" or "needs for a normal life"? Is there any specific term?

Are you looking for 'Home range' (see also the definition in Encyclopaedia Britannica)? Generally, 'home range' is defined as the entire area an individual animal uses, while the 'territory' is the subset of the home range that is actually defended from conspecifics (in animals that show territoriality). 'Home range' is often delimited by the types of environments used and movement patterns of individuals.


Human Evolution in Modern Times I understand that evolution occurred to form the current hominids from a common ancestor millions of years ago. As evolutionary processes take a long time, is there proof of evolution occurring with humans today?

Yes, there are examples. First: If you want to say, that humans and monkeys evolved, than it is better to say that they evolved from a common ancestor. This makes quite a difference.

If you are looking for examples of human evolution then one of the most obvious traits under evolutionary selection is pigmentation. There is a clear correlation with lattitude (and this UV-index):

The changes in pigmentation occured - seen from a evolutionary perspective - pretty recent when humans moved out of africa and to other regions (see here).
See these papers for more details:

The evolution of human skin coloration
Colloquium paper: human skin pigmentation as an adaptation to UV
radiation.
Epidermal pigmentation in the human lineage is an adaptation to
ultraviolet radiation.

Other examples would be the tolerance for lactose (the sugar contained in the milk) in adults which arose during the last 5-10.000 years. Normally only babies can process these sugar which is contained in large amounts in the mothers milk. When they are weaned, usually the enzyme is not expressed anymore. However with the settling of the humans and the domestication of cattle this changed, so we can still drink milk and eat milk products without producing intestinal problems. See here for more details:

Genetic signatures of strong recent positive selection at the lactase
gene.
Adult-type hypolactasia and regulation of lactase expression.

A third example would be the sickle-cell anemia, which happens due to a point mutation in the human hemoglobin protein. This causes an aggregation of the hemoglobin molecules in the red blood cells which then leads to a reduced elasticity (see here for more details). It also leads to a protection against malaria (most likely by the reduction of the life span of the erythrocytes). The areas with high prevalence of the sickel cell anemia in africa correlate pretty nicely with the distribution of malaria.

An Immune Basis for Malaria Protection by the Sickle Cell Trait
Sickle Cell Anaemia and Malaria

If you look further, you will find a number of different examples, where evolution is present after humans went through a genetic bottleneck (meaning the number of humans was drastically reduced).


Humans have Cannabinoid receptors. Does that mean we're meant to consume cannabis? I know the answer is no. But what then explains the name of these receptors being specific to Cannabinoid found in cannabis? Aren't Cannabinoid receptors exclusive to Cannabinoid? Why are they named like that, if not?

Receptors
Any drug or compound with specific effects has a receptor. You can read about this general concept in Goodman and Gillman's The Pharmacological Basis of Therapeutics. Chapter 1 introduces the concept, chapters 3 and 5 expand further. As far as the history of this concept is concerned, receptors mediating the specificity of action was first clearly articulated by Paul Ehrlich (in the context of dyes and toxins), and further developed by John Langley (and Ehrlich again in response). Cannabis and cannabinoids are not unique in this regard. Illicit and therapeutic drugs of all kinds have a target binding sites (receptors). In almost all cases, these receptors are bound by endogenous compounds as well.
Does having a receptor mean we should consume something?
There was a case to be made that having a great number of receptors that bind psychoactive compounds in cannabis means there is a physiologic role for some cannabinoid (especially given the pattern of expression) and suggested the existence of an endogenous cannabinoid before it was discovered. This was discussed in the nature paper that first identified the receptor and its functional expression and in the science paper that reported the discovery of endocannabinoids. Generally, it doesn't suggest that we are "meant to consume cannabis". Toxins and poisons also have receptors, and we certainly don't want to consume those.
As far as the name is concerned, the comment by @user137 is correct. Receptors are sometimes named by exogenous drugs that activate them, in particular when these compounds are discovered and studied before an endogenous ligand is found. Opioid receptors are another example.


How much time does HIV live outside the body? I'm wondering HIV viability outside the body of an infected person, for example in a knife that contains blood of an infected person, with N virus cells. (N could be for example, 1000).
Some virus might live more than others, then I'm asking the half-life of it.

The general response to that question is not long, the HIV is a weak virus and that once exposed to air, it can survive for maybe a few minutes at best.

BUT Under specific conditions, HIV can survive for a far longer period of time, sometimes for hours or even days if the right temperatures, pH balance, light exposure, and humidity are achieved.  It is a very difficult set of conditions but is nevertheless possible.

Source : How Long Can HIV Live Outside of the Body ?

In certain conditions, the virus can survive outside the body for several weeks.
Survival depends on which body fluid it is in, volume of the body fluid, concentration of the virus within it, temperature, acidity, and exposure to sunlight and humidity.
HIV transmission has not been reported as a consequence of contact with spillages of blood, semen or other body fluids.

