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Will a person with two copies of the same set of chromosomes be normal?
Would a (theoretical) woman (because she must have two X's), that both sets of
her chromosomes were 100% identical, be "normal"?
Would she be healthy, or would she have genetic problems as a result of that?
Would all her egg cells contain the same copy, identical to all others in her
body?
Thanks very much for any answers!

It sounds like this person would be close to what you get with "pure lines", aka inbred strains in laboratory animals:

A population of identical homozygotes constitutes a pure line. Pure lines "breed true"; that is, they maintain their phenotype indefinitely if genetic crosses are restricted to members of the pure line (see True Breeding).

You get those by inbreeding for enough generations that the individuals become genetically identical, or monozygous for every allele at least.
And on the effect of being a homozygote for all genes:

Inbreeding in allogamic organisms bring the deleterious recessive alleles to homozygosity; the immediate consequence is an increase in the frequency of defective offspring, or, in another words, an increase in the genetic load of the population. This phenomenon is called inbreeding depression or inbreeding degeneration. As inbreeding continues, the deleterious alleles are selected out and eventually disappear.  The original heterozygous populations are often more fit than the resulting pure lines because they profit from heterosis and balanced polymorphisms; the main advantage of pure lines is the quick production of many individuals with the same well-adapted genotype

It sounds like she would only have genetic problems if she had problem genes; bad alleles are more likely to be harmful if you're monozygotic for them because there are no other alleles to compensate, but if you only have the good alleles to begin with there's no harm. You would have problems in cases where having two different alleles is itself superior to having a single one of any; for things like immunity for example that can be the case. Or being heterozygous for the sickle-cell allele in malaria country, for another standard example.
I don't know if any of those things would be harmful enough that we'd call that woman "unhealthy" or "suffering from genetic problems" though. I think if it did, it would be more a statement about how the human genomes contains these specific alleles that you have to be heterozygous for than about the intrinsic harm of being the combination of two identical haploid genomes.
As for whether her egg cells would all be identical, they should be since homologous recombination should be switching identical bits of DNA with each other, but that's ignoring mutations. Which shouldn't be ignored, because every human has on the order of 100 mutations that weren't in their parents. Still, compared to how much DNA there is in the eggs overall it would also be reasonable to call them identical.

She would be completely healthy (if no disease causing alleles are present). This is because only one of her X chromosomes will be active. https://en.m.wikipedia.org/wiki/X-inactivation

Last question is redundant... If no other X chromosomes are present then only one version exist and can be passed on

@JeppeNielsen I understood the question to be about all chromosomes, not just the X chromosome (the woman and X chromosome thing being specified because obviously a man cannot have all pairs of chromosomes be 100% identical). And the last question being redundant is irrelevant, all that matters is that the OP asked it, and also it isn't redundant if you take mutations and errors in recombination into account.


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Why are bugs attracted to light bulbs but not flames?
Just now, a housefly was bugging me a lot and I wanted to get rid of it. My mother suggested me to turn off the lightbulb and off it went. However a small flame was burning in my room. Why didn't the housefly get attracted to the flame (although it was a luminous flame)?
My first guess is because of the high temperature a flame produces. This Wikipedia article states that:

A 300 watt tubular halogen bulb operated at full power quickly reaches a temperature of about 540 °C (1,004 °F)

And a charcoal fire can produce temperatures between 750–1,200 °C (1382-2192 °F). Source.
I've seen small bugs getting attracted to large halogen lights in sports complexes. Although these two temperature ranges are a sizable difference apart, 540 °C doesn't seem cool at all. Is it really due to temperature, or is there some other reason?

It could be something to do with them learning to avoid flames over many years. Fire is more of a natural occurrence than halogen bulbs. It could biologically coded within them to avoid flames. The same way the average human would run at the sight of a tarantula, but doesn't get hugely scared if they just saw a plastic model of a spider, insects may know innately that fire is harmful, but newer man-made sources of light may not invoke the same biologically-driven behavioral response.

Not all animals are attracted to light but those that are are motivated by mating behavior. Some female moths will seek a light source and release pheromones drawing the males to the light. The old stories about a moth flying into a flame is a myth

It has nothing to do with temperature, but with the color of the light. Insects are especially attracted to lights with short wavelenghts, especially Ultraviolet (UV) light. Yellow and red light attract far less insects. (Rich & Longcore 2006). PDF
White light, like the one emitted by an average light bulb, consists of a broad spectrum, that includes UV. Halogen lights also emit UV. Flames on the other hand emit mostly red and yellow light.
Unless the flames burn at a very high temperature, then the flames turn blue. To illustrate this, my parents used to have a candlelight on gas they used during camping. This light burnt at a very high temperature, and hence the flame had a bluish color. And it did attract insects, especially moths.

source: Stack Exchange

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Why are aminoglycoside antibiotics particularly effective for aerobic gram negative bacteria?
Aminoglycosides are short chains of sugar molecules with some -OH groups substituted with amine groups. As far as I understand they function by causing bacterial ribosomes to misread RNA and create non-functioning proteins. These proteins both stop providing essential functions of the cell and increase permeability of the cell to aminoglycosides, eventually leading to the death of the cell. What I don't understand is why this mechanism is specific to aerobic, gram-negative bacteria. Surely membrane permeability would be roughly the same for both classes? And also ribosome structure? Any help would be much appreciated.

Anaerobiosis is incompatible  with effective intracellular accumulation of aminoglycoside antibiotics such as streptomycin and gentamycin.

After an initial binding step involving outer membrane lipopolysaccharide the kinetics of the uptake of aminoglycosides exhibit two energy-dependent processes (EDP I AND II). EDP I  is the slow, rate-limiting stage and is dependent upon the membrane potential ΔΨ, but the details of the process are unclear. EDP II is more rapid and may be triggered by membrane changes arising as a result of translation errors caused by the antibiotic accumulated in EDP I since protein synthesis inhibitors block the transition from EDP I to EDP II.
EDP I requires  a threshold value of ΔΨ, and there is evidence that this threshold often cannot be achieved under anaerobic conditions.
This summary is based on information in this review from 1987.  I haven't been able to find any more recent information.

Aminoglycosides are positively charged and hence more drawn towards the the Gram negative bacteria as the LP in their outer membrane is negative.

Welcome to Bio. Could you add some more background and some sources behind your interesting answer? As of now your post is more of a short comment. Thanks.

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Measure of environmental impact on phenotype
Let me begin by disclaiming that I am nowhere near a biologist by competence or education and that I am simply interest in some of its fields of study as a matter of general curiosity. So excuse my ignorance.
I've been recently pondering the concepts of genotype and phenotype. This page succinctly summarizes the difference between the two.
I was curious if there are scientific measures, and how accurate they are, for the impact of environment on the phenotype of a specimen. Hypothetically, if the environment had no effect, the phenotype would be 100% determined by the genotype. But, in a simple approximation, phenotype = genotype + environment. Does modern biology have a measuring system for how much the environment affects the ultimate observable features of an organism, on top of what its genotype does?

In between a long comment and an answer...
For a review of the theory behind the causal variables of phenotype, one might want to have a look at Biology Why is a heritability coefficient not an index of how “genetic” something is?.
One can investigate the impact of a specific environmental variable onto the phenotypic variance but the environmental as a whole is typically computed as whatever is left when other sources of phenotypic variance have been explained. As such you might want to read about estimations methods for heritability and maybe esp. the post How do heredity and regression to the mean work with respect to intelligence?.

Phenotype is often discussed at a fairly coarse level. In biology classes we ponder simple genotypes from Mendelian genetics, and discern that the pea plant with the YY genotype bears yellow pea seeds.
Consider a suspension of tumor cells being grown in a petri dish, however. A fairly straightforward way to asses the phenotype of the cells is by confocal microscopy
Say you grow the same cells, but some at normal oxygen and some at lower oxygen. Refer to the following figure:

In B, the investigators are using fluorescent antibody label, as you'd use in flow cytometry, to perform confocal microscopy. At 1% oxygen for up to 21 days, the phenotype of the same cells profoundly differ (reference). Flow cytometry can also be used to identify difference in phenotype that arise from environmental factors.
Take for example T cells isolated from you blood. I can change the phenotype based on surface receptors detected from flow cytometry, by adding different cytokines to the culture medium. If I add interleukin-12, I'm most likely to differentiate my T cells to discernibly type-1 helper or cytotoxic cells. I can tell due to the presence or absence, or abundance of markers such as CCR5 or CXCR3.
And if you sequence these cells, you get the same material. Epigenetic changes are harder to wrap your head around. In the hypoxia example, the lack of oxygen is thought to change the phenotype by modifying the way the cell machinery can access and express key genes associated with the hypoxia phenotype.
The take home point here, is that in order to discern the techniques that are available to you, it's important to define the system you're researching. For example, I have no idea how they determine the environmental impact on animal species. But, I can sit here and rattle off techniques to analyze single cells or systems of cells.


