Does DNA helicase or topoisomerase actually "unwind" DNA?

Got a short piece of three stranded rope handy? (I don't think they make two stranded rope.) Hold the rope firmly in each hand about 5 cm apart. Twist in the direction opposite the winding. The strands of the rope will separate in the region between your hands. The unwinding and the separation of the strands are, um, inseparable from one another. You can't separate the strands without unwinding.

The heilcase unwinding is merely straightening out the double helix in a very local area. This separates the strands such that one strand can serve as a template for transcription or replication.

But a consequence of the unwinding in the local region where the strands are being separated, is that other nearby regions get more tightly wound. This occurs because the DNA is far too long for the ends to spin around to accomodate this unwinding. These more tightly wound areas are what is refered to as supercoiling. The topoisomerase alleviates this stressful coiling. https://en.wikipedia.org/wiki/Topoisomerase

So, the answer is both helicase and topoisomerase result in the unwinding of DNA.


Two heterozygote mice for skin color are reproduced. Find the probability that in 3 children 2 will be dark and one white

You are on the right track, but you have to keep in mind there are multiple ways to have two dark and one child in a group of three. You have to add the probabilities of each unique outcome that results in two dark and one light child. So, the probability is (1/4) x (3/4) x (3/4) PLUS (3/4) x (1/4) x (3/4) PLUS (3/4) x (3/4) x (1/4)


Free radicals are damaging because their unpaired electrons (or not fully filled valence shell) makes them highly reactive species. They are often considered together with highly oxidizing "reactive oxygen species" (ROS) such as peroxides. They are especially problematic for cell membranes and DNA. In the latter they can react with (oxidize) heterocyclic bases.

As suggested first by Gerschmann et al. (1954), since oxidative damage to cells and cell structures is seen to accumulate with age, the corollary of this could be that aging is a result of oxidative damage. The very fact that cells have antoxidant enzymes such as superoxide dismutase (SOD) suggests that suppression of these species is important in the cell.

Many (but not all) ROS originate from mitochondria during cell metabolism. Therefore, it has been suggested that by regulating metabolism (that is, reducing the metabolic rate) the "rate of living theory" (Harman 1981) the rate of oxidative damage can be reduced. One way to do this may be calorie restriction.

This idea seems to fallen out of favour though. Another possibility is that the rate of mitochondrial ROS has nothing to do with metabolic rate per se; rather it might simply be a longevity determinant.

However, having said all this there is evidence that ROS are actually crucial in a number cellular pathways. It may be that it is the deregulation of pathways managing ROS that can contribute to aging rather than simply damage accumulation with age.

Gerschman, R., Gilbert, D. L., Nye, S. W., Dwyer, P., and Fenn, W. O. (1954). "Oxygen poisoning and x-irradiation: a mechanism in common." Science 119(3097):623-626.

Harman, D. (1981). "The aging process." Proc Natl Acad Sci U S A 78(11):7124-7128.


A summary of what we know so far includes that for B cells to become plasma cells they need BLIMP-1. For memory cells CD40 engaging with CD40L on B cells is required. CD40 is expressed on Th cells and thus they are also necessary for memory cell development. Problem is though, it's really damn confusing after that. It really isn't known but if you're interested in this stuff consider reading this review which talks about memory cell differentiation and this which discusses plasma cell differentiation.

The image below helps (taken from this review)

PC = Plasma Cell, MBC = Memory B cell


Do all animals exhibit comparable reflex velocity?

Simply stated, the reflex speeds of diverse animal species should not be the same. First, even within an individual, signal conduction speeds actually vary between nerves, on a fairly significant range of about two orders of magnitude. Conduction speeds between species, and likely even between individuals, will differ. Second, not all species possess the same reflexes, which can be, in fact, quite elaborate neural events. To qualify speeds for similar reflexes, one must use closely related species. I did find one article that found the pupillary light reflex in monkeys is essentially similar to that of humans, but this information is not sufficient to speak of the similarities between reflexes in general between the species.


Are there verbs for "undergo mitosis" and "undergo meiosis"?

I'm actually not sure myself. If I were to use something, I would go with "Mitos'd" and "Meios'd".

However, you may not win over many fans, depending on the audience. If it's with students or maybe a professor, you could get away with shortening the processes. If it's in any formal setting, be as precise and descriptive as possible. It's not a lot of trouble to be more accurate and add "underwent" to the sentence.


Can some prokaryotic cells be larger than eukaryotic cells?

Prasinophytes are the smallest known eukaryotes. They are around 0.5 µm in diameter.

Thiomargarita namibiensis is the largest known prokaryote. They are around 100-300 µm in diameter.

So, yes some prokaryotes are much larger (up to about 500 times larger) than some eukaryotes.


Integration of several environmental signals

What you are looking for sounds like the mechanism for a fold-change detector. I would recommend looking at these two papers:

The incoherent feedforward loop can provide fold-change detection in gene regulation

As an example of this working in a real system, I recommend looking at the NFkB pathway, as recently detailed by Suzanne Gaudet:

Fold Change of Nuclear NF-κB Determines TNF-Induced Transcription in Single Cells

Here are a few others that I found just by searching for "Fold change detection"

Comparing Apples and Oranges: Fold-Change Detection of Multiple Simultaneous Inputs

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0057455

Efficient fold-change detection based on protein-protein interactions

I'm sure by looking at the referenced papers in the above you can find more examples as well.


Why do neutrophils need to die after pathogen phagocytosis?

Macrophages can certainly phagocytose living cells, as you can read in Sompayrac's "How the Immune System Works", Chapter 1 and 2, but they do need an "eat me" signal of some kind in order to do it. For a bacterium that might be lipopolysaccharide and mannose. For endogenous cells, there is a balance of "eat me" and "don't eat me" signals. Apoptosis, in addition to neatly packaging up potentially toxic intracellular components, involves downregulating the don't eat me signals and upregulating the eat me signals. Macrophages can phagocytose live cells that seem to have some sort of problem (for example, tumor cells), but they are much more efficient at phagocytosing apoptotic cells.

As far as why the neutrophil has to die, in addition to making them more efficient targets for phagocytosis, they die pretty quickly anyway. There is some debate about the exact length of their life span, but from the time they're released by the bone marrow, the average circulating life span is probably less than 24 hours, regardless of whether they exit the blood stream as part of an inflammatory process or not. The exact function of this short lifespan is the source of some speculation, but we do know that, after being recruited in the inflammatory response, apoptotic neutrophils help suppress that inflammation, playing an important role in regulating the processes that sent them out into the tissue in the first place.

Sompayrac's book is a good overview, but if you want to read the gory details this is a good review.


Non competitive inhibitors and Uncompetitive

I am not really sure to understand completely your question, but both non competitive and uncompetitive inhibitors affect the rate (Vmax) of the reaction by decrease it. In fact in both case, the enzyme (E) takes longer to transform the substrates (S) in to products (or to release it).
To better allow you understand I put below two mechanism of action for uncompetitive inhibition and non competitive inhibition.
Uncompetitive inhibition

Uncompetitive inhibition is unique in that the inhibitor binds to the enzyme-substrate complex. This could imply that the binding site for the inhibitor is accessible only after the enzyme has bound to its substrate. This reduction in the effective concentration of the E-S complex increases the enzyme's apparent affinity for the substrate through Le Chatelier's principle (Km is lowered) and decreases the maximum enzyme activity (Vmax), as it takes longer for the substrate or product to leave the active site.

Non competitive inhibition

Non-competitive inhibition models a system where the inhibitor and the substrate may both be bound to the enzyme at any given time. When both the substrate and the inhibitor are bound, the enzyme-substrate-inhibitor complex cannot form product and can only be converted back to the enzyme-substrate complex or the enzyme-inhibitor complex [...]
This type of inhibition reduces the maximum rate of a chemical reaction without changing the apparent binding affinity of the catalyst for the substrate.

Hope this could help.


When a fungal spore germinates in a suitable location, the growing mycelium will spread underground in all directions. In the ideal situation, the result is that the mycelium will become circular. Over time, the center of the mycelium will die out whereas the newly formed mycelium (underground) will develop the familiar mushrooms above ground and this will result in a fairy ring.


For how long can a raven stay airborne (a week or more)?

Can't be very sure about ravens but the maximum recorded flight duration is of Common Swift — 10 months.
Alpine swifts also remain airborne for up to 6 months.

Pigeons can fly up to 1800km in a long flight. From this article (pubmed):

  In the United States, the longest pigeon races involve flights of 1800
  km and, because substantial financial rewards accrue to the owner of
  the fastest pigeon, there is severe selection for those pigeons that
  home the fastest.

Wikipedia article on pigeons says that they can fly at 80km/h but I suspect because the other wikipedia page on flight speeds says that average flight speed of peregrine falcon is 65-90km/h. So assuming that average speed of pigeon is 60km/h it should be able to fly for 30h. According to this paper, the speed with minimum power consumption is 8-9m/s (~30km/h). At this speed they should be able to fly for 60 hours. In the same paper it is estimated that the maximum continuous power output is ~10.5 W; if a pigeon has 11g of stored fat (per 400g body weight — assumptions from the same paper), and given the calorific value of fat — 38kJ/g, it can fly upto 38 × 11 ÷ 10.5 = ~40h. This means that the best trained ones can perhaps manage to fly for 2.5 days straight.

Now ravens are heavier (~3 times heavier) but are more aerodynamic and can fly faster. However, I guess they cannot perhaps fly 7 days straight.


Are genes known or at least conjectured to evolve cyclically ?

Welcome to Biology.SE Sylvain!

  I observed recently that some people born the same year in not too distant areas (say, in the same country whose size is not too big, like France) share similar phenotypical features, for example they look like each other though they are not of the same family.

You are likely doing a confirmation or some kind of extended Barnum effect.

You will need to provide a rigorous study for this claim and not just a vague feeling you're having.

  If confirmed, [..]

This piece of sentence suggests that you agree with my previous comments. We expect the OP to provide reference for a claim on which the question lies. One cannot ask "Why do elephants have such a huge genome?" without providing an evidence that they do have a huge genome.

  [..] this would suggest that some alleles are more common within a given period,

If there is such effect it is much more likely caused by shared environment than by shared genetic. Have a look at this post to understand the underlying sources of phenotypic variance.

  and hence that the global evolution of the human genetic pool could be statistically determined.