Source : HIV transmission & testing, Survival outside the body


How is Glycophorin A and straphylococcal related to Escherichia coli and what does readily purified mean in this context? I am reviewing the paper "Glycophorin A Dimerization Is Driven by Specific Interactions between Transmembrane Alpha-Helices."  There is a statement in the abstract which I don't understand:

"The transmembrane alpha-helical domain of interest is fused to the C-terminus of staphylococcal nuclease.  The resulting chimera can be expressed at high levels in Escherichia coli and is readily purified."

As I understand it, this describes that an alpha-helix within Glycophorin A is fused to straphylococcal nuclease?  Then, how does Escherichia coli come into the discussion and what is meant by being readily purified?

Basically, they engineered a vector which, when transfected to E. coli, produces transcripts of -and thus proteins to- a fusion gene which produces these transmembrane α helices conjugated to the staphylococcal nuclease. In other words, the E. coli are just factories for producing proteins:

  Expression, Extraction, and Purification of SN/GpA - For high
  levels of SN/GpA production, pT7SN/GpA was transformed into E.
  coli MGT7 (kindly provided by D. LeMaster), containing the plasmid
  pLYS-S.

And the reasoning therein was proposed in the discussion,

  We report here the use of a chimeric protein to show that
  the presence of just the transmembrane domain of GpA, fused
  to a normally monomeric soluble protein, is sufficient to
  mediate the dimerization of this artificial membrane protein
  -in SDS

What they mean by readily purified is that the protein can be extracted relatively easily, and in the experimental method they explain some commonplace methods of purification:

  One-step purification of milligram quantities of SN/GpA from the
  extract could be achieved by reversed-phase HPLC utilizing an acetonitrile/isopropyl
  alcohol/water gradient on a semipreparative Vydac
  C4 column. Alternatively, purification of larger quantities was
  achieved using two rounds of cation-exchange chromatography...

  ...The chimera SN/GpA131, but not truncated forms, could alterNaCl,
  50 mM Tris-HC1, 5 mM EDTA, 1 mM PMSF, 0.025% NaNa,
  natively be extracted by sonication of the pellet after cell lysis in 1 M
  pH 7.9, containing no detergent. This extraction was of similar
  efficiency to that with Lubrol, and was utilized in the preparation of
  material for generation of transmembrane peptide by trypsin treatment.


Is this bird a woodpecker? This bugger is pecking on the side of my house. I don’t know anything about birds, but it doesn’t look like your typical woodpecker.

That is a red breasted nuthatch.(https://www.allaboutbirds.org/guide/Red-breasted_Nuthatch/id

Include a location next time,it helps with identification.


Limits of gene editing I was reading some articles about CRISPR and the world of gene editing, but then a lot of questions for which I couldn't find any answer online came into my mind. Those are all about how far can we edit an organism. So here is the general question, followed by some other to narrow down a little bit this broad subject:
What are the limits of gene edition?

Can one edit the genes in its entire body? (as a human, or a multicellular organism)
What are the risks? I heard that some people who did try gene therapy ended up having some of their modified cells turned into cancer. Was is because of gene incompatibility  or because of error during the gene editing process?
Can we go as far as adding some chromosomes or changing an entire chromosome? For example, if a male human would like to change their sex, could they switch all their Y to an X?

EDIT: I decided to accept the answer from @MattDMo. However, I'm still interested in some development (clues with other technologies...)

Your question is very broad, but I'll try to address each of your points briefly.

It would be nearly impossible to edit the genes in every cell of a human being or other complex organism simply due to the number (and accessibility) of cells. A full-grown human has in the neighborhood of 30 trillion cells - 30,000,000,000,000. Cells in locations such as the brain and central nervous system are protected by the blood-brain barrier, which would keep most gene therapy vectors from accessing those cells. There are other reasons why editing each cell in the body is virtually impossible, such as vectors accumulating in the liver, but this is one of the main ones.

Cancer is indeed a risk from gene therapy in general, although DNA editing technologies like CRISPR in particular have a lower risk due to thTe circumstances surround exactly how the therapy is delivered to the nucleus of the cell where DNA resides. Other risks include potentially serious or fatal systemic inflammation due to an immune reaction to the viral vector which carries the CRISPR "machinery". Off-target effects can occur due to the wrong cells being targeted (although this risk is generally lower with CRISPR). Additionally, there is the very small but non-zero chance that the genetically-engineered vector could somehow regain its native infectious capability. Newer generations of gene therapy have significantly reduced this chance, however.

Very briefly, no. DNA is made up of "letters" (A, T, C, and G) called bases or base pairs, and typical CRISPR constructs only operate on 10-20 bases at the most — usually it's just one or a couple that are changed. A typical human chromosome has millions of base pairs encompassing hundreds to thousands of genes, so editing, adding, or removing an entire chromosome is simply out of the realm of possibility with this technology.