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Why do we feel headache after ice cold drink?
Whenever we drink ice cold drinks, after a couple of seconds, suddenly we feel intense pain rising from upper nose to forehead. What is reason behind this pain after too cold drink and why it's felt in that particular part of head?

This is called sphenopalatine ganglioneuralgia: https://en.wikipedia.org/wiki/Ice_cream_headache

The cold drink causes the blood in blood vessels of gums to freeze. This stimulates nerve endings and causes a sensation in brain.


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Does sunlight kill rotavirus?
Does sunlight Kill Rotavirus? Maybe freezing? Norwalk or similar. Its a practical question for bedding.

So you have bedding contaminated with rotavirus? These can live more than a week in a variety of conditions. Freezing will not do the job and sunlight won't either. I'd recommend a high temperature wash/dry cycle with bleach. Most other disinfection methods will bleach your fabrics anyways. What you should really do if they're extremely soiled is discard them, however.

According to this study, both a high temperature wash (57C) and full spectrum sunlight will kill rotavirus.
It would appear that a washer with a sanitation cycle (newer models often have a cycle that hits or exceeds 165F) would be your best bet for treating bedding.
See Figure 2.

Oof, that figure though... I presume the y-axis should be labeled "log activation"? And the units aren't FFU/mL they are plotting a dimensionless ratio of FFU(t)/FFU(0). Importantly, though, if log10(FFU(t)/FFU(0)) = -2, that's only a 99% reduction which may not be enough for OP. Still, I have trouble trusting a source that can't label their axes properly.

I think it is correctly labeled.  If you measure at time(t) and find 5 units still alive, and at beginning of experiment (t0) you had 100 units alive.  Then log10(5/100) = log10(.05) = -1.3.    A Y axis value of -2 would mean that 99% of the initial population of rotavirus was inactivated.

Point taken about 99% not being enough though.

The y-axis numbers are correct, the word "inactivation" is not. If "inactivation" is plotted it should be something more like [FFU(0) - FFU(t)]/FFU(0), where inactivation=0 means the FFU is unchanged from baseline. 5 units alive should be greater inactivation than 10 units alive but on the chart it is less. Clearly what they are actually plotting is activity.

My concern is OP's issue has to do with bedding, whereas the paper here is testing inactivation in liquid broth or what have you. I don't think the two media are comparable.

@CMosychuk Also a good point: presumably in a broth there is fairly direct access to the light, whereas with bedding there may be many nooks and crannies not exposed to direct light and therefore the broth test is probably a significant overestimation of the susceptibility to sunlight.

OP asked if sunlight can kill the virus. Apparently full spectrum light can. It is certainly valid to question the ability of sunlight to access the nooks and crannies of bedding. Personally, I found the info about heat particularly useful, as many new washing machines have a heated water sterilization setting that exceeds 57C. The slope of the line for heat indicates it likely be a 99.9 percent reduction in virus particles after 5-10 minutes of this temp (-log10 = 3).


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Location of microbes causing eliminated diseases
Do eliminated diseases like polio, smallpox etc still exist in locations they have been eliminated from or in the wild or did we just make them go extinct like the dodo?

Whether a disease can be eradicated or not depends on its reservoir. To be eliminated it needs to be eliminated in all places and organisms it can thrive in and spread from. This makes diseases like rabies for example hard to eradicate altogether because it can exist and spread in many different animal species.
Polio and smallpox however both have no non-human reservoir, which makes it possible to eradicate them. There is no "in the wild" for them to persist in because humans are "the wild" for them. So smallpox the disease has indeed been made extinct like the dodo; polio we're not quite there yet but we seem to be close.
I said "smallpox the disease" because "smallpox the virus" still exists in two laboratories in the US and Russia.
Polio, as I said, isn't an "eliminated disease" yet (as of May 2017), but since you mentioned it, the main places it persists now are Afghanistan and Pakistan.

so lets say tommorow we get vaccine which kill malaria and vacciante all human malaria will die cause it need human to survive ?

No, because it doesn't. Malaria's main host is a mosquito, and while it does require a secondary host (that the mosquito bites) to complete its lifecycle, that secondary host doesn't need to be a human.


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introduction of system biology to bench biologists
I am trained as a bench biologist and I want to learn about system biology and introduce a system biology type of analysis into my study. Can somebody recommend books and websites about system biology for biologists?

Don't have any good suggestions, but I suspect that the answer will depend critically on how strong your math background is. Can you add a few details about that? i.e., how familiar are you with calculus, differential equations, and linear algebra (matrices)?

"Systems biology" is an incredibly broad category.


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Spider identification assistance Phoenix
Anyone know what kind of spider this is? They seem to be in the walls of my house...

LocationL Phoenix, AZ, USA

That's a nice silhouette of a male Southern House Spider, Kukulcania hibernalis.  That bizarre body, with the gigantic, forward-projecting, 'jackknife' chelicerae is unique and unmistakable.  These are quite harmless spiders.  A link to some useful information is below:
https://bugguide.net/node/view/26400

Sure does look like a Hobo spider but your photos don't show everything more
Photos could possibly pinpoint the spider and try to stay away this spiders could be a serious concern(really serious) and they're known to bite you even though you're not doing anything

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Can living cells be imaged with electron microscopy?
According to this article from October 2009, http://news.mit.edu/2009/electron-microscope

"Electron microscopes are the most powerful type of microscope,
  capable of distinguishing even individual atoms. However, these
  microscopes cannot be used to image living cells because the electrons
  destroy the samples."
"Now, MIT assistant professor Mehmet Fatih Yanik and his student,
  William Putnam, propose a new scheme that can overcome this limitation
  by using a quantum mechanical measurement technique that allows
  electrons to sense objects remotely. Damage would be avoided because
  the electrons would never actually hit the imaged objects."

Is it possible yet to image living cells with an electron microscope? If not, has there been any advance in this direction?

As far as I can see, this remains only a proposal, though it isn't quite my field, so it's possible someone has presented results at a conference somewhere.
Taking a look at the citations of the original paper [Noninvasive electron microscopy with interaction-free quantum measurements, Putnam and Yanik
Phys. Rev. A 80, 040902(R)], there don't seem to be any experimental implementations: https://scholar.google.com/scholar?cites=17617747827527972037
From the news story you linked: "[Yanik] expects the work will launch experimental efforts that could lead to a prototype within the next five years." A good reminder about making time estimates!

what is your field/occupation? Just curious to know if it's the answer of a microbiologist , a physicist or what

I'm a physicist who works in biology, so if this became big, I'd probably have heard about it. (But I'm not an imaging specialist or an EM person - that's my caveat!)

if this idea would actually work someday, do you think it would be able to image cells only superficially, or could it get inside and below the surface of the cell?  Does a traditional electron miscrocope only scan objects superficially?

Not sure! I think it is possible to scan some depth (100s of nm?) with traditional EM, depending on energy, but less than the size of a typical eukaryotic cell. Because of this, there are methods for "slicing" cells to look at the interior, or milling away parts of the surface. Obviously this is pretty destructive, too!

According to this http://www.mpq.mpg.de/4867802/13_02_21, they were about to start "testing the theory" in 2013  with a budget of 4 million and the work was going to last 3 years and a half.. they dont say in which date they were going to start

@Pablo In my opinion, if something like this became feasible to the point that researchers of biology (rather than EM physics) were able to use the technique, it would very quickly become known to just about everyone in biology because it would be such an important step. These groups got a grant to try it out because it would be a big deal and because they came up with a plausible mathematical approach - from the recent citations linked by AJK it seems like they are still working on the physics, and still far from the biology.

well, if you ever get news on this dont forget to update the topic.. I thought something like this was close to happen when I started reading news about scientists being able to read people's thoughts and words they were thinking, but aparently for doing that they only needed to know the cells and neurons superficially, knowing which neurons became activated during a speech, or measuring electrical activity and blood oxygen levels

@Pablo The thought reading experiments are very different from this, completely unrelated, and a bit overstated. They are based on fMRI or EEG and are dependant on a substantial training sequence to teach a model about patterns of brain activity observed in a single subject in a limited number of situations.

According to this "but living cells and tissues and whole, soft-bodied organisms require chemical fixation to preserve and stabilize their structure." https://en.wikipedia.org/wiki/Scanning_electron_microscope . Does it mean it's possible?

While it may not be possible yet to image live cells with EM, it is possible to image live animals. For one example, Ishigaki et al. (2012) imaged live ticks (Haemaphysalis flava) with scanning electron microscopy. They could even see the ticks moving their legs inside the microscope for about 1 min after they went in the chamber. The ticks were still alive after they were removed from the vacuum inside the microscope. Half of those exposed to the vacuum and the electron beam died within the next two days, but the rest remained alive for at least two more weeks. Apparently, ticks that were only put inside the vacuum all survived just fine. It was only when they were blasted with the high-energy electron beam that their chances of dying increased.