Sure, it can but this is not a consequence of the above supposed observation nor by the above hypothesis for the supposed observation.

Of course, specific processes could cause some cyclic process in evolution. A population overshooting carrying capacity could go under an oscillatory behaviour around this carrying capacity. As population size affects genetic diversity, such cyclical behaviour can have some impact. However, this is quite negligible. Also, there might be fluctuating selection (typically fluctuating on a seasonal basis) but this tends to be rather negligible for species of long lived individuals. I am sure you can think of some complex mechanism in structured populations would could yield to some oscillatory behaviour as well.

  One can go one step further and see the considered genetic pool in a given range as a quantum-like system governed by some kind of Schrodinger's equation. I think here of a theoretical framework like Laurent Nottale's scale relativity that could explain these similarities.

I don't understand that part. I know pretty much nothing in quantum physics (have basic understanding in general relativity but not in Nottale's attempt to merge relativity and quantum physics). You might need to expand your thoughts I guess if you want biologists to understand where you're heading. However based on the above, I suspect, there is no reason to think this cross-talk would matter in any way.

  Have such questions been considered so far?

I doubt so, because I don't think any of it makes much sense (no offense).


Why do people look different after a long sleep?

Puffy eyes are caused by fluid build up in tear ducts from extended periods of lying down. Gravity from sitting or standing slowly drains them during the day. The crusty 'sleep' that accumulates in the corner of your eyes is the residue from basal tear liquid that has seeped out of the eye and evaporated during the night.


Help in identifying an unknown arthropod

It is the larva of household casebearer moth (a Lepidoptera), named after the larval stage. It is scientifically called Phereoeca uterella.

It is found through out South and North America.

  The larva constructs a protective case from silk and camouflages it with other materials such as soil, sand and insect droppings.

References:

Wikipedia
bugguide

Further reading: Household Casebearer, Phereoeca uterella by
Juan A. Villanueva-Jimenez and Thomas R. Fasulo


Is there a way to determine how many times a given cell divided?

Yes, its called the HayFlick limit. A cell will divide until their telomeres reach a critical length,which is usually around 40 to 60 cell divisions. The cells then enter cellular senescence and cease to divide. However, cells may also stop dividing due to (ROS) or reactive oxygen species, cell to cell fusions, or activation of oncogenes, the latter of which is a gene that has the potential to cause cancer.


I'd like to know the name and a few details of a certain time-keeping structure in the human brain

You are probably referring to the suprachiasmatic nucleus.

Note that, although this is the central clock, there are also so-called "peripheral clocks", for instance in the liver, pituitary and other organs that can finely tune rhythms in the organism.

You may also want to have a look at the Wikipedia page for circadian clock and references therein.


Yes, and a quick search for viral in-vitro assembly will turn up tons of results. — it's a little more complicated than that! — but it's not usually done as such, which I will explain.  Basically, there are four things you might want to do:

You want to make large amounts of virus and study it. If so, then all you need to do is infect your cell culture with your virus and let it replicate.  Some are obviously easier than others — from my own experience, HIV is pretty easy but Hepatitis C is a real PITA — but that's essentially it.  This obviously presumes you already have some virus stock on hand for infection.  You could also transfect the culture with full-length viral plasmids, which leads me to...
You want to study some specific aspect of the virus.  That's cool!  Most people aren't just concocting virus.  Generally, for viruses that humans can get, it's generally recommended/heavily encouraged to only use what you need for safety reasons.  So, for example, you might transfect the one protein you think is important to see what it does by itself.  After that, you might transfect the cell culture with the full virus, but with one important gene knocked-out.  I used to make single-round HIV by using a plasmid for full-length HIV without a functioning envelope gene and another plasmid for VSV envelope; new HIV particles would be made infectious because of the VSV gene but after infecting they no longer had that gene anymore.  Basically, a limited version of the virus, which leads me to...
You want to make virus-like particles.  These are one of the better-named things in science and are just what they sound like — particles that look a lot like virus, but aren't.  Generally, they're empty shells.  We can use these for all sorts of things, from vaccine studies to other genes and diseases.  Techniques can vary, but generally it's similar to the above.
You want to introduce some other gene to a cell culture system, using a virus backbone for transduction; think "I want to fix these cells... permanently."  Generally, these viruses are usually based on adenovirus or lentivirus (aka HIV) because they will insert their genes into the cell's genome, so the gene will persist.

Item 4 is probably closest to what you specifically meant.  Here's a free review on the use and safety of retroviral vectors in humans, and here's a nifty one in fish.  As for which viruses it's applicable to, well, that varies a lot by virus, host, culture system, and so on.


This appears to be a bird mite (or possibly rat mite) in the genus Ornithonyssus of the parasitic family Macronyssidae.

 Credit: user Aewills on bugguide.com

Identification:

From Central Exterminating Co.:

  The mites are distinguished from most other common, structural species by the very long legs and very long mouthparts. These long, pointed chelicerae and palps stick well out in front of the head region. The 8 legs are very long and well separated, allowing for good mobility by these mites. The body is oval, with the thorax and abdomen combined to a single segment without separation. The color is light grayish in unfed mites to reddish orange in mites recently having had a blood meal. The fowl mites often seem to have a patchy, mottled appearance of dark areas.

Distinguishing between species is difficult.

Blaine Mathison mentions the following features useful for identifying these mites to lower taxonomic levels under magnification [source: bugguide.com]:

chelicerae shape
dorsal plate breadth and degree of dorsal coverage
spiracle present between legs
genitoventral plate width
sternal plate shape and presence of setae

(see the linked post for pictures and more detail).

You can see videos of these mites crawling on people here and here.

Regarding their affects on humans:

From Penn State Extension:

  Bird mites have piercing mouthparts that enable them to take blood meals from their
  bird hosts. Although the mites will inadvertently bite people, they cannot reproduce without their bird hosts...

  As the mites search for an alternative host, they will crawl onto the skin and conduct an exploratory bite to test the appropriateness of the host. The mite will move on, possibly trying the host again, but will not feed. These bites are felt as a “prick” and a resultant rash and itching, sometimes intense, will occur. Some individuals are apparently capable of sensing the crawling of the mites on the skin. The irritation produced by the bite is enhanced by the injection of the mite’s saliva that can cause a localized histamine
  response.

Management:

Remove birds (and especially nests) from on or near the building. Check for any holes in your building that could be large enough to allow birds inside. Again, these mites need birds to reproduce, so if you eliminate the birds eventually these will disappear. See PSU Extension and Central Extirminating Co. for more suggestions.


Confusion regarding niches in evolution theory

I think part of the confusion is that these terms are very loosely defined.  Also this discusses evolution in terms of taxanomic radiation, e.g. macroevolution at large spatial and temporal scales.

Problem 1 is that you haven't been clear about what kind of competition, inter or intraspecific competition?  These will have opposing effects generally which can counter balance each other [1]
[2].  When a species is free from interspecific competition, but under high intraspecific competition, that will promote an adaptive radiation, which concurrent morphological changes.  The most famous example of this would be Darwin's finches as studied by the Grants [3].  With a lack of interspecific competition, the finches exhibited rapid morphological divergence.  Following the logic of this, you'll see that lack of competition will lead the kind of rapid taxanomic radiation the video is discussing, especially over a longer time scale.

However increased interspecific competition will have two effects. It will reduce the number of available niches for an existing species to expand into [4], this generally will drive specialization of a species, which tends to limit genetic diversity which will lead to less "raw material" for evolution to work with. This specialization though is also technically evolution.  However with fewer niches, the new species tend to arise via replacement of existing species in an existing niche, as opposed to an adaptive radiation.

So you can see how actually both conclusions are right depending on the type of evolution and competition being considered.

More interspecific competition -> More specialization (one type of evolution), less adaptive radiation (another type of evolution)

More intraspecific competition -> More adapative radiation, less specialization.

I hope that helps answer your question.


The short answer is crocodiles may be secondarily cold blooded, but the long answer is warm blooded and cold blooded is not a binary condition but a spectrum.

It has to do with how much heat you generate with your own tissue as all organisms generate some heat and gain some from the environment when they can. on one end you have extreme ectotherms (some insects) at the other extreme endotherms (such as arctic mammals) and a huge range between them covering nearly every level of metabolic activty. The ancestors of crocodiles (Crocodylomorpha) were terriestial and highly active and was thus likely near the warm blooded end of the spectrum and thus with a four chambered heart. They actually look like what you would get if you tried to turn a crocodile into a wolf.  But it is believed that as the line that led to modern crocodiles adapted more for an aquatic environment they switched back to a more ancestral metabolism. Although  I should mention crocodiles and esspecally alligators are capable of producing considerable metabolic heat and activity even for prolonged period, more than other "reptiles", comparable to slowest metabolism mammals. they kep many anatomical adaptation to a higher metabolism as they also aid in diving and still benefit their higher metabolisms.


How does the mechanism which controls blood pressure in the brain work?

Blood pressure is sensed in blood vessels by baroreceptors. Baroreceptors are stretch-sensitive nerve fibers located primarily in the aortic arch and carotid sinuses. The baroreceptors send afferent fibers via the glossopharyngeal nerve to the nucleus tractus solitarii in the dorsal medulla in the brainstem. From there, efferent cardiovascular neurons send projections to the medulla and spinal cord. There are also stretch-sensitive receptors in the heart and pulmonary vessels, called cardiopulmonary receptors that use the same nerural connections as the baroreceptors.

The baroreflex loop results in activation of sympathetic or parasympathetic fibers to the heart, the smooth muscle of the peripheral blood vessels, and other organs such as the kidney to maintain arterial pressure at normal levels.

In a simplified scheme, increased pressure stimulates baroreceptors, which attenuates the sympathetic outflow to the peripheral vessels and the heart, restoring pressure to normal levels. The parasympathetic influence will dominate which is mediated by acetylcholine. Conversely, a decrease in pressure relieves the baroreceptors and increases sympathetic outflow. Sympathetic activation causes a release of noradrenaline that leads to vasoconstriction and increased cardiac output and hence an increased blood pressure (see Fig. 1).

Fig. 1. Control of blood pressure. Source: Human Physiology (2011).

Reference
- Cougias et al., Med Sci Monit (2010); 16(1): RA1–RA8


I think this is a Barbary dove (or Ringneck dove). See this image (from the here):

More information can be found here and here. The second pages shows also images of different color variations.


Book request: systematics and evolution of vertebrates

I really like Liem et al.'s Functional Anatomy of the Vertebrates: An Evolutionary Perspective.


Flybase is a generally useful source for Drosophila anatomy/physiology including the nervous system. From there I found this link which has some neuroscience-specific info.


What species is this bird (found in Cousset, Switzerland)?

This is really hard to tell given the quality of the picture. What size was it?

Could be Emberiza citrinella, the so-called yellowhammer - a year-long resident in Switzerland. It is about 16 cm in size and its breeding season starts beginning to mid-April and males are advertising for females in a golden plumage.

Again, this is only a best guess and without a better quality image it can never be more. RHA pointed out in the comments that the head of the bird in your image appears to be darker than one would expect in E. citrinella, suggesting it could also be E. melanocephala - the black-headed bunting, Spinus spinus - the Eurasian siskin, or Serinus serinus - the European serin. But consider this:

The bird on your picture appears to have a somewhat dark head but it does not seem to be black (but with the resolution it is hard to tell). E. citrinella males have brown stripes on their head that can be more or less pronounced (see examples in Google search for yellowhammer) - blurred, this fits the brown head in your picture.
In your comment, you give the bird's size as the size of a house sparrow which exactly fits E. citrinella.
E. melanocephala males have a pitch black head and the range it can be found does not fit your location. There are reports of vagrants but in combination with the brownish head in your picture this seems somewhat unlikely to me.
Sp. spinus and Se. serinus are smaller (max. of 12 cm in length) than what you describe.
Se. serinus is a partial migrant in Switzerland which decreases the probability of finding it in April, compared to a year-long resident. Additionally, it also only has brown stripes on its head.

In summary, I think the the most parsimonious call is that the bird on your picture is E. citrinella. However, keep in mind that it could also be one of the other species mentioned above, with E. melanocephala - given your size description and the dark head - perhaps being the second most likely identification.


How can some animals see ultraviolet or infrared light?

Short answer
In mammals dedicated UV cones have been found, as well as photoreceptors with secondary peak-sensitivity in the UV range. In fact, human blue cones are sensitive to near-UV.

Background
In humans, the visible spectrum is generally accepted to range from 390 to 700 nm. Figure 1 shows the spectral sensitivities of the various photoreceptors in humans.

Fig. 1. Spectral sensitivity of the four receptor classes. Source: Wikibooks; Sensory Systems

In invertebrates sensitivity to near-UV is quite common. However, some rodents (mice, gerbils and gophers) also feature a peak in sensitivity at 359 - 511 nm. In these rodents and some marsupials sensitive to UV, it is thought to be attributable to a specific dedicated type of cone sensitive to near-UV (Jacobs et al., 1991; Winter et al, 2003). Near-UV is referred to as UV-A, encompassing 315 - 380 nm.  Likewise, birds seem to feature a dedicated, fourth cone class to detect UV (Benett & Cuthill, 1994).

In the color-blind flower bat, UV sensitivity has been attributed to a photoreceptor with two peak sensitivities - one in the green range and the other around 365 nm and running down to 310 nm (Winter et al, 2003). Hence, UV sensitivity can be conferred by cones with broad sensitivities ranging into the UV range.

In fact, the aphakic human eye (eyes with the lens removed after cataract surgery are aphakic) has been shown to be sensitive to near-UV. As can be seen in Fig.1, the blue cones are actually pretty sensitive to near-UV. It appears that the lens absorbs much of the UV, rendering UV light useless to humans with healthy eyes (Griswold & Stark, 1992).

Infrared (IR) sensitivity in snakes is mediated by pit organs and not via the eyes. Basically they are heat sensors and likely don't mediate vision as such (Newman et al., 1982). I was not able to find any relevant information on IR vision, or how it should be mediated. In fact, I doubt IR is used for vision at all, i.e., to reconstruct the visual scene. IR vision is used more in the form of general heat detection.

References
- Benett & Cuthill, Vis Res (1994); 34(11): 1471–8
- Griswold & Stark, Vis Res (1992); 32(9):1739-43
- Jacobs et al., Nature (1991); 353: 655-6
- Newman et al., Sci Am (1982); 246(3): 116-27
- Winter et al, Nature (2003); 425: 612-4


It may never have happened again, however, since all lifeforms on Earth today are similar on a molecular level (DNA), suggesting a common origin.

An important distinction to make here is that all extant life on Earth has a common origin.

It's completely possible that abiogenesis occurred many times, but whatever organisms emerged as a result became extinct early on or are not preserved in the fossil record.

  Immediately after the first spontaneous abiogenesis, environmental conditions on Earth changed dramatically, making a repeat impossible.

Nope. The red bands and subsequent dating techniques suggest it took a very long time for a change to occur.

  The first organisms that arose consumed any subsequent organisms...

Possible, but we have solid data suggesting the first functional organisms were autotrophs. That is, they made their own food from whatever they were exposed to, and the predator/prey relationship had yet to play a major role.

  The common origin theory is in fact false, despite the similarities between organisms, and abiogenesis did occur multiple times in the same way.

The Common Origin Theory - as you've defined it - is almost certainly true. DNA is a constant, as is RNA, mitochondria, etc.

That, however, doesn't mean abiogenesis couldn't have happened more than once. As I said above, the Common Origin Theory applies to extant (living) species, not necessarily all organisms that have ever existed. Species go extinct all the time.

  Spontaneous abiogenesis never occurred on Earth after all because the conditions never allowed it; instead, a proto-organism arrived on Earth from a planet where the conditions do (Panspermia).

That merely pushes the question of abiogensis back a bit. Why did it evolve on another world and not Earth, then? How did it survive in space? Why was it so well suited to Earth's environment if Earth-like planets are (relatively speaking) rare?

  The standard theory of geological history is wrong (i.e. the Earth was in a "fertile" state for much longer before the eventual origin of life than commonly thought, due to some unknown mechanism causing radiometric dating to give wrong results).

Estimations and conclusions have come from more than radiometric dating. We have fossil records, geological records spanning continents, and even ice-core records from the poles that both confirm radiometric dating and establish themselves as independent evidence.

  None of these seem likely to me, yet even less likely I find the idea that life arose spontaneously almost immediately (within a few hundred million years, possibly even faster) after the Earth's crust solidified, and never again afterwards.

Why?

  What are the currently held theories on that matter? Both random speculations and references to relevant publications are welcome.

This SE is not the place for random speculations. I don't have publications handy, so I may return and edit my answer when I have the impetus.

The most widely held theory is that all extant life, with a few possible exceptions, has evolved from a single organism that existed billions of years ago. That organism may or may not have been the only one to arise. If it was one among many variations of progenitors, we have yet to find the progenitors in the fossil or biological records. Given the extremely long time span between now and the beginnings of life, we don't expect fossil records to exist of all the organisms that existed some 3 B.Y.A. so the best we can do is speculate on what might have existed to account for what we see today.


Optimality theory

Optimality theory is a concept of linguistic. See wiki > Optimality theory. This is probably not what you were referring to.

What is optimality

Optimality is the condition under which something is maximized! In behavioural ecology, this something is often fitness and the condition is often measured in terms of magnitude/intensity of a behaviour.

Optimality models

In ecology, we call optimality model any model that separate the benefits and costs (in terms of some measurement, often fitness) of a given phenotype (often behaviour). By weighing benefits and costs one can figure out what is the optimal phenotype. The principle is extremely simple. Such graphs are quite standard:

In the graph, the X-axis represents the magnitude of a phenotype (often a behaviour) and the Y-axis represents the benefit and cost of this behaviour (with the same scale) often in terms of fitness.

By definition, the fitness is maximized when $B-C$ is maximized. In other words, compute B-C and look for the maximum (through derivation) and you found the optimal phenotype (often behaviour). In the above graph, the optimal phenotype is a little bit left to the position of the B label.

Optimal foraging theory

Foraging behaviour has been subject to much investigations using optimality models. We refer to this body of knowledge as Optimal foraging theory.


blue/white screening - results are opposite as expected

Given the fact that the negative control uncut plasmids are producing white colonies, it seems that there have been significant mutations within the lacZ gene in the plasmid, causing the uncut plasmids to become white due to inactivation of the gene.

I would suggest purchasing a new batch of pBluescript, or if that is not possible for whatever reason, perform a miniprep on one of the blue colonies and sequence its multiple cloning site to verify that the MCS is present and not mutated before continuing. If you are not going to buy a new batch of plasmids, it would also be prudent to verify the plasmid's length using gel electrophoresis.

The most likely explanation is that the plasmids are mutated, and therefore you are getting bad results in the blue/white screen.


fastq-dump can write to stdout ; the -Z option allows you to do that. This, you can pipe to any downstream process. [An example]. Also see the SRA-toolkit manual.

I guess someone asked this question in biostar too.


The fingers and toes (for example) ARE at lower temperatures than the interior of the torso.  It's why it's so easy to get frostbite on the extremities. As for temperature regulation of the testes, you have to also consider that humans evolved without clothes...i.e. The testes just "hang out" and get lots of airflow, as opposed to modern times, when they are typically under (usually) more than one layer of clothing.

Also, for reference, I took some quick IR temp readings on myself:

Room temp: 19.9C

Fingertip: 27.0C

Palm: 31.8C

Axilla: 34.6C


Is there an "evolutionary species similarity calculator"?

Since the simple value of percentage of nucleic acid identity over whole genomes isn't very useful in taxonomy, you won't find these values published in a database, even if they were computed by someone in the process of other work.

One project that provides ready-for-consumption phylogenetic trees based on similarity metrics, by using orthologous genes between species, is OMA. They compute all orthologous genes between two species, and they are now at 1,235 species:

http://www.biorecipes.com/Orthologues/status.html

You could then read off the "distance" between cat and mouse from the eukaryotes tree. This value would then be more meaningful than the nucleic acid identity percentage.

Apart from the trees, using their OMAbrowser you can get for any species pair the number of common orthology groups, i.e., the number of common genes between those two species.


The Raynaud phenomenon is a recurrent vasospasm that is associated with cold temperatures and emotional stress [1]. Excessive vasoconstriction leads to hypoxia. The cause of vasoconstriction is a hyperactivation of the sympathetic nervous system [2] and probably the lack of parasympathetic response. The mechanism is thought to involve both central neural issues and peripheral impairment (subclinical polyneuropathy) [3]. The resulted chronic hypoxia leads to pain, atrophy and sometimes even ulceration [2].