Live ticks in SEM
Notice that the scale bars in panels B-F should be in $\mu m$, not $mm$

This is not the first study to succeed in imaging live organisms with electron microscopy; that was Pease et al. in 1966. It appears that in some insects the ionizing beam induces the polymerization of "extracellular substances" into a thin (~5 $\mu$m) membrane that acts as a protective "nano-suit" (Takaku et al. 2013). Takaku et al. (2013) could induce the formation of a similarly protective thin membrane by using polysorbate 20, a broadly used surfactant. Artificially inducing the formation of similar "nano-suits" may be a more promising way to image live cells with electron microscopy rather than relying on quantum mechanical measurements. Takaku et al. (2013) even go as far as to speculate that the natural formation of similar "nano-suits" may have acted as a protective shield for prokaryotic extremophiles that could have invaded the earth during early evolution (panspermia hypothesis).

References

 - Ishigaki Y, Nakamura Y, Oikawa Y, Yano Y, Kuwabata S, Nakagawa H, et
   al. (2012). Observation of Live Ticks (Haemaphysalis flava) by
   Scanning Electron Microscopy under High Vacuum Pressure. PLoS ONE
7(3): e32676. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0032676
 - Pease, R.F.W., Hayes, T.L., Camp, A.S. and Amer, N.M., (1966). Electron microscopy of living insects. Science, 154(3753):
   1185-1186. http://science.sciencemag.org/content/154/3753/1185
 - Takaku Y., Suzuki H., Ohta I., IshiiD., Muranaka Y., Shimomura M., and HariyamaT. (2013). A thin polymer membrane, nano-suit, enhancing
   survival across the continuum between air and high vacuum
   PNAS 110 (19): 7631-7635. 10.1073/pnas.1221341110

I'd love to see how well waterbears survived.

@Daniel Given that tardigrades are able to survive orbiting in space, as you are probably aware of since you brought them up, I am confident that they can do at least as well inside the EM column.

Indeed. Anyone got a spare electron microscope and some tardigrades? And why on Earth hasn't this experiment been done already? Quick! Let's publish!


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Did birds descend from a single or multiple species of dinosaur?
It seems like there are mixed results because sometimes I read about a single missing link, like an archaeopteryx that somehow single-handedly explains all modern-day birds, but then I see conflicting articles about how different birds are descended from different dinosaurs like a t-rex or a velociraptor and so on. Which theory is correct? Did birds all descend from one common ancestor or multiple?

The answer is "one common ancestor", but I'll expand.
All organisms descend from one common ancestor so that question is not quite well-posed, but what you are actually asking I think is whether birds all descend from one common ancestor that was a bird, or whether their common ancestor wasn't a bird, which implies that different branches of birds became birds independently. In other words, are birds a "polyphyletic" group or a "monophyletic/paraphyletic" one (the difference between the latter is whether all of that common ancestor's descendants are birds, or whether it also had descendants that aren't birds).
The answer to that is that modern birds are monophyletic: they all descend from a common ancestor that, itself, was a bird. (and that common ancestor doesn't have any descendants that aren't birds)
But modern birds aren't the whole story - their group originates in the Cretaceous, and there are many groups of birds that are clearly recognizable as birds but also aren't modern birds - they might have teeth, they have subtle but unavoidable skeletal differences, etc. Like Enantiornithes and Confuciusornis. In other words, modern birds absolutely, unambiguously have a common ancestor that was itself a bird, which isn't hard because animals we would recognize as "birds" were already common by the time it appeared and the ancestor of our modern birds was just one of them. Whether those older, "extended" groups of birds themselves descend from a single species is harder to tell because fossil evidence is all we're going on, and it's even harder to tell when we go closer to the origin of birds and they no longer look unambiguously like birds. But at that point it's not so much a matter of "did this group originate from one ancestor or several" but "are these fossils that we've been putting in this group as closely related as we were assuming?" and "did this trait that these different fossils have evolve in their common ancestor, or did they evolve it independently, and what about those other fossils that seem related but don't have the trait: did they lose it from the common ancestor who had it or are they a sign that the common ancestor didn't have it to begin with?". Like, you might get different answers depending on how you define "bird". BUT paleontologists these days like monophyletic groups, so whichever groups they call "bird", those will have a common ancestor that was a "bird".
The Wikipedia page for Avialae expresses some of the issues with what "bird", or "Aves" means in the context of paleontology. To quote:

Aves can mean those advanced archosaurs with feathers (alternately Avifilopluma)
Aves can mean those that fly (alternately Avialae)
Aves can mean all reptiles closer to birds than to crocodiles (alternately Avemetatarsalia [=Panaves])
Aves can mean the last common ancestor of all the currently living birds and all of its descendants (a "crown group"). (alternately Neornithes)

"Avialae" is one of those "extended groups of birds", in that paleontologists will often refer to any member of that group as "birds", but there's still a wide gap between "Avialae" and "Neornithes"; some stepping stones on that gap:
Neornithes (modern birds) are part of
Euornithes (birds have a certain articulation oriented like modern birds, as opposed to Enantiornithes, or "opposite-birds", who have it the other way, in addition to other differences like having teeth; note this page has a cladogram), which is one branch of:
Ornithothoraces (all descendants of the common ancestor of Euornithes and Enantiornithes), which is part of
Avebrevicauda ("short-tailed birds", to distinguish them from long-tailed Avialans like Archeopteryx) which is part of
Avialae, which as mentioned is basically birdinosaurs that could fly like Archeopteryx but it doesn't stop there because that's part of
Paraves, a group of dinosaurs that by and large had wings and feathers including the four-winged dinosaurs like Microraptor gui, which if we saw today we'd recognize as not like other birds but would we recognize as not a bird, really? That's part of
Pennaraptora, which is the first group to contain names that we definitely think of as not-birds; this group contains birds as well as Oviraptor and Deinonychus, but to quote the page:

The earliest known definitive member of this clade is Anchiornis, from the late Jurassic period of China, about 160 million years ago.

And Anchiornis, as its name suggests, is bird-like, feathered wings and all. This is where we get into "wait, Velociraptors were basically like turkeys?" reactions (Deinonychus is Jurassic Park's "Velociraptors").
(also these points are where the groupings become disputed, or fast-changing, or ambiguous between groups that are defined based on phylogeny, or similarity, or others and you can get different results depending on which group's Wikipedia page you look at; for example the Wikipedia page for Theropods puts Avialae directly under Maniraptora).
Pennaraptora is part of Maniraptora, which also contains your velociraptors, and Maniraptora is part of Coelurosauria which also contains your Tyrannosaurs. At this point we have clear non-bird dinosaurs, although it's likely they all had feathers.
I don't know which articles you read saying some birds would have descended from T-Rex and others from Velociraptor; that seems completely counter to what we know today of bird evolution, even if we extend "birds" to "Avialae" or even "Paraves". In fact the only way it would work is if we call T-rex or velociraptor themselves "birds". What you could have is conflicting articles about how close birds are to T-rex or Velociraptor; that part of the family tree is based entirely on fossils and so new fossils can change our understanding of how things are related... But the current phylogeny that makes, say, Avialae a group that's quite a few nodes away from velociraptors, and both of those a couple of nodes away from T-rex, seems quite robust. We have found many, many bird and proto-bird fossils in the last few decades that have clarified the picture on that scale (you can get an idea of how many by clicking the various links).
One thing those many, many bird and proto-bird fossils also made clear is that the traits of modern birds (feathers, wings, toothless beaks, etc) didn't evolve in a simple line from non-bird to bird. Many of those traits evolved convergently in several lineages, were lost in some, maybe regained in others, and feathers in particular turn out to be a widespread dinosaur feature that cannot be considered a uniquely bird trait anymore (unless we want to call T-rexes "birds"). Still, saying "beaks evolved several times" or "feathers evolved several times" doesn't mean that birds, let alone modern birds, evolved from several different ancestors. It can mean that the common ancestor of birds had lots of variously bird-like more-or-less distant cousins living around the same time.

to add for years one of the definitions of aves was the most recent common ancestor of Archaeopteryx and the common chicken and all of that ancestor's descendants.


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What is two photon calcium imaging?
I have encountered the term "two photon calcium imaging" in a few papers.
I have tried to look in the internet but can't understand what this technique actually is.
I will be very happy for recommendations for a good internet source.
For example:

what does the "two photon" means?
how does the implement look like?
Is it sensitive to absolute voltage or voltage changes?
Does all relevant (genetically engineered) neurons light in the same color?
Is it the color that is measured or the intensity of the color?
Is the purpose of this technique single neurons or brain pathes?