References:

Bakst R, Merola JF, Franks AG, Sanchez M. Raynaud's phenomenon: pathogenesis and management. J. Am. Acad. Dermatol. 2008 Oct;59(4):633-53. doi: 10.1016/j.jaad.2008.06.004. PubMed PMID: 18656283.
Wikipedia contributors, "Raynaud's phenomenon," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Raynaud%27s_phenomenon&oldid=613954124 (accessed June 27, 2014).
Koszewicz M, Gosk-Bierska I, Jerzy G, Bilińska M, Podemski R, Budrewicz S, Adamiec R. Peripheral nerve changes assessed by conduction velocity distribution in patients with primary Raynaud's phenomenon and dysautonomia. Int Angiol. 2011 Aug;30(4):375-9. PubMed PMID: 21747356.


Why is the human body able to repair a broken bone and not a heart muscle?

Part of the answer may be(*) that in bone, you have still stem cells everywhere (blood capillaries that grow until checked and osteoblasts), i.e., also in the vicinity of the wound. The same applies to skin, by the way, where the epidermis continues to produce skin layers until eternity. This facilitates repair enormously, as new cells won't have to move far to take their place.

Contrast this with heart or spinal cord, where the placement of the cells took place in early development when distances were small and most cells were undifferentiated. Also, no tissue like epidermis was left in the vicinity that could act as a near source of new cells.

(*) I said "may be" because 1. I have no ref for this, and 2. I have no idea to what extent other factors are involved. I would be thankful for counterexamples.


How are chromosomes counted at the end of mitosis in a plant cell?

I think I know what is confusing you.
A chromosome can have one or two chromatids. If you have two chromatids, you don't necessarily have two chromosomes. This is what happens during S-phase, during replication. Before the S-phase each chromosome had one chromatid, after the replication, it has two. So the number of chromosomes stays the same.

In the karyogram (the picture with all chromosomes), each object is one chromosome. Usually those will be double-chromatid chromosomes, and you will see a nick (like here). After these chromosomes divide, you get two separate objects → two identical chromosomes.


I suggest you to take the tutorial you can found from here
Before the $(-;-)$ there is the specific location of the gene in the DNA. Between the brackets you have your specific genotypes at the location marked before. So, whatever is inside the brackets is referred to a single nucleotide polymorphism (SNP) found in your gene. If there is nothing, as the case of the screenshot that you provided, is possible that they are not able to determine the SNP (so the SNP is not found and this information is missing).


It is possible to perform gene-level population genetics analyses on microbiome-derived bacterial species.1,2 † However, the biology of bacteria and the nature of metagenomic sequencing data make such analyses difficult and intractable to many of the well-worked tools of population genetics. Here are some of the things you should keep in mind as you build a conceptual framework for understanding the field:
Bacterial genomes are flexible
The term "allele" connotes gene variants, and the underlying assumption of analyses involving alleles is that each (diploid) individual in a population has one or two alleles of a given gene.  When considering a bacterial population, specifically all the cells that constitute a species, some genes will not be present in all cells. For this reason, "allele" is not frequently used in discussions of complex bacterial communities.  For well-studied species like E. coli and K. pneumoniae with many complete strain genomes, plotting the number of genes found across genomes gives a characteristic U-shaped distribution.3  For a given species, this suggests that many genes are present in most strains, and many genes are present in only one or two strains.  The simple thing to do is to constrain your analysis to the gene set that you observe to appear in all ‡ individuals in a population (the core genome, to use a pangenomics term), but this likely excludes genes that are important for niche-specific fitness like virulence factors, antibiotic resistance genes, carbohydrate degradation operons, etc.  Recently, this problem has been addressed computationally by representing pangenomes as weighted graphs with genomic features at nodes 4 and by building composite reference genomes from strain genomes data encoded as reference graphs.3 #
Metagenomes are messy (but getting cleaner!)
Horizontal gene transfer is likely a frequent occurrence in microbiomes,5 confounding analyses that rely on strict inheritance. Since microbiome sequencing is often short-read, the problem of horizontal gene transfer is exacerbated by the difficulty in reliably assembling transferred genes with specific metagenome-assembled genomes.  As noted by Maximillian Press, there are several ways to address this issue. At the bench, proximity ligation sequencing can supplement traditional metagenomic assembly-by-alignment using the ground truth of physical closeness.5,6 Likewise, single-cell isolation combined with multiplexed whole-genome amplification greatly reduces complexity of assembly.7  At the computer, sequence composition (i.e. kmer content) and coverage profiles can be leveraged to associate metagenomic contigs in bins,8,9 which are like pseudo-genomes.§ If you're lucky enough to have long-read sequencing data, many of the problems associated with assembly of short reads are no longer an issue,10 with the added bonus that SMRT and nanopore sequencing produce methylation data -- unique methylation profiles can be used to infer which contigs likely belong to the same genome or to associate extragenomic contigs (e.g. plasmids) with their hosts.11,12  All of this to say that getting complete genomes from microbiome sequencing is non-trivial, but there are many techniques and tools at your disposal.
Microbiome data is relative
Much of population genetics deals in counted data -- $n$ individuals with allele $a$, $m$ individuals with allele $b$, and so on. Concerning microbiomes, the absolute abundances of individual microbes are not recoverable from sequencing alone. Microbiome data is therefore said to be compositional.  Like RNA-seq, gene or organism abundances derived from metagenomic sequencing are relative, and, importantly, many of the assumptions underlying the statistical analyses applied to absolute counts do not hold for compositional data.13,14  Thankfully, statisical tools for population-level analysis of microbiomes have been developed,15,16 though their widespread adoption has been slow.
Microbiome members are often interdependent
As hinted at in the question update, bacteria display a type of community altruism, where an individual cell with a specific gene can influence the fitness of neighboring cells that lack the gene.  For an example, see my answer to Will all bacteria become resistant against all antibiotics in the long term? concerning secreted β-lactamases.
Therefore, spatial association is an added factor when considering population dynamics of a genetically heterogeneous bacterial species.  Some methods that address cell-cell spatial proximity in microbiomes include sequencing of cryofractured fragments 17 and probe-based spectral imaging.18 Even if microbes are not spatially associated, different microbes may play complementary roles in the iterative metabolism of large carbohydrates into small metabolites.19,20
Surely, this discussion is incomplete, though I hope my answer has given you the footing you need to continue your own exploration to find the appropriate resources for your research.  For a more in-depth discussion of the points I've addressed here, see What Is Metagenomics Teaching Us, and What Is Missed?,21 particularly the sections titled Strain-Level Analyses and Ecoevolutionary Modeling.

† I recommend keeping up with the publications of Ran Blekhman, Peer Bork, and Katie Pollard.
‡ Core genome membership seldom requires that 100% of individuals represented by that genome contain the gene in question, and setting such a strict cutoff would likely exclude truly essential genes that were not found associated with a given strain due to gaps.  In practice, core genome cutoff thresholds are on the order of 90%.
# The senior author for reference 3 made a great explanatory Twitter thread.
§ Contigs and Bins and MAGs, oh my! As with any field, metagenomics has field-specific jargon. Coursera seems to have a good lecture that includes these concepts and how they relate to eachother.

References

Garud NR, Pollard KS. Population Genetics in the Human Microbiome. Trends Genet. 2020 Jan;36(1):53-67. doi: 10.1016/j.tig.2019.10.010.
Priya S, Blekhman R. Population dynamics of the human gut microbiome: change is the only constant. Genome Biol. 2019 Jul 31;20(1):150.
Colquhoun RM et al. Nucleotide-resolution bacterial pan-genomics with reference graphs. bioRxiv 2020.11.12.380378.
Gautreau G et al. PPanGGOLiN: Depicting microbial diversity via a partitioned pangenome graph. PLoS Comput Biol. 2020;16(3):e1007732.
Kent AG et al. Widespread transfer of mobile antibiotic resistance genes within individual gut microbiomes revealed through bacterial Hi-C. Nat Commun. 2020 Sep 1;11(1):4379.
Stalder T et al. Linking the resistome and plasmidome to the microbiome. ISME J. 2019 Oct;13(10):2437-2446.
Chijiiwa R et al. Single-cell genomics of uncultured bacteria reveals dietary fiber responders in the mouse gut microbiota. Microbiome 8, 5 (2020).
Alneberg J et al. Binning metagenomic contigs by coverage and composition. Nat Methods. 2014 Nov;11(11):1144-6.
Kang DD et al. MetaBAT, an efficient tool for accurately reconstructing single genomes from complex microbial communities. PeerJ. 2015 Aug 27;3:e1165.
Kolmogorov M et al. metaFlye: scalable long-read metagenome assembly using repeat graphs. Nat Methods 17, 1103–1110 (2020).
Beaulaurier J et al. Metagenomic binning and association of plasmids with bacterial host genomes using DNA methylation. Nat Biotechnol. 2018;36(1):61-69.
Tourancheau A et al. Discovering and exploiting multiple types of DNA methylation from individual bacteria and microbiome using nanopore sequencing. bioRxiv. 2020.02.18.954636.
Tsilimigras MC and Fodor AA. Compositional data analysis of the microbiome: fundamentals, tools, and challenges. Ann Epidemiol. 2016 May;26(5):330-5.
Gloor GB et al. Microbiome Datasets Are Compositional: And This Is Not Optional. Front Microbiol. 2017 Nov 15;8:2224.
Shi P et al. Regression analysis for microbiome compositional data. Ann. Appl. Stat. 10 (2016), no. 2, 1019--1040.
Kurtz ZD et al. Sparse and compositionally robust inference of microbial ecological networks. PLoS Comput Biol. 2015 May 7;11(5):e1004226.
Sheth RU et al. Spatial metagenomic characterization of microbial biogeography in the gut. Nat Biotechnol. 2019 Aug;37(8):877-883.
Shi H et al. Highly multiplexed spatial mapping of microbial communities. Nature. 2020 Dec.
Kundu P et al. Species-wide Metabolic Interaction Network for Understanding Natural Lignocellulose Digestion in Termite Gut Microbiota. Sci Rep 9, 16329 (2019).
Selber-Hnatiw S et al. Metabolic networks of the human gut microbiota. Microbiology. 2020 Feb;166(2):96-119.
New F, Brito IL. What Is Metagenomics Teaching Us, and What Is Missed? Annual Review of Microbiology. 2020 74:1, 117-135.