Thanks!

what does the "two photon" means?

Ordinary confocal microscopy uses single photon of laser light to excite the molecule of fluorescent dye.
In two photon microscopy you use two photons, with lower energy, which cannot excite the molecule of dye on their own, but their interference in a specific place leads to summation of their energies and to excitation.
This has benefits such as decreased phototoxicity and increased precision (resolution) especially in z-plane.

how does the implement look like?
  Does all relevant (genetically engineered) neurons light in the same color?

There are two types of fluorescent dyes for 2-photon Ca2+ imagining. Since you want to measure local concentration of Ca2+, you can either use a chemical which chelates the calcium ions and changes its conformation and fluorescent properties based on that e.g. fura-2.
Alternatively, you can prepare fused protein from calmodulin ( CALcium MODULated proteIN) and some fluorescent protein e.g. GFP and transfect the cells with this product.
This means you can transfect different cells with different GFPs and get different colors. Depends on the actual experiment design.

Source

Is it the color that is measured or the intensity of the color?
  Is it sensitive to absolute voltage or voltage changes?

You can analyse fluorescence intensity changes. The derived fluorescence intensities and ratios are plotted against calibrated values for known Ca2+ levels to learn actual Ca2+ concentration. Source

Is the purpose of this technique single neurons or brain paths?

Actually, with a good interpretation of the data it can be used for analysis of both.
For more information about calcium imaging, see for example: http://www.cell.com/neuron/fulltext/S0896-6273(12)00172-9
or http://www.pnas.org/content/100/12/7319.full
or corresponding wiki articles:
https://en.wikipedia.org/wiki/Two-photon_excitation_microscopy
https://en.wikipedia.org/wiki/Calcium_imaging


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Lactobacillales vs LAB (Lactic acid bacteria)
As far as I understand bacteria of order Lactobacillales are all LAB (Lactic acid bacteria). So often "Lactobacillales" and "LAB" are used interchangeably.
But I also thought that this is not the whole truth, because there are LAB which are not of order Lactobacillales.
Can anyone elaborate on this topic and is there a paper/review explaining the consensus on this topic?

Lactic acid fermentation is the most common type of fermentation among Eubacteria, and it's found on several genera.
Actually, regarding the fermentation types, we can say as a general rule:

Ethanol fermentation: found in Plants and Fungi.
Lactic acid fermentation: found in Bacteria and Animals.

That being said, according to the Todar's Online Textbook of Bacteriology,

Although many genera of bacteria produce lactic acid as a primary or secondary end-product of fermentation, the term Lactic Acid Bacteria is conventionally reserved for genera in the Order Lactobacillales.

And according to Lactic Acid Bacteria: Microbiological and Functional Aspects, Fourth Edition:

They [LAB] belong to the Phylum Firmicutes, Class Bacilli and Order Lactobacillales.

These genera are: Lactobacillus, Leuconostoc, Pediococcus, Lactococcus, Streptococcus, Carnobacterium, Enterococcus, Oenococcus, Tetragenococcus, Vagococcus and Weisella.
The problem here is that not all lactic acid producing bacteria are called a LAB. Therefore, Lactobacillales and LAB can be used interchangeably. However, you cannot say that all bacteria that perform lactic acid fermentation are LAB.
Sources:

Textbookofbacteriology.net. (2017). Online Textbook of Bacteriology. [online] Available at: http://textbookofbacteriology.net/index.html [Accessed 3 May 2017].
Lactic Acid Bacteria: Microbiological and Functional Aspects, Fourth Edition
En.wikipedia.org. (2017). Lactobacillales. [online] Available at: https://en.wikipedia.org/wiki/Lactobacillales [Accessed 3 May 2017].

Thanks a lot for your reply. I found this sources already. Is there any review/paper confirming this as the consensus among taxonomists?

Have a look at this book, page 2: https://books.google.com.au/books?id=tFjsAuo5WocC&printsec=frontcover&dq=lactic+acid+bacteria&hl=en&sa=X&redir_esc=y#v=onepage&q=families&f=false


text:
Basic molecular biology of nucleic acids book for a mathematician studying DNA and RNA formally?
I am a mathematician studying DNA and RNA language from the perspective of Formal Language Theory.
Note that I am aware of these posts:

best book for a comprehensive introduction to biology for a computer science graduate interested in undertaking research in bioinformatics
Introductory biology text for an outsider
Material recommendation: molecular biology for mathematicians and computer scientists

I consider my situation more specific, I am specifically dealing with DNA and RNA, so what I need is a basic text that deals with this two structures, rigorous but still accessible.
As an example I quote a paper I am reading:

(...) Inverted repeats are prevalent features of nucleic acids (...)

I would like trustable references for the fact that these features indeed exist, which is fundamental for my work, and maybe a shallow explanation for what they biologically imply, but I do not want to delve into what these features mean (It would be great to understand them from a biological perspective but that is not my priority)


text:
What causes sleep inertia?
Sometimes after a nap, I wake up in a state of grogginess. I learned that this is actually called sleep inertia. I'm able to find lots of methods to overcome this, but what causes it in the first place?

This is due to states of brain activation promoted by the reticular formation, specifically with the ascending reticular activating system that mediates the general activation of the upper areas, for sleep these areas should promote states of relative low activity promoting the cerebral activation profiles during sleep, it is also interesting to study the descending reticular activating system that mediates the general muscular activation that is generally inhibited during sleep (except clinical problems among others) (that is why you can not make muscular efforts when waking up, try an experiment: try to clench your fists strongly when you are awakening).

Try adding some sources to your points. It would help and form a much better answer.


text:
Are there any animals that celebrate communally?
Are there any animals that are known to celebrate events? For example, we humans might celebrate a birthday or passing an important test. An event causes us to perform some sort of celebration that is motivated simply by joy and not any sort of survival instinct.

To clarify, I am more interested in positive celebrations. I know a number of animals having mourning behaviors (which absolutely count as a response to external events, no denying); I'm just more interested in celebrations in a positive sense.

I'd like to take this one step further.
Are there any cases proven or postulated of animals celebrating. I don't necessarily need something firm and proven, could be a theory.

This is a very interesting question! Thanks for the clarification as well.

What is the difference between a celebration and a bunch of animals happy about something together?  For example, a bunch of happy dogs racing around like crazy because their owner came home?

I expect there are two elements to what a "celebration" is, maybe three: social animals displaying joy to each other over the same event (where Will's happy dogs might apply); 2) doing so in a ritualized fashion (this is where I expect most examples to fail); 3) doing so on a differed timescale (ie not exactly after the celebrated event happened) (this one I not only expect not to happen much if at all, it seems it would be hard to impossible to observe). I think if any animal does this it would be highly intelligent and social ones, ie orcas, elephants, bonobos, parrots...

So far I've found "greeting ceremonies" among orcas; I can't seem to find a definite source on them but you'll see references if you google it, it's a ritualized behavior when orcas from a certain group meet each other after being separated awhile. Might not be what we'd call a "celebration" (after all we have "greeting ceremonies" too and we don't always call them "celebrations" per se). Orcas do illustrate one potential problem tho: if it's culture-related it's a behavior we're unlikely to observe in captivity, and might be disrupted by environmental change/human intervention.

Hmmm, good question Will. I suppose that does qualify.

Rozenn, If you can make an answer I'd gladly flag it best answer. Definitely matches what I was looking for :)

Koko (the gorilla) celebrates Christmas.

Celebrations were originally being performed as metaphysical rites with the aim of connecting with the divine intellect.

The communal yipping of coyotes?  https://www.adirondackalmanack.com/2014/03/coyotes-decoding-yips-barks-howls.html  Of course determining whether this counts as "celebration" requires getting into the coyotes' heads...

An event causes us to perform some sort of celebration that is motivated simply by joy and not any sort of survival instinct.

Celebrations usually mean large group activity but a play can be considered an event which is simply by joy and not any sort of survival instinct, and hence would fit your question. One can easily spot their pet playing around with objects when they are sitting around, busy in something 'boring' for the pets, like - reading a newspaper. But here it can be argued that pets have learned to do this to get the attention of the owner, and hence associated benefits.
Well, plays of pure enjoyment have been documented in wild animals too.

I once observed a young elk in Rocky Mountain National Park, Colorado, running across a snow field, jumping in the air and twisting his body while in flight, stopping, catching his breath and doing it again and again. There was plenty of grassy terrain around but he chose the snow field. Buffaloes will also follow one another and playfully run onto and slide across ice, excitedly bellowing “Gwaaa” as they do so (Canfield et al. 1998).