Why does the rabies virus have such a long incubation period?

This question may not be particularly answerable.

The only available information about this specific case is in the original article (Shankar et al. Ann Indian Acad Neurol. 2012 Jul-Sep; 15(3): 221–223. doi:  10.4103/0972-2327.99728); they say only:

  The anatomical site of viral latency and the mechanism of reactivation of rabies, a neurotropic virus, remains an enigma to be unraveled.

Other reports in the literature of long incubation periods (>7 years, the previously reported maximum seems to be 14 years) are scattered/old/speculative, e.g. Gavrila et al.  Ann. Inst. Pasteur 1967 Vol.112 No.4 pp.504-15:

  Discussing these cases of prolonged incubation periods, the authors point out that in rabies the incubation period can vary within very wide limits and that it is possible in areas where the disease is enzootic that, in very exceptional cases, the disease can develop after an incubation period which may sometimes greatly exceed the maximal limits now admitted, and that, as for example in cats [this Bulletin, 1965, v. 62, (1106)], stress conditions and so forth may lead to the generalization of the virus until then quiescent at the point of entry.

Plotkin 2000 Clinical Inf Dis 30:1 says

  the reasons for this long latency are unknown ...
   in the absence of specific prophylaxis, the virus becomes hidden, only to invade the CNS weeks, months, or years later. Where is the virus during this period? There is some evidence for slow replication in muscle cells and for latency in macrophages, but there is no certainty that these account for the long incubation periods.

There has been an experimental study on skunks (Charlton et al. Acta Neuropathologica June 1997, Volume 94, Issue 1, pp 73–77) that suggests there is some infection of muscle cells at the injection site, but otherwise not much is known about the mechanism.

I would guess that vaccination would be effective if it were administered soon enough, but it will probably be hard in these surprising cases to identify the disease soon enough.


Questions of the type, "why does organism X have feature A?" invite teleological (just so) explanations which are difficult to substantiate. For example, the number of teats on a cow are difficult to explain in terms of providing milk to humans!

We should look to evolutionary history to explain human traits, not "just so" stories. The simple answer is that humans are primates, and primates have similar bodies and lifestyles. If there's a single pressure that lead to the number of teats in primates, it's likely the arboreal niche, not the mean litter size. Indeed, litter size is usually a plastic trait, even in primates, and is certainly not an accurate predictor of the number of teats.

There are no strict restrictions on nipple numbers in humans; they can occur anywhere on the milk line. So humans tend to have two nipples because that's what primates tend to have, because of our evolutionary history.

A better answer than this one would locate a candidate common ancestor to the primate and non-primate lineages and make reference to the embryonic development of the mammary tissue.


Are Asians more genetically homogenous than other races?

I will side-step the question of 'race', as you seem to be using it (like most people) in the sense that has no scientific basis, but the answer to your question goes something like this:

The amount of genetic variation in a given population is mostly the function of the geographical distance from Africa. Roughly, populations in Africa are most genetically variable as they are the oldest (they have been there for the longest time in human evolutionary history and therefore there was a long time for mutations to accumulate in their genomes). Because all the other populations in the world have originated from these original African populations, they have a subset of that original variation - they are less variable. The further you get from Africa the less variation remains (a very simplistic scenario: a group of Africans left and settled down in the Middle East; then a group of Middle Easterners went further up to Europe and further east to India; then the Indians moved further north and east etc. etc.; in each stage, only a subset of the previous variation would be travelling along).

A famous image depicting this phenomenon is in Ramachandran, S. et al. (2005). Support from the relationship of genetic and geographic distance in human populations for a serial founder effect originating in Africa. Proceedings of the National Academy of Sciences of the United States of America, 102(44), 15942–15947. doi:10.1073/pnas.0507611102 figure 1B

On the Y axis you have a measure of genetic relatedness (more relatedness = less variation) and on the X axis you have rough geographic distance that takes into account major geographic barriers (like seas etc.). Green is Eurasia and blue is Australia and Oceania. Red is variation within the groups (so, Europeans only, Australians only etc.) The variation  between the populations explained by this geographic distance is close to 80% - which is huge. If I get this right, it means that most of the genetic differences between people in different populations are a simple consequence of living outside Africa. And the variation within each population is tiny (12%) compared to the between population.

This is a simplified view, because we now know that there were other species of humans that lived when our ancestors left Africa, and that thay had sex together as our ancestors spread around the globe, so a small portion of the others' DNA is still present in us today. Also this picture may be slightly different depending on what region of the genome you're looking at. But the major picture stands.

Going back to your question - "Asians" (populations with ancestry in east Asia) are on average more genetically homogenous than "Australians", "Americans", and "Africans".

EDIT: A paper I like that should explain all this much better: Barbujani, G., & Colonna, V. (2010). Human genome diversity: frequently asked questions. Trends in genetics : TIG, 26(7), 285–295. doi:10.1016/j.tig.2010.04.002 link


What is the effect of persistent hypothermia on cardiac performance?

Winter swimming and infarcts

The publication Long-term risks of cardiac and cerebral vascular diseases increased following winter swimming in the cold seawater which came out just some weeks ago shows a link between long-term winter swimming and CVD.
I think this is the best evidence so far about the possible link.

WYSIWYG's comment has some good general idea:

  Many processes are affected by temperature including metabolism and
  growth rates. Reaction rates increase with temperature but not in case
  of catalysed reactions where the catalyst can operate at only an
  optimum temperature.

Some related topics

temperature effect on the rate of protein degradation

So further studies

protein degradation in the heart in persistent hypothermia
...

Effect of persistent hypothermia on processes of cAF

[1]

Let's have cAF (chronic atrial fibrillation) here as an target.
Electrophysiological study shows that cAF-related remodeling is typically divided into three categories: 1) electrical, 2) contractile and 3) structural.
They cause respectively

1) shortening of both the action potential (AP) duration and effective refractory period (ERP)
2) possibly a result of impaired Ca2+ intracellular handling
3) changes of cellular level (hypertrophy, glycogen accumulation and modified mitochondrial morphology) and tissue fibrosis

cAF's processes in persistent hypothermia

I cannot say now more anything about persistent hypothermia and cAF by confidence.
Those mechanisms of Koivumäki et al are cellular processes, while the representation of the heart requires integrative analysis in the cellular, tissue and organ levels.

In cellular level

Only some catalyzed reactions can work in persistent hypothermia. TODO consider which enzymes of the heart and body work in low temperature in short-term and long-term cases. Depletion cases too.
Effect of persistent hypothermia on the outflux of Calcium (probably, slows down).

In tissue level

I can say without rigor that electrical coordination is uncoordinated in tissue fibrosis.

In organ level

I say say without rigor that the mean electrical axis should be determined and fixed in the study.
Effect of Arterial hypertension must be fixed. Sokolew-Lyon index can a starting point for the indicator but better indicator is required with higher specificity.

Persistent hypothermia from the extreme side (Sauna)

[2] Regular Sauna is with better hemodynamic function; however, the association of sauna bathing with cardiovascular and all-cause mortality is not known.

so possible effect of persistent hypothermia can be

lower hemodynamic function if no compensation mechanism
better hemodynamic function if some compensation mechanism (genetics; unknown)

Some research topics

Effect of Persistent Hypothermia on the Arterial Hypertension. This may be associated with coagulopathy, especially in the lower limb.
Effect of Persistent Hypothermia on Atherosclerosis. It would be very nice to see long-term study about the effect of regular 4-7 winter swimming on the cardiovascular risk score, SCORE and others.

Sources

In Silico Screening of the Key Cellular Remodeling Targets in Chronic Atrial Fibrillation. Koivumäki et al. Computational Biology.
Association Between Sauna Bathing and Fatal Cardiovascular and All-Cause Mortality Events, here

Please, see the reference of the publication for more better view.


Nerves (including cranial nerves) are constituted of neurons, and other supporting cells and structures (e.g. myelin sheath and extracellular protein matrix). Neurons are highly specialized cells that have a particular cellular anatomy:

As you can see, the cell body (or soma) contains the nucleus, and projects it's axon towards other structures in the body, sometimes more than a meter away! Cranial nerves (like other nerves) are a collection of the axons, not the cell bodies themselves. The cell bodies reside together, in the brainstem, forming what we call nuclei. So that's simply what they are.


Why do we urinate more often in winter compaired to summer?

There is no 100 % sure answer for this as, obviously, nobody is that much interested in studying about urination. But there are some theories, of which the most popular and accepted one is cold diuresis.

  Cold-induced diuresis, or cold diuresis, is a phenomenon that occurs in humans after exposure to a hypothermic environment, usually during mild to moderate hypothermia.

According to this theory, what exactly happens is this (I'll explain in steps for better understanding):

When your body senses cold or low temperature of environment, it constricts the blood vessels near your skin and external organs and restricts your blood to the inner core of your body to maintain its temperature.
Thus, it causes the blood pressure to increase as there is same amount of blood in lesser volume.
This induces negative feedback on ADH (a vasoconstrictor) i.e. its secretion is reduced.
Now when blood vessels in kidney get proper amount of blood (as blood vessels aren't constricted now), they sense high blood pressure and try to reduce it as soon as possible.
So they transfer more amount of water from blood to bladder which fills the bladder more quickly and causes an urge to urinate.
Thus, we urinate more in colder climate.

There are some more theories related to it too, but they aren't as popular. According to another theory, when we are exposed to cold weather, aquaporins are inhibited around the body, making it impossible for water to be taken in by cells, leaving a lot more of it in the blood. Again, the body will try to balance that pressure, pulling water from the blood and storing it in the bladder. You can get a more frank and interactive explanation here.


What is the closest species to humans in animal kingdom?

Others have given great answers, so I'll just support their answers with this diagram and a little further background on how to think about relatedness in evolutionary context.

Since the author in this excerpt makes no mention of Bonobos, I would imagine that, by chimpanzee, he really meant the genus Pan, which includes both Bonobos and Common Chimps. But that does not necessarily matter.

Relatedness, in modern taxonomy, depends purely on common ancestry, not necessarily on similarity of specific traits. As others have explained, we make theories about ancestry relationships based on many criteria and logic, not just variation in one gene. In this tree, you should think of A, B, and C as theoretical, extinct common ancestors of the species below them in the tree. The list of apes at the bottom represent the relevant extant species species only. Bonobos and Common Chimps have a more recent common ancestor (C) than either Bonobos and Humans (B) or Common Chimps and Humans (B). This is why @mgkrebs said that both qualify equally as most closely related, because the common ancestor of each pair is the same.

Few would disagree that Bonobos do seem to be more similar to humans than Chimps are to humans, but that actually does not mean they are more closely related evolutionarily! Theoretically there are two ways this could happen even if Bonobos and Chimps are equally related to humans, either our common ancestor with Chimps and Bonobos also shared the traits we have in common with Bonobos and Chimps changed, or Bonobos and Humans happened to develop these similarities independently. The former is a simpler explanation, but either are possible for each similarity. Again, the key in understanding this is in thinking about the theoretical ancestor species, B and C. The only way Humans could be more closely related to Bonobos than chimps is if the common ancestor, B, was a descendant of C, which seems extremely unlikely and as far as I know is not supported by the genetic research in this area.

Our common ancestor with Gorillas (A) on the other hand is much "earlier" than our common ancestor with Chimps and Bonobos, so Gorillas are less closely related to use than the group containing Bonobos and Chimps.


Help with jellyfish species identification

Be warned that these are just best guesses - as you said yourself, these aren't great images for identification as they appear to be simple drawings:

1) this looks a lot like Aurelia aurita - though the lack of any internal patterning in the drawing makes me think perhaps otherwise.

image source: https://www.leisurepro.com/blog/wp-content/uploads/2017/05/shutterstock_272438348.jpg, https://holidays-majorca.co.uk/wp-content/uploads/2017/01/Aurelia-Aurita-S-300x225.jpg

2) possibly a Turritopsis dohrnii or nutricala - if so then this is the 'immortal' jellyfish. shape of bell is correct and the lappets seem reasonably close, it's just the internal structures that I'm not sure about.

image source: https://www.cairnsholidayspecialists.com.au/shared_resources/media/irukandji-jellyfish-in-far-north-18836_400x322.jpg

3) Very unsure about this one, but potentially a Atolla wyvillei? definitely has some visual features in common and I can't find anything else that's similar. I can also see how an artist would derive that image from this species.

Image source: https://www.mindenpictures.com/cache/pcache2/90194947.jpg, https://c8.alamy.com/comp/E45A4H/deepsea-medusa-jellyfish-atolla-manubrium-gulf-of-maine-atlantic-E45A4H.jpg

I hope these at least give a starting point and are of some help, I think the nature of those images will make it hard to get many better answers. Good luck!!


What is the latency between paired neuronal responses in the brain?

Short answer
A rough indication of the delay in monosynaptically connected cortical neurons is 6 - 14 ms.

Background
As @Jonathan correctly states, there are many variables involved in neuronal delays. However, because you ask for an estimate of the order of magnitude of the neuronal delay between two coupled neurons in the neocortex, I will suffice by providing the latencies reported form one study that seems to meet your demands very well. In this study the latency data on horizontally connected neurons in monkey prefrontal cortex in layer III were reported González-Burgos et al (2000).

The authors inserted stimulating electrodes to evoke action potentials and used distant recording electrodes to measure the responses in cells located distally from the stimulation site (Fig. 1).

Recording setup used in González-Burgos et al (2000).

They report that delays between monosynaptic connections range between 6 - 14 ms. Fig. 1 shows that these latency estimates depend on the position of the stimulating and recording electrodes, i.e., which part of the presynaptic cell is stimulated and which part of the postsynaptic cell is recorded. Most notably in the recording setup used, longer axon collaterals will have resulted in longer latencies. The authors conclude that the conduction velocity of the horizontal axon collaterals was 0.14 ± 0.04 m/s and the synaptic delay was estimated at 2.29 ± 0.49 ms.

Reference
- González-Burgos et al., Cereb Cortex (2000); 10(1): 82-92


Elevated position effect on recovery times from upper respiratory infections at rest?

Physiology

My conjecture.
The slightly elevated position causes greater venous return (work against gravity by smooth musculature and thoracic pump).
Why this is happening this way is partially based on my question here about Fast standing and the heart's insufficient accommodation of the increased venous return.

where the venous return reacts first the change in the position from supine by shifting the VR1 to VR2.
The stroke volume increases initially to SV1 to SV2, while the end diastolic volume from EDV1 to EDV2.
The increased stroke volume cannot be maintained long time so the cardiac output shifts to the right from CO1 to CO2.
So the initial stroke volume SV1 is the same as SV3 (not in the picture).
However, the EDV has increased (EDV3 >> EDV1) which increases much the lymphatic drainage.
Lymphatic drainage is not dependent on the stroke volume.
Increased lymphatic drainage then again increases the circulation of lymph.
This then again supports the recovery from the upper respiratory infection where the fine regulation between

the thoracic pump,
respiratory pump, and
smooth musculature

determine the final effect of the body position on the recovery times.
The size of the thoracic cavity puts some limitations, for instance.

Cardiology

In some cases, the upper respiratory infection can cause myocarditis.
This will decrease the functioning of the heart and cause possible

premature atrial contraction, and/or
premature ventricular contraction.

Elevated position helps small arterioles of left ventricle supply preload.
Otherwise, ectopic beat can be heard or also called "epics beat" which is sign of the two previous conditions.

The nurse is educated to listen to the patient and ask for possible jolts and flips in the chest.
Elevating position in such a case can help because of better supply for preload in the left ventricle.

Pathophysiology

Upper respiratory infection is often acute respiratory infection (acute respiratory distress syndrome).
There is an increased permeability of the vessels.
The fluids and plasma proteins are going through alveoli.
Acute hyaline membranes are formed.
Cytokines play a big role in this process.
To maintain lymph retention, the result of increased venous return compensates.

These patients can breath normally in the sitting position.
There are also other reasons for the infection:

overweight - the greater intra-abdominal pressure $\to$ more liquid diffused into the lungs OR other organs are suppressed.
Big chest suppresses lungs such that the architecture can change.

Pharmacology

There are different drugs which effect is dependent on posture and position of the body.
Hypertension is a common disease which amount increases during ageing in population.
Let's take hypertensive drugs as a case study.
Peripherally acting sympathoplegic drugs are generally dependent on posture more than centrally acting ones.

In hypertension treatment, the peripheral acting sympatholegic drugs are used often in combination with diuretics.
Blood pressure can be under control when blood volume is 95% of normal, but much too high when blood volume is 105% of normal.
So this study should be considered with no hypertension and hypertension.

Sources

For Pharmacology, Basic and Clinical Pharmacology, 11th edition, Katzung et all.


Standard datasets for testing new multiple sequence alignment algorithms?

I would suggest you PAcAlCI or Prediction of Accuracy in Alignments based on Computational Intelligence, though the acronym in wierd the tool is good for testing new Sequence Alignments. They

But before you start testing your algorithm, I suggest take a look at these papers:

[1] Who Watches the Watchmen? An Appraisal of Benchmarks for Multiple Sequence
Alignment

[2] Issues in bioinformatics benchmarking: the case study of multiple sequence alignment

PS: I haven't tested or used the tool myself.


What is this very tiny (3mm) centipede-like insect?

That is a dermestid larva. A beetle from the family Dermestidae https://en.wikipedia.org/wiki/Dermestidae, common name, skin beetle. They eat dried skin, or flesh, and are generally the last insect to feed on a carcass. They are the bane of insect collectors, because they eat dried insects right off the pin.


That is a horntail, family Siricidae. https://www.insectimages.org/browse/taxthumb.cfm?fam=455
They are a family of sawflies. Not technically wasps, but they are Hymenoptera.


Name and Behaviour of Arthropods near a Cactus

It's hard to tell from these photos (you'll need a macro lens for good shots), but they seem indeed to look like mites (Acari).

There are mites that feed on rotting cacti, Bonomoia opuntiae for example. There is a film here about this cactus mite.


What would sanitiser fail to do that detergent and warm water would do in cleaning glasses frame that isn't 'visibly soiled'?

The earsocks on Oakley brand sunglasses are made of a proprietary hydrophilic rubber called Unobtanium 1.  From what I can find, Unobtanium is likely a styrene copolymer 2, possibly a formulation called Kraton G 3.  Polystyrene is insoluble in water, but soluble in ethanol and 2-propanol (isopropanol) 4, which are the most common alcohols used in sanitizers.
So, as suggested by @Cell, soapy water is likely recommended by the manufacturer because it is unlikely to damage the glasses, whereas alcohol-based cleaners may degrade the soft rubber components.

https://www.oakleyforum.com/threads/how-to-restore-old-unobtainium-that-has-gone-sticky.10821/
https://www.oakleyforum.com/threads/rubbers.21973/page-2
https://kraton.com/products/KRATON_G.php
https://www.bangslabs.com/common-solvents-and-non-solvents-polystyrene


At first I was skeptical about this question but then I did some researching and apparently, a certain amount of oxygen is indeed taken up from the surroundings through the upper layers of our skin. In fact, the paper titled "The cutaneous uptake of atmospheric oxygen contributes significantly to the oxygen supply of human dermis and epidermis. states that

  the upper skin layers to a depth of of 0.25-0.40 mm are almost
  exclusively supplied by external oxygen, whereas the oxygen transport
  of the blood has a minor influence.

Here is another paper that you would find interesting. In short, I would say that its not just the fingers but O2 diffusion into cells take place over the whole body.


Can some human groups evolve into new species?

Absolutely it is possible for the current human species to evolve in to two distinct species in the future. Barriers to reproduction, such as physical isolation, help the process along as it allows differences to accumulate. Gene flow allows hybridisation (not in a species to species sense, but sub-population to sub-population sense) which will impede the process of speciation because it allows genetic variation which is unique to one population to move to the other.

Differences occur between populations, which can lead to speciation, by the mechanisms of evolution - mutation, migration, drift, and selection. Different mutations occurring in sub-populations allows the two to become genetically incompatible, leading to speciation. Gene flow from a third population may make the first two too different to reproduce (see also ring species). Drift and selection may cause genetic variation which allows reproductive compatibility between two populations to be lost, further generating genetic differences. Selection in different directions (e.g. the environment of the two populations is very different) can hasten speciation, as seen in a classic Drosophila experiment.