Certainly, there was no motive here apart from having fun.
I would encourage you to go through this article - Bekoff, M. (2000). Animal Emotions: Exploring Passionate NaturesCurrent interdisciplinary research provides compelling evidence that many animals experience such emotions as joy, fear, love, despair, and grief—we are not alone. BioScience, 50(10), 861-870.
Speaking of the celebration, such as - birthday, or the largest homo sapiens gathering Kumbh Mela, I would also be interested to know of some group of animals doing it periodically.
Reference:

Canﬁeld, J., Hansen, M. V., Becker, M., & Kline, C. (1998). Chicken Soup for the Pet Lover’s Soul. Deerﬁeld Beach, FL: Health.

Exactly what I was looking for :)

Good answer but this answers the question "Do animals have fun?" and it is much more evident. Celebration is very different.

You want scientists to measure animal emotions and social behaviours, and they rarely agree about animal psychology unless it's measured chemically and physically.
Celebration (behaviour for events) is not a word defined zoological science research. You can imagine that thirsty elephants that walk for 3 days to find a riverbank have a celebration when they arrive there.
Scientists don't use the word alien planet to mean exoplanet, and they don't use the word cyberspace to mean internet. For that reason, the word celebration is mostly a dramatic and reporting term that a scientist would be uncomfortable to use with proof as the basis of a document.

Could you please add sources for your claims?


text:
What is an inclusion forming unit?
What is inclusion forming unit load? I found it when reading this article.
What does this measure and what information can be gained form it? Does this represent the amount of bacteria within a person? What's the difference between inclusion forming units and colony forming unit?
I am from a mathematical background, so can someone please explain these in simple terms?

Depending on the development cycle of Chlamydia tend to appear in two forms, the elementary body and the reticulate body. As outlined in the excerpt below, the reticulate body can be found as inclusions in a cell's cytoplasm when stained with iodine. So yes, your initial guess of inclusion-forming units (IFUs) being a measurement of how much of Chlamydia spp is present in a sample (cell or tissue) is correct.
It is similar to the concept of Colony Forming Units (CFU) which is a unit used to estimate the number of viable bacteria or fungal cells in a sample. Viable is defined as the ability to multiply via binary fission ("division in half") under controlled conditions.
Applying the concept of CFU to the above an inclusion-forming unit may be understood as a unit to estimate the number of Chlamydia cells in a sample. The difference between CFU and IFU would be as follows, CFU counts are normally taken for bacteria/fungi grown in a controlled environment. CFU counts also only account for viable cells, dead cells are disregarded. This is in contrast to IFU counts as we do not have a controlled environment as such and depending on what staining method you use, IFU counts may or may not account for dead cells too.

Chlamydia may be found in the form of an elementary body and a reticulate body. The elementary body is the nonreplicating infectious particle that is released when infected cells rupture. It is responsible for the bacteria's ability to spread from person to person and is analogous to a spore. The elementary body may be 0.25 to 0.30 μm in diameter, and it mainly consists of C. trachomatis, C. pneumoniae, and C. psittaci. This form is covered by a rigid cell wall (hence the combining form chlamyd- in the genus name). The elementary body induces its own endocytosis upon exposure to target cells. One phagolysosome usually produces an estimated 100–1000 elementary bodies.
Chlamydia may also take the form of a reticulate body, which is in
  fact an intracytoplasmic form, highly involved in the process of
  replication and growth of these bacteria. The reticulate body is
  slightly larger than the elementary body and may reach up to 0.6 μm in
  diameter with a minimum of 0.5 μm. It does not present a cell wall.
  When stained with iodine, reticulate bodies appear as inclusions in
  the cell. The DNA genome, proteins, and ribosomes are retained in the
  reticulate body.

Link to Wikipedia page - excerpt was taken from there.


text:
single use traits
Are there any known traits (in any organisms) that serve exclusively one purpose?
(Counterexample: Giraffes long neck help them reach less available food AND communicate sub-sonically).
If so is that the exception rather than the rule?
This will be used for a human evolution paper, in which I would suggest that the descended hyoids in hominins and modern Homo sapiens could have serve multiple purposes, such as size exaggeration and language. I want to debate an argument that a similar descension in deer evolved, or was selected for, for only one use (i.e. size exaggeration) and that this correlates to human larynx evolution, by citing literature (if available) that demonstrates that organisms use features for multiple purposes more often than not.

Comments are not for extended discussion; this conversation has been moved to chat.

if you mean a physiological trait, a butterfly wing with a fake eye is only there to look like a fake eye. when moth species turned black during the coal peaks of the industrial revolution, it was to make them hide against the black backgrounds.

There is no rule to this, advantage is advantage however it is achieved. Slection does not care how it yields a net advantage just that it does.

If by trait you mean any phenotypic trait there are boatloads of enzymes which have only one function.  Phosphofructokinase-1 is good only for adding another phosphate to fructose-6-phosphate.
If you want big things there are plenty of those too.  The gallbladder's only function is to add bile to the intestinal contents.  The quadriceps femoris has only the function of extending the leg at the knee.  The abducens nerve controls the lateral rectus muscle of the eye and that is all.  Beta cells in the islets of langerhans in the pancreas are only good for making insulin.  You can't make them do anything else but that.

Actually the rectus femoris part of the quads also crosses the hip joint and thus in involved in hip flexion as well.

You seem to be thinking only of molecular function but even an enzyme with a single molecular function can have multiple cellular functions, be involved in various pathways and processes etc. There are actually relatively few proteins involved in one and only one function and it is very likely that they too are involved in many we just don't know about. Same for the rest of your examples: that we know of only one function does not mean there are no more.

@terdon: If I play the bass drum, but with the band I play many different pieces, is my function different with each piece?  Or am I performing the same function in different contexts?

@Will that's a very, very long and complex discussion actually. The meaning of "function" in biology is very unclear. Especially when you consider the different levels one can function on (from the molecular to the cellular to the tissue or organismal, from complex systems and emergent properties down to simple chemical reactions). If a receptor kinase activates the same MAPK pathway in different tissues but results in opposite effects is it still the same function? What if the same receptor activates a different pathway?

In fact,  PFKA1 which you mention has multiple functions: ATP binding, fructose binding, metal binding, it is involved in the metabolism of fructose and of mannose, it exists with three different types of subunits in different tissues. Is that the same function? Is it even the same protein? It all depends on how you define function and after spending 4 years doing a post doc on this sort of thing, all I can say is that it is very hard to define.


text:
Longest transcripts without isoforms
Does anyone know what genes produce the longest mRNAs? I am planning a project on synthetic introns and want to use stuffer fragments to vary intron size. Obviously they must not contain any splicing sites, hence I plan on buying cDNA clones.
It would be incredibly appreciated if someone could point fingers at transcripts that are 12...20 kbp long (and ideally have no other known isoforms or cryptic splicing sites).
Thank you!

In which organism? BTW, since you're ordering cDNA anyway, I imagine most of the non-cryptic splice sizes will be gone anyway.

mammalian, prefferably mouse

Do you mean "longest transcript without introns"?  if you want a gene with only a single isoform, I'd parse the latest mouse gtf, and look for genes with only a single transcript line.  You can get the gene length (though oddly enough, not the transcript length) in there too.

These question here is refering to the longest cDNAs. No matter if they contained introns before. The final product mustr not contain any splicing sites

To R!

Download the most comprehensive GTF file from Gencode for mouse.
Do the following in R (I'll put comments in the code so you can hopefully follow along):

library(GenomicFeatures)

#Load the GTF file and make a TxDb object
txdb = makeTxDbFromGFF("gencode.vM13.annotation.gtf", format="gtf")

#Make a GRangesList, with transcripts split per gene
grl = transcriptsBy(txdb, by="gene")

# Filter the GRangesList for genes with one annotated isoform
grl2 = grl[which(elementNROWS(grl) == 1)]

# Make a new GRangesList of the exons per gene from above
grl = exonsBy(txdb, by="gene")
grl = grl[which(names(grl) %in% singleIsoformGenes)]

# Get the length of each single-isoform gene
lens = sum(width(grl))

# Get the top 10 single isoform genes by length
head(lens[order(lens, decreasing=T)], n=10)

You then get the following output, with gene IDs on top and lengths below that:
ENSMUSG00000020255.8 ENSMUSG00000101609.1 ENSMUSG00000104211.1
              123179                84395                74456
ENSMUSG00000109536.1 ENSMUSG00000109125.1 ENSMUSG00000047888.9
               30942                25241                17327
ENSMUSG00000022262.7 ENSMUSG00000066108.7 ENSMUSG00000033826.9
               15630                14964                14583
ENSMUSG00000032855.5
               14170


text:
Human Digestion of Cellulose?
Most animals can digest the cellulose in grass because of the anaerobic bacteria called Fibrobacter succinogenes living in their rumen (gut). The bacteria produces the enzyme cellulase and is therefore able to break down the β-Glucans(1,4) glycosidic bond in the cellulose. Animals like cows and giraffes grow up to be very large simply on a diet of grass!
Is there a way for humans to ingest the Fibrobacter succinogenes bacteria and be able to digest cellulose?

Animals can digest the cellulose. Most animals (incl. humans) cannot. The one who can are only thanks to this symbiotic relationship with a anaerobic bacteria that you describe.

@Remi.b I think the question was centered around whether or not humans could ingest the cellulolytic bacteria and attain that symbiotic relationship/ability.

@HarrisWeinstein Sure. I just wanted to highlight this point which might have been of confusion for the OP.

The few animals that can digest cellulose have to have HUGE guts to provide enough space for enough bacteria to be worth it, or they have to do the rabbit thing and eat their feces to run it through multiple times. Cellulase is slooow.

This is the type of question that could rather go on WorldBuilding.SE rather than on a science website.

This isn't a complete answer, but searching Google Scholar for "Fibrobacter succinogenes human" I found this paper:
The cellulose-degrading microbial community of the human gut
varies according to the presence or absence of methanogens
The abstract of which begins this way:

Cellulose-degrading microorganisms involved in the breakdown of plant cell wall material in the human gut remain rather unexplored despite their role in intestinal fermentation. Microcrystalline cellulose-degrading bacteria were previously identified in faeces of methane-excreting individuals, whereas these microorganisms were undetectable in faecal samples from non-methane excretors. This suggested that the
  structure and activity of the cellulose-degrading community differ in methane- and non-methane-excreting individuals.

Note also in Table 1, Fibrobacter succinogenes is one of the strains that seem to have been detected, so that answers the part of your question that seems to ask if humans can incorporate those bacteria into their gut fauna: yes, some already do.
This suggests to me that:

some humans do have a limited ability to digest cellulose through their gut bacteria, though this ability is probably limited enough that "humans can't digest cellulose" can still be considered true in the large scheme of things,
the challenge in digesting cellulose isn't so much getting the gut bacteria in there, but providing them with an environment where they will thrive and digest a lot of cellulose. This is probably where the specialized gut structures of ruminants come in; it becomes not so much a matter of digesting cellulose, but of digesting it well enough that you can live off of it. I'm guessing this is also related to the differences the paper found between people who excrete methane and those who don't but I wasn't able to figure out what that was supposed to be related to (is it a cause or an effect of the presence of certain gut bacteria? is it related to diet, genes, something else? I couldn't find that information in the paper though I didn't read every word)
according to the paper there isn't much research done into this.
the paper gives no info as to how significant those cellulose-digesting bacteria are to the host's energy balance, which I imagine is what you're really interested in. Is it significant, is it too small to be noticeable, does the host even benefit at all calorie-wise? They don't address that question in the paper.

In this article it later says:
"For example, in the work of Van Soest's group10 11 in which healthy
volunteers were fed controlled diets with the addition of cellulose from
either cabbage, bran, or
a purified cellulose (Solka Floc), average cellulose
digestibility was 74% on the control diet, 75% in the cabbage, about 53%
in the bran but only 25% from the Solka Floc."
This is to illustrate how naturaly sourced cellulose is way more digestable than a chemicaly isolated one. So the answer is that cellulose found in vegetables is 53%-75% broken down. The article also mentions that it seem to vary between people.
The Human digestion system is very much similar to this of primates. In fact, a noticable difference is that the human gut is actually relatively longer. Primates feed on huge amounts of cellulose. It seems obvious that it is energetically beneficial for them. An adult male gorilla will eat up to 30kg of plant matter a day!
So yes, without independetly breaking this stuff down, we seem to do fine with a little help from our friends. Their big contribution is not surprising considering the fact that more than 80% of the cells in the human body does not carry his genes (most commonly because it is bacteria, but sometimes because it is fungi). Methane btw, is just one of three common byproducts of the bacteria breaking cellulose down. That is why cattle growing has a severe adverse effect on atmospheric ch4 (extremely potent green house gass).

This doesn't seem to answer the question. Can you please [edit] your answer so that it addresses the exact question?

Please don't copy and paste swaths of text. Instead, extract the relevant information to answer the question and combine that with other sources to generate your own synthesis of the solution to the question at hand.

Thank you for your answer, you gave some very interesting information! :) @Krugo


text:
How does repair take place on leading strand in eukaryotes?
I am currently reading molecular biology of the gene by Watson to develop an understanding of the mechanism of replication and repair.
Under the topic mismatch repair of DNA, they mentioned that eukaryotes lack a homolog of MutH. The repair takes place from the nicks developed on the lagging strand before ligase acts on Okazaki fragments.
How then does the repair take place on the leading strand as there are no nicks on the leading strand?
And also, because eukaryotes lack Dam Methylase, how does the repair system recognize which nucleotide of the mismatched pair is incorrect?

I could be mistaken, but I think eukaryotic MutL homologous have intrinisc nuclease activity.

It does not mention so in the text so I am just confused about this.

I'll keep the answer to this as concise as possible. The major mismatch repair (MMR) pathway used by eukaryotes is the MutS$\alpha$-MutL$\alpha$-dependent MMR. See the diagram below for its mechanism:

The pathway initiates when MutS$\alpha$ (Msh2–Msh6) binds to a mismatch. This is followed by binding of MutL$\alpha$ (Mlh1 and Pms2). PCNA then activates MutL$\alpha$ to incise the nascent strand and the DNA ends are used for removing the replication error. After this, the repair is completed by correct DNA synthesis and ligation (note that this pathway works in both leading and lagging strands). DNA replication and MMR are temporally coupled in a manner that may be related to the regulation or appearance of the signals used for MMR. Also, pay attention to the point that the opposite strand is used as reference strand for repair and the strand to which MutL$\alpha$ binds is the one at which Pol$\epsilon$ (or Pol$\delta$) replicates as the DNA polymerase and the PCNA act as the signal for MutL$\alpha$ activity.
See this paper (also the image source) by Kunkel and Erie (2015), they describe this process and a lot of things related to it, including its regulation and signals, in much more detail. I haven't talked much about the details here as the paper is a much better source to understand them.
References:

Kunkel TA, Erie DA. Eukaryotic Mismatch Repair in Relation to DNA Replication. Annu Rev Genet. 2015;49:291–313. doi:10.1146/annurev-genet-112414-054722

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Human body reaction to gamma rays
I attended a meeting where the speaker claimed that a human body reacts to the exposition to gamma rays reducing the amount of acetylcholine. Is this thing scientifically proven? I cannot find any source that confirm this thesis.
- Update -
The source from which the speaker based his theory is this paper. Excluding the fact that here gamma rays seem not to be mentioned, is this a reliable source?


text:
Do colour-blind people see white?
I know that white colour is perceived on excitation of red, blue and green cones simultaneously.
It is also said that a colour-blind person doesn't see a particular colour and just perceives it as a shade of grey.
If their (for example all red) cones are affected, then how do they perceive white colour?

Clarification: Will a person with defect in red cones perceive white colour when green and blue colour only fall on his retina?
So, basically he will detect RBG and BG both as white.
If not then how will he be able to differentiate?

"People with deuteranomaly and protanomaly are collectively known as red-green colour blind and they generally have difficulty distinguishing between reds, greens, browns and oranges. ... To these people the world appears as generally red, pink, black,white, grey and turquoise." Depends on what type of color blind. http://www.colourblindawareness.org/colour-blindness/types-of-colour-blindness/

If red is absent then how is white colour perceived?

@krythic Why don't you write this as an answer?

@Marzipanherz I don't care about this branch of stack exchange. Why don't you do it? Free points.

I am color blind. I see very bright blues and reds. I nearly never fail to see a red light, a red sign, a blue one, on a different background like a green tree. if you have double genes for it you get it worse. my vision is near perfect for all except color blind tests. only error ive noticed is for blurryness, is one eye sees stars less like pin dots than the other eye. very color blind people have worse color sight, there are many types.

as long as they have rods black white and  greyscale will always be possible.

Question: What kind of vision perception issue is it when the student sees similar intensities/shades of red and white as the same color (that is, red)? (So, red marker on a white board disappears...) What if this person also sees blue as green and yellow and red as orange? Wouldn't it be more than tritanopia? If so, what would this be called?

It's definitely not white or grey generally, it's a mix of other colors, they often have low resolution of a particular color so that it's less visible rather than visible and grey.