Will the population you mention ever become a non-human/novel species? Who knows, but they are certainly interesting - as you've realised, their isolation by geographic barriers will help differences to accumulate between them and other human populations that could lead to speciation.

I suggest reading more about evolution and speciation here!


What is the molecular mechanism of odorant transduction signaling pathway?

Information available on this is huge. I will pin point main points. Generally this signalling will involve four components viz. receptors, transduction machinery, perireceptor processes and downstream processing of chemosensory information.

Receptors
First step is to receive signal (here odorant or chemicals). Following figure shows comparison between primary chemoreceptor neurons in vertebrates, insects, and nematodes.

These neurons constantly undergoes birth-maturation-death and process is well studied in many model systems.

Signal transduction

After stimulus is received, it needs to be transfer inside cell for further processing. In this case, generally transduction happens via GPCR signalling. These neurons use two widely used signalling cascades. Following figure shows main components in this signalling ( (a):vertebrate olfactory receptor neurons (b): lobster olfactory receptor neurons),

Perireceptor Processes

These process are important for receptor activation and transduction. They can be any type like mechanical or biochemical.

Downstream processing

There is huge information available at the level of pathway. Following figure represents main components in two model systems.

For finding genes, you have to search in specific part of this process (like this is good example of receptor genes in human).

I would strongly recommend reading chapter 4 of "The Senses - Comprehensive Reference". All above information is taken from this book. Another good open source reference is The Neurobiology of Olfaction, this reference has all things you need for free.


The paper you link finds that there is not a significant correlation between body mass and resting heart rate in humans. While there is a well known negative correlation across mammals:

This is the ever-popular mouse-to-elephant curve that is found in one form or another for lots of physiological measurements.

I'll suggest, but have no evidence, that the lack of a significant correlation in humans is simply a result of there not being enough range in body mass among humans to allow finding a significant result. When the range of one variable is small, the association between that and another variable necessarily lessens. For example:

Although the linear relationship between the two variables is largely similar, when the range of x is truncated, the coefficient of determination, $R^2$, decreases. The correlation goes from 0.97 to 0.7. In this case, that might still be "significant", but I suspect that in humans that variation is much greater in resting heart rate.

It would have been nice if that paper included the actual data on HR, but they act like it doesn't exist just because it was not significant.


Why is a gene for a fluorescent protein used rather than one for an enzyme that produces fluorescent molecule?

GFP has a lot of advantages:

The detection of the fluorescence works directly and doesn't need a lysis step or the uptake of a reagent.
Fluorescence can be detected directly using a fluorescence or confokal microscope with the cells. This can be done while growing them on plates (works for bacteria and eukaryotic cell culture).
You can sort labelled cells using a flow cytometer.
direct tagging of proteins and their subsequent localisation on the cell is possible.
GFP is rather stable in the cells and not toxic.


What are some effective strategies for testing whether a trait is an adaptation?

See if the trait gives any significant advantages as compared to absences of trait. Also if the trait is present in almost all organisms and no variation is found, then see if it has any use. Like appendix is found in almost every human; although it can be surgically removed, normally it is present, but is useless in humans.


If a human is stranded with beer but no water, should they drink it?

There is quite a lot of misunderstanding about alcohol (and caffeine) as a diuretic. It's not nearly as cut and dry as you're presenting.

There is no answer to your question. Sodium and water are very tightly regulated, and a lot has to go wrong before they fail. If alcohol could easily derail water regulation, there would be far, far fewer alcoholics in the world.

Alcohol is primarily a toxin, not primarily a diuretic. The diuretic effect of alcohol depends partly on your hydration status. If you're fully hydrated, you'll produce slightly more urine on drinking an alcoholic (>2%) beverage than when you drink water. If you're dehydrated, your body will conserve the water more. The more alcohol in the drink, the less value it has as a rehydrating solution.

You won't find good studies because it's not a scenario truly worth studying. The toxic effects of alcohol are already known and bad enough. It would be unkind to conduct a study where higher concentrations of alcohol were the sole fluid available and length of survival on animals, let alone humans.

N.B. There have been lots of studies with acute alcohol intoxication and diuresis because that is a scenario that occurs, and which can be mitigated.

Effects of a moderate intake of beer on markers of hydration after exercise in the heat: a crossover study
Hydration Status and the Diuretic Action of a Small Dose of Alcohol


The process of measuring the effect of nootropics would be the same as for any other drug: Do a double blinded placebo study and the follow the parameters you hope to influence. For example do "brain tests" if you want to test for enhanced brain function. If there is any function of your drug in the body, you will see a difference between the treatment and the control group. You could start by reading the Wikipedia article about Nootropics which is quite exhausting and also has quite a lot of references and go on with these two papers "Does taking vitamin, mineral and fatty acid supplements prevent cognitive decline? A systematic review of randomized controlled trials." and "Cognition enhancers between treating and doping the mind."


How is the exogenous DNA protected from degradation during bacterial transformation?

Different bacteria have different modes of transformation and as I understand it is Haemophilus influenzae that takes up the single strand whereas ?Streptococcus [i am not sure which bacteria it is] takes up dsDNA.

I intuitively think that DNAses are not that common like RNAses. Moreover, natural competence is associated with stress and is even triggered by DNA damage. Therefore we can speculate that DNA repair proteins will be prevalent and DNAses will be low in the cell, under these conditions. The chance of foreign DNA being damaged goes down.

In the case of artificial transformation, I guess the entire concept of heat shock is a way of providing stress. Moreover, the lab strains such as DH5alpha have certain mutations which disable them from recognizing a plasmid as "foreign".


gene expression fold change threshold limit

As I mentioned in your previous post. If your reference gene undergoes changes then replace it with another reference and if even that doesn't work out then use a spike in. You must normalize. Interpreting the raw values can be erroneous- there could be a loading bias. Don't think much- repeating RNA isolation and/or qPCR is not a very hard job. And as Chris said, use two references if you can.
BTW, if you are fine with it then can you tell what is the gene that you are studying and what is the treatment
w.r.t what is a significant fold change.
There is no hard and fast rule to determine what is an acceptable fold change. In some robust systems a minor perturbation in the gene expression will not translate to any great biological outcome whereas there can be sensitive systems in which minor changes can affect the cell state. These things depend on how the gene is integrated in the regulatory network.


You can find some, but not all, gene frequencies in a range of populations at The Allele Frequency Net Database - Allele, haplotype and genotype frequencies in Worldwide Populations.

However, your question is broad genes have a lot of variation within them, the most basic being Single Nucleotide Polymorphisms (SNPs) and you've already been pointed to one source of information (SNPedia which is new to me) but you can look at the variation of allele frequency of SNPs in different populations by looking at dbSNP1.  Note they have a subset for variation associated with clinical phenotypes.

1 This may be the source on which at least some of SNPedia is based as dbSNP has been around for a very long time.


Why animals can move and plants cannot in general?

Animals and plants are both classified as Eukaryotes, and as such can form large, complex, multi-cellular organisms. There are several major differences at the cellular level that distinguish the 2 Kingdoms (Animalia and Plantae). Without getting technical, the most crucial difference in relation to your question is that plants contain chlorophyll, and as such can generate their own food using sunlight.

This is very important when you consider that plants (by definition, those Eukaryotes that contain chlorophyll) have therefore evolved to be very efficient at converting sunlight to 'energy', whereas animals have evolved without this option and have to eat what food they need. So they have instead evolved mechanisms that allow them to forage, or even to hunt, for their food.

At some point, a unicellular organism incorporated chlorophyll, leading to multicellular plants in the course of evolution. The ancestor of animals evolved independently from the last common ancestor of plants and animals. Therefore, plants and animals are quite diverged, e.g. in mating 'rituals' (in plants this involves flowers and seeds - whereas in animals there are mating and gestation periods), and systemic changes, such as the immune system and the circulatory system (these are generally much more complex in animals than plants). All of which has stemmed from the difference in evolutionary pressures applied by the choice of food-source.

As you have pointed out, there are exceptions to all rules, so not all plants have chlorophyll, but as a rule it is the case! (Wikipedia: "Some plants are parasitic and may not produce normal amounts of chlorophyll or photosynthesize.").


Why is gastrin not acing paracrine manner primarily, when it acts mainly on cells nearby its release?

Paracrine signalling would mean not merely that gastrin is signalling the same organ, but that it is signalling nearby cells in the same organ - so that a few parietal cells close by respond, while the others perhaps would ignore the signal because maybe the paracrine signal would be degraded.  While the distinction is not absolute - there are shades of gray in all these things - blood gastrin tests are commonly done and medically relevant ( https://medlineplus.gov/ency/article/003697.htm ).  Because you can look at gastrin level as a whole-body characteristic, it is certainly appropriate to call it an endocrine signal.

Though their role is less emphasized, bear in mind that there are gastrin-producing G cells in the duodenum as well, and gastrin affects other digestive organs.


Find how much times blood is filtered in the kidney?

I'll try to dissect your teachers answer for you:

  1/12*60=5 liter blood

no explanation required here

  0.55*5=2.75 liter plasma of blood.

only the plasma is filtered in the kidney (the 45% cell content remains in the blood stream), so out of the 5 l blood, only 2.75 l need to be filtered.

  The plasma is filtered 60 times is 24 hours. (how did she find that?)

the kidney filteres 7.5 l per hour so if the whole blood plasma has 2.75 l, then in one hour the whole blood is filtered 7.5/2.75=2.73 times. In one day the whole blood is filtered 2.73*24=65.5 times (the numbers are slightly rounded).


Role of calcium chloride during competent cell preparation

Although we do not have any conclusive proof about how $CaCl_2$ works, the suggested mechanism is much similar to what you have suggested. When $CaCl_2$ dissociates in aqeous solution, $Ca^{2+}$ ions bind to the phosphate groups in DNA as well as the inner core of lipopolysaccharides in cell membrane (Dagert et al, 1979), neutralizing them. After this, heat shock allows uptake of this DNA into the host (how heat shock works is also not known; it is suggested that increased temperature creates pores in cell membrane, see this answer). For visual representation, see this diagram (from here):

Regarding $MgCl_2$, the role of $Mg^{2+}$ is not completely understood either. However, $Mg^{2+}$ is known to promote cell growth (Hanahan et al, 1983). It might be because $Mg^{2+}$ is an important factor required for functioning of ribosomes (Nierhaus et al, 2014). Anyhow, its role in increasing competence seems to be lesser than that of $Ca^{2+}$.