Here's a page where you can mouse over a color wheel and see a version in color blind mode:
http://www.archimedes-lab.org/colorblindnesstest.html

The first type of cone is primarily sensitive to short wavelengths (blue), another to medium wavelengths (green) and one to long wavelengths (yellow). The yellow cone is usually referred to as the red cone. While its sensitivity peak lies in the yellow wavelength band, it is also quite sensitive to red. A single cone cannot detect color, as it provides only a scalar number indicating the total light energy it absorbs. For example, the red cone by itself cannot distinguish red from yellow, green or orange. Red is detected by a combination of high activation of the red cone, low activation of the green cone and no activation of the blue cone. This page has a very comprehensive graphs and a first hand account of Tritanomaly
Evolutionary gene mechanisms have a particular knack of varying vitally important organs and functions, arm length, walking gait, hair type, color, and colorblindness is perhaps an expression of high variance to a survival critical and modular organ which animals have a high variance in depending on their habitat and survival requirements.

Thanks. One last query: consider a person who has defect in red cones, now if we put Blue and green light on his retina will he detect it as white? Since red cones are anyhow not functioning in his eyes , will he perceive it as white? If not then by what mechanism will he perceive white colour?

when all the cones are signalling a balanced range across the spectrum he will see it as white. I changed the answer with an extra graph to explain that the cones are not RGB, they have broad reception, with a page to a guy who says how he got used to greens being grey or white and reds being confused with  yellow and orange. None of the cones sense precisely red so there won't be a very narrow reaction to red colors.

Well, we can't see things as colorblind can (I have very strong reason to think  even non-colorblind people don't see colors identically due to veriations between cone cells sensibility). Given page does not give us their perception. Colorblind people can see some impossible colors, for example. For us it is a mystery until a device is made capable of affecting cone cells selectively. And I'm not sure achromatopsia makes people see everything grey. Grey is a composition of all three types of cones being involved. But their cones, I guess, don't work.


text:
Can someone identify this species?
When I was about 5 or 6 years old, a tiny yellow puffball with 2 black spots which I think are eyes landed on my finger. I didn't dare breath, and after a few moments it flew away. Is there any such species that is similar to my description?

Welcome to Biology.SE. Given your description, it is very difficult to answer your question. Try to think of any feature you remember, any characteristic that might help the id. Maybe try to draw or post a picture that resembles what you have seen. As is, your question might be down-voted or closed as too broad.

Sounds like a bee/bumblebee covered in pollen.

It might be helpful to add location, season and daytime of the event.

It's really tiny, about 2 times the size of a pen point


text:
What is the name of this big tree with look of banyan branches?
Location is India, Tree is so huge & some branches are hanging like Banyan.

Its Hanging Branches look:

& Finally its leaf:

So what is it then?

Looks like a fig, it has large number of species.

Did you find any fruits of the same?

Looks like Ficus, maybe F. benghalensis


text:
Photosystem 1 and 2; P680/P700; Chlorophyll a/b
I am getting slightly confused about how the above relate to each other. My current understanding is that P680 and P700 refer to the primary pigment reaction centres in Photosystems 2 and 1 respectively, with the numbers giving the peak wavelength of absorption. Now I initially thought that one of these primary pigment reaction centres must be composed of chlorophyll a and the other of chlorophyll b, hence the slightly differning absorption wavelengths. Instead, here it seems to suggest that the primary pigment reaction centre is always chlorophyll a. Most sources I have looked at do not specify what forms the primary pigment reaction centre (the Wikipedia article on photosynthetic reaction centre, for example, does not state for the general case of for photosystem 2; however it does mention that photosystem 1 has a special pair of chlorophyll a molecules at the centre).
So my specific questions are:

Is the primary pigment reaction centre in both photosystem 1 and 2 (i.e. P700 and P680) a pair of chlorophyll a molecules?
If so, what is chlorophyll b? Is it simply an accessory pigment?
Finally, if it is the case that the primary pigment reaction centre is chlorophyll a in both cases, how can it be that it absorbs at a different wavelength in the two photosystems if it is the same molecule?

Regarding your questions #1 ("Is the primary pigment reaction centre in both photosystems a pair of chlorophyll a molecules?") and #3 ("How can it be that it absorbs at a different wavelength in the two photosystems if it is the same molecule?"):
Both reaction centers in Photosystem I and Photosystem II contain only chlorophyll a. According to Lodish (Molecular Cell Biology):

As in the bacterial reaction center, at the center of each chloroplast photosystem is a pair of specialized reactioncenter chlorophyll a molecules, which are capable of undergoing light-driven electron transfer. The chlorophylls in the two reaction centers differ in their light-absorption maxima because of differences in their protein environment. For this reason, the reaction-center chlorophylls are often denoted P680 (PSII) and P700 (PSI). (emphases mine)

Regarding your question #2 ("If so, what is chlorophyll b? Is it simply an accessory pigment?"):
Chlorophyll b has a different molecular structure (and, therefore, a different absorption spectrum) and it's less abundant in the chloroplast than chlorophyll a. Here is an image depicting their molecular structures and absorption spectra:

(a) Chlorophyll a, (b) chlorophyll b, and (c) β-carotene are hydrophobic organic pigments found in the thylakoid membrane. Chlorophyll a and b, which are identical except for the part indicated in the red box, are responsible for the green color of leaves. β-carotene is responsible for the orange color in carrots. Each pigment has (d) a unique absorbance spectrum. Source: "OpenStax College, The Light-Dependent Reactions of Photosynthesis. October 16, 2013."
Both chlorophyll a and b are present in the antenna complex. Still according to Lodish:

As in photosynthetic bacteria, each reaction center has an associated antenna that consists of a group of light-harvesting complexes (LHCs); the LHCs associated with PSII and PSI contain different proteins.

However, most of chlorophyll b is associated to PSII antenna complex, not PSI, which is one of the main differences between PSII and PSI.
Source: Lodish, H. (2000). Molecular cell biology. 4th ed. New York: W.H. Freeman.

PSII generates H+ and O from water - the H+ acidifies the thylokoid lumen, IIRC. PSI, drives a process that pumps out H+, again IIRC. Doesn't this mean that the photon adsorption rates of PSII and PSI must be closely balanced? If so, then wouldn't PSII's capacity to tune its adsorption spectum be a mechanism to balance photochemistry?

The antenna pigments are predominantly chlorophyll b, xanthophylls, and carotenes. Chlorophyll a is known as the core pigment. Their absorption spectra are non-overlapping and broaden the range of light that can be absorbed in photosynthesis. The carotenoids have another role as an antioxidant to prevent photo-oxidative damage of chlorophyll molecules. Each antenna complex has between 250 and 400 pigment molecules and the energy they absorb is shuttled by resonance energy transfer to a specialized chlorophyll-protein complex known as the reaction center of each photosystem. The reaction center initiates a complex series of chemical reactions that capture energy in the form of chemical bonds.
  Source : https://googleweblight.com/i?u=https://en.m.wikipedia.org/wiki/Light-harvesting_complexes_of_green_plants&grqid=SbEQ4daG&hl=en-IN
In land plants, the light-harvesting antennae around photosystem II contain the majority of chlorophyll b. Hence, in shade-adapted chloroplasts, which have an increased ratio of photosystem II to photosystem I, there is a higher ratio of chlorophyll b to chlorophyll a.This is adaptive, as increasing chlorophyll b increases the range of wavelengths absorbed by the shade chloroplasts.
  Source: https://googleweblight.com/i?u=https://en.m.wikipedia.org/wiki/Chlorophyll_b&grqid=UwAfK7V5&hl=en-IN

So, both reaction center have chlorophyll A, which can absorb a range of wavelengths with maxima 662 nm.
Although, peak differs for two photosystems because of antenary proteins. More chlorophyll b in PS II transfers more energy to chlorophyll a at peak 680 nm.
More carotenes and xanthophyls in PS I transfers more energy to reaction center at 700 nm peak.

From what I understand both photosystems contain chlorophyll a, although they are modified differently in each case which changes their absorption spectra accordingly.
Sources:
en.wikipedia.org/wiki/Photosystem_I
www.ncbi.nlm.nih.gov/pubmed/11687208
www.ncbi.nlm.nih.gov/pubmed/11786359
Chlorophyll b is a pigment that differs from chl a by a single functional group:

And so it also has a different absorption spectrum:

As mentioned by Goel, some plants (or plant parts) that grow in shadows have a higher ratio of PSII (contains the majority of chlorophyll b en.wikipedia.org/wiki/Chlorophyll_b, Plant physiology and development by Taiz and Zeiger 6e, chapter 9) to PSI which results in an increased amount of chlorophyll b pigments in their photosynthetic tissues. This gives them an advantage as they absorb rays with wavelengths that are missed, or not absorbed efficiently, by the leaves that shade them.


text:
Nucleic acid extractions
Is it fine to leave pulverized plant tissue in CTAB buffer at -80 degrees over night? will the buffer remain effective to generate good quality nucleic acids?