P.S.: during the experiment, $Mn^{2+}$, $Rb^+$ and $K^+$ also work effectively along with $Ca^{2+}$ (Hanahan et al, 1983).

References:

Dagert, M.; Ehrlich, S. (1979). "Prolonged incubation in calcium chloride improves the competence of Escherichia coli cells". Gene. 6 (1): 23–28. doi:10.1016/0378-1119(79)90082-9. PMID 383576
Douglas Hanahan, Studies on transformation of Escherichia coli with plasmids, Journal of Molecular Biology, Volume 166, Issue 4, 1983, Pages 557-580, ISSN 0022-2836, http://dx.doi.org/10.1016/S0022-2836(83)80284-8.
Nierhaus K.H. $Mg^{2+}$, $K^+$, and the ribosome J. Bacteriol.  2014 196 3817-3819


Substrates of cytochemical reactions in this immunostaining

It's hard to understand the question, but in any immunocytochemical staining such as the above, you have two different types of reactions:

the antibody binding to the target (in this case, some laminin)
the peroxidase-based colorimetric reaction with DAB. DAB (3,3'-diaminobenzidine tetrahydrochloride) is oxidized in the presence of hydrogen peroxide to form a brown precipitate, which becomes the stain.

The fact that is an indirect immunostaining implies that you have a non-conjugated primary antibody against laminin and a secondary antibody against the Fc part of immunoglobulins of the species in which the first antibody was raised. This secondary antibody will be conjugated with HRP (horseradish peroxidase, the enzyme responsible of generating the peroxides that will oxidize the DAB).

For a more complete reference of immunocytochemical stainings, you can read: http://www.ihcworld.com/_books/Dako_Handbook.pdf


Seeing new colours with new photoreceptors

Each human optic nerve contains between 770,000 and 1.7 million nerve fibers, So it will be beyond human grasp to swap eyes in the near future, genetic eye and optic fiber development has to happen in the womb. Eye grafts require some kind of neural nanotechnology which is probably multiple generations away.

If you replace a human photoreceptor with another color, the result is: un-demonstrated/unknown.

Genetically engineered photoreceptor color swap (swap UV and blue)  which sends impulses to the same optic nerves as the previous color, may, and probably would work fine.

If you switch one eye to CMY and keep the other as RGB, it should have a usable result.

If you switch both eyes to CMY it's fine too, we would expect that there would be a fair vision perception, perhaps equivalent to RGB in clarity.

If you design a fetus with 4-5 photoreceptors and let it develop normally, It would have an unknown result. Perhaps the baby would have augmented vision, perhaps troubled. It's not know and many scientists would love to know the result.

I'd wager that a human with 4-5-6 colors of photoreceptors can be genetically engineered to see, within our lifetime.


Cucumbers have an anti-inflammatory effect that reduces puffiness. The
  vegetable not only has a high water content, it but it's often stored
  in the refrigerator and comes out cold. This means that the water
  hydrates your skin, and the cool temperature decreases the flow of
  blood to the space around your eyes. Together, additional hydration
  and reduced blood flow can sooth the skin around your eyes and
  alleviate swelling

Source

Also it has silica.


Steps to confirm if predicted miRNA is good or bad

There won't be any duplicates in miRBase (for a given organism). Choose the taxon nearest to your organism if you are doing homology based discovery. If you want to take all/many organisms then you can use fastx_collapser to collapse redundant sequences. However you will lose the name of the miRNA. You can use awk also for this and it will keep the sequence header from the first organism in the list.

awk '/>/{$0=h} !(/>/){if($0 in a){next} else{a[$0];print h"\n"$0}}' organism1.fa organism2.fa ... organismN.fa

Make sure that there are no extra newlines, otherwise you might need a small modification

To know if something is an expressed miRNA you would need to do a small RNA sequencing. There are some tools like mirdeep and mirSVR which you can use to discover miRNA sequences.


Can the characteristics of an offspring depend on the locality of its conception also?

Genetic makeup can not vary with the place of conception, but certainly the way genes are expressed can change with change in place of conception. Such changes are called epigenetical changes. Epigenetic change is switching on or off of genes which can be achieved by various method:-

1)  DNA methylation

2)  Histone modification and

3) RNA associated gene silencing

In theory, change in place of conception, can result in silencing or activation of differential genes in foetus. In fact there is this nice article which discusses how maternal nutrition switches on or off six genes in foetus 1 and [2]. Even stress can cause such epigenetic changes [3]. These environment triggered changes may also result in change of phenotype. For example in mice, the agouti viable yellow (Avy) gene which is a retrotransposon and is found in upstream of the agouti gene. The Avy elements are generally methylated and hence are shut off but in Agouti mouse, they are unmethylated and therefore switched on, which leads to a yellow coat.Though this methylation or unmethylation in agouti mice has not been proved to be a result of environmental factor, but in a strict theoretical sense this can happen (with some or other phenotypic trait)

1] Painter R.C., Roseboom T.J., Bleker O.P. Prenatal exposure to the Dutch famine and disease in later life: an overview. Reproductive Toxicology 20, 345-52 (2005).

2] Maternal nutrition at conception modulate DNA methylation of human metastatic epialleles(NCBI)

3] Exposure to stress even before conception cause genetic changes to offspring(science daily)


Reason for specific location of a gnat swarm?

'Gnat' is the common name for a number of species of tiny flying insects in the Dipterid suborder Nematocera (https://entomology.ca.uky.edu/ef632), including Ceratopogonidae (biting midges), Chironomid midges (non-biting midges) and Simuliidae (blackflies). Like many other Diptera, a lot of these species mate aerially in swarms: the males gather using visual cues to determine swarm location. I'll try to add more detail to this later on why they go for specific locations, but in the meantime here are some papers on mating swarms in some of the groups normally called 'gnats':

General papers on swarming behaviour in Diptera:

Downes, J. A. 1969. The swarming and mating flight of Diptera. Annu.
Rev. Entomol. 14: 271–298.

Swarming behaviour of the family Ceratopogonidae:

Downes, J. A. 1955. Observations on the swarming flight and mating of
Culicoides (Diptera: Ceratopogonidae). Trans. R. Entomol. Soc. London
106: 213–236.
Campbell, M. M., and Kettle, D. S. 1979. Swarming of Culicoides
brevitarsis Kieffer (Diptera: Ceratopogonidae) with reference to
markers, swarm size, proximity of cattle, and weather. Australian. J.
Zool. 27: 17–30
Zimmerman, R. H., Barker, S. J., and Turner, E. C. 1982. Swarming and
mating behavior of a natural population of Culicoides variipennis
(Diptera: Ceratopogonidae). J. Med. Entomol. 19: 151–156.
Blackwell, A., Mordue, A. J., Young, M. R., and Mordue, W. 1992. The
swarming behavior of the scottish biting midge, Culicoides
impunctatus (Diptera, Ceratopogonidae). Ecol. Entomol. 17: 319–325.

Swarming behaviour of the family Chironomidae:

Gibson, N. H. E. 1945. On the mating swarms of certain Chironomidae
(Diptera). Trans. R. Entomol. Soc. London 95: 263–294.
Oliver, D. R. 1971. Life history of the Chironomidae. Annu. Rev.
Entomol. 16: 211–230.
Fyodorova, M. V., and Azovsky, A. I. 2003. Interactions between
swarming Chironomus annularius (Diptera: Chironomidae) males: role of
acoustic behavior. J. Insect Behav. 16: 295–306.

Swarming behaviour of the family Simuliidae:

Moorhouse, D. E., and Colbo, M. H. 1973. On the swarming of
Austrosimulium pestilens MacKerras and MacKerras (Diptera: Simuliidae). Australian J. Entomol. 12: 127–130
Hunter, D. M. 1979 Swarming, mating and resting behaviour of three species of black fly (Diptera: Simuliidae). Australian J. Entomol. 18: 1–6


Although there exist some differing opinions mostly to do with brain function, the best answer is definitely the heartbeat. Here's why:

In some ways the human body really does operate like a machine. The process of delivering oxygenated blood is THE foremost example of a time-critical activity that must occur constantly in order to maintain life. That process stops when either breathing or pumping of the heart ceases, and since the circulation of the blood is more immediately critical than breathing it makes sense to place more weight on that criterion.

Some medical conditions can lead to a person being essentially "Brain-dead" before they are biologically dead, but these situations are almost always extreme outliers to the general discussion of alive vs dead. Furthermore, the arguments surrounding that state too often and too easily cross over into philosophical/metaphysical commentary.

The only serious wrinkle to the argument above is hypothermia. This wrinkle is encapsulated quite nicely in the old medics' axiom "You're not dead until you're warm and dead." And it is well documented that hypothermic patients can sometimes be revived after long periods of time - in excess of a half hour - using special techniques and equipment (to prevent frostbite).

Bottom line: Has the subject's heart been pumping any blood (including during CPR chest compressions) in the last 10 minutes? Is the subject hypothermic with a core temperature below 95 degrees Fahrenheit? Answers of "No." and "No." mean that the subject is no longer living.


Why is it that bacteria and fungi cannot develop resistance against essential oils?

Here are my thoughts on this, taking your example, oregano oil.

The active anti-microbial ingredient in this essential oil is carvacrol. The WP article states that it probably acts by disruption of the membrane.
 There appear to be no examples of carvacrol resistance, as suggested by your question. In mammals the compound is detoxified in the liver via esterification to increase solubilty, thus promoting excretion.

Assuming that we can create a situation with a strong selective pressure for the development of resistance in a microbe, what would that resistance look like? If the carvacrol does indeed disrupt the membrane, then it is probably useless to develop intracellular degradation - what is needed is the secretion of an enzyme that is able to inactivate the compound, analogous to the β-lactamases that inactivate antibiotics like penicillin (which also has an extracellular mode of activity).

Furthermore, unlike β-lactams, carvacrol is insoluble in water. This suggests to me that most of the time, in the natural environment, free-living bacteria will not experience significant levels of the compound.

In summary - it may be difficult to evolve a system for the degradation of a lipophilic compound, and because it is lipophilic it may be that it is rarely a problem for bacteria unless they are being subjected to laboratory tests for antimicrobial activity.