Someone push back but freeze-dried or frozen in liquid N2 is shown to be preferable, typically.


text:
How many molecules are generally required for cell signallng processes for given cases?
I know its really a broad topic but I am interested in just few cases:

Quorum sensing
neurotransmitters for the communication of images/ general information
hormones/pheromones

I actually want to know that does a single or hundreds of molecules are needed to communicate information from one cell to another.
I searched but approx number of molecules, I can't find anywhere.

A cell can interact with other cells in zillions of ways. You can send information from one cell to other cells via neurotransmitters, hormones, pheromones, electric signals, magnetic resonance ,leukotrines etc.
In general a single type of molecule is enough to send such information. Like you require only Acetylcholine(Ach) as neurotransmitter to transmit various nerve impulses.
But, even for a single type, you require thousands of molecules. Like 1 molecule of Ach can do almost nothing and would immediately be broken by Acetylcholinesterase. You require 1000s of such molecules.
You can modify the communicating information via different types of transmitters. You can use GABA or glycine to supress any information exchange or use dopamine to enhance it. But again you will need many molecules of GABA or Glycine.
For visual pathway,  you can use no. of types of transmitters like glutamate, glycine, gaba, dopamine, acetylcholine, substance P etc.
Neurotransmitters for visual pathway.
Hormones are transmitters that are required in small quantities. But,  again you require certain concentration. There is normal blood concentration of various hormones like 80 pg/ml for calcitonin.
Quorum sensing use transmitters like AHLs. Again a certain threshold value is required for them to act.
Again,  to produce these transmitters you have to go through a rigorous process of transcription, translation and post-translational modifications.
So, for cell to communicate a rigorous process is used.


text:
What is this bird called?
I've found this bird.
Does anyone know what is it?

Since Asia is pretty big: Where in Asia is this taken?

You should ask him, I don't know him personally but he looks like a good bloke, he does remind of a Geoffrey though

It is White breasted Kingfisher also called White throated Kingfisher. Halcyon smyrnensis.

Why this is Halcyon smyrnensis?

Halcyon kingfishers are mostly large kingfishers with heavy bills.

According to wikipedia this genus has 11 species, some workers also include genera Pelargopsis, Syma and Todirhamphus.

Out of all the 11 species only two are comparable to H. smyrnensis; Halcyon badia and Halcyon coromanda.

Halcyon badia is an African resident.

Additional information:

They are “sit and wait” predators of small ground animals including large insects, rodents, snakes, and frogs, but some will also take fish.

The genus Halcyon in the current sense consists mainly of species resident in sub-Saharan Africa, with a couple of representatives in southern Asia, one of which, the white-throated kingfisher, occasionally reaches Europe. White-throated and Ruddy kingfishers (Halcyon coromanda) are at least partially migratory.

it looks much more nice but has a lot in common

Added more information to establish as why it is your bird and the similarities are not due to chance. Check google for images from different angles. @griffonvulture


text:
How many possible codons?
Consider a codon of the form NNK (where N = Adenine, Cytosine, Guanine or Uracil & K = Uracil or Guanine).  How many codons are now available? I know if all were available there would be 4^3 = 64 codons. How many are possible now? When I have tried combinations manually I got it to be 32, is this correct?

4 * 4 * 2 = 32.

What is being meant by N and NN of NNK? Does it means the first 2 nucleotides have to be same?

Yes, 32 is correct.
Technically, I have nothing to add what Gerardo Furtado and a tiger haven't already mentioned but a graphical representation of all permutations might help to understand this a bit better.
For the first 2 positions in the codon we have 4 bases to choose from (adenine, guanine, uracil and cytosine). So this can mathematically be represented as 4 x 4 = 16 or visually as:

Now, for the next position (the position of interest) we only have two bases to choose from (uracil and guanine). Leaving us with 4 x 4 x 2 = 32 different permutations, or visually:

You are welcome. I am glad it helped.

Yes, it is.
Gerardo Furtado has already provided a short answer in the comments, but allow me to explain why.
The 4^3 = 64 if all bases can be chosen freely comes down to 4*4*4=64, because you can choose from 4 options for each of the 3 bases.
If you restrict the possibilities of one of the bases, e.g. there are only 2 options for the third base (as in your example), the formula changes to 4*4*2=32, as you can choose from 4 options each for the first 2 bases and from 2 options for the 3rd base.
Edit:
If the 2 'N's from 'NNK' have to be the same, you can choose the first base freely (4 options), the second base is already defined (it has to be the same as the first base, 1 option) and there are 2 options for the 3rd base as described above. Thus, we get 4*1*2=8 possible codons
I hope I could clear this up.

Good explanation. For completeness, it would be extremely unusual if NNK denoted that the first two bases had to be identical: first off, it’s not the convention; IUPAC ambiguity codes are character wildcards, not variables in the common mathematical sense. And secondly, there’s little biological reason to consider codons where the first two bases are identical.

I absolutely agree.


text:
Why do nerve fibres rotate?
Background: Lemniscus (Latin lēmniscus, ribbon) is a strap of second order nerve fibres which twist as they ascend to the brainstem.

Why do these these nerve fibres rotate?
 What could be the functional significance of such rotation?
I think that rotation is somewhat less beneficial because firstly it causes increase in length thereby increasing the conduction time , secondly it may decrease structural integrity of such a bundle of axons.

Why downvote????

I didn't downvote, but I think you are overestimating the amount of twisting that occurs, it isn't going to affect length substantially. If you mean the quarter-turn twist that makes caudal inputs turn lateral and rostral inputs turn medial then indeed this is a very minor twist. Not everything in biology is significant in terms of function, often things are significant for development; a slight twist might help to coalesce the fibers. I'd also say that the structural integrity argument makes no sense, think about how a rope is constructed via twisting smaller fiber strands for strength.

Okay. Does this make any functional significance just like decussation?

It is probably relevant for the orientation of the homunculus in, for example, the VPL of the thalamus, but I think it's more an issue of it being important that there is a spatial organization of the fibers, rather than any particular orientation being important.


text:
Was HindII the first restriction endonuclease to be extracted?
Background:
Guided by wikipedia and pmc I found this paper by Hamilton O. Smith. and .Daniel Nathans.

A
  restriction
  enzyme
  is
  a
  component
  of
  a
  restriction-modification
  system
  of
  a
  given
  specificity
  within
  an
  organism.
  The
  R-MT
  system
  consists
  of
  two
  enzymatic
  components,
  a
  restriction
  endonuclease,
  and
  a
  modification
  enzyme
  sharing
  similar
  (or
  identical)
  recognition
  specificity.
  We
  would
  like
  to
  propose
  that
  the
  genus-species
  designation
  be
  used
  as
  an
  R-M
  system
  name
  according
  to
  the
  following
  rules.
(1)
  The
  genus
  and
  species
  name
  of
  the
  host
  organism
  is
  identified
  by
  the
  first
  letter
  of
  the
  genus
  and
  the
  first
  two
  letters
  of
  the
  species
  to
  form
  a
  three-letter
  abbre-
  viation
  in
  italics.
  For
  example:
  E.
  coli,
  Eco
  and
  H.
  influenzae,
  Hin.
(2)
  Strain
  or
  type
  identification
  follows
  the
  genus-species
  abbreviation
  in
  non-
  italicized
  symbols,
  e.g.
  EcoB
  or
  EcoK.
  In
  cases
  where
  the
  R-M
  system
  is
  genetically
  specified
  by
  a
  virus
  or
  pla,smid
  the
  italicized
  genus-species
  abbreviation
  of
  the
  host
  is
  given
  and
  the
  symbol
  for
  the
  extrachromosomal
  element
  follows
  in
  non-italics,
  e.g.
  EcoPl,
  EwRI,
  etc.
  In
  occasional
  cases
  where
  it
  might
  be
  necessary
  to
  specify the
  host
  strain
  as
  well
  as
  the
  extrachromosomal
  element
  the
  strain
  identification
  symbol
  may
  be
  inserted
  parenthetically,
  e.g.
  Eco(B)Pl.
(3)
  When
  a
  particular
  host
  strain
  has
  several
  different
  R-M
  systems,
  these
  are
  identified
  by
  Roman
  numerals,
  thus,
  the
  R-M
  systems
  from
  H.
  injluenzae
  strain
  d
  would
  be
  HindI,
  HindII,
  HindIII,
  etc.

Main question:
Now HindII was -

extracted from  Haemophilus influenzae
the strain was strain Rd, so d
and it was the 2nd enzyme to be isolated? Hence II.

So how is it the first Type II RE?

H.O. Smith, K.W. Wilcox, and T.J. Kelley, working at Johns Hopkins University in 1968, isolated and characterized the first restriction nuclease whose functioning depended on a specific DNA nucleotide sequence. (wiki)

I don't know how widely this has been accepted but Roberts proposed in 2003 that the italics should be dropped (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC152790/). I used to be a stickler for using italics, but I now prefer without.

I'm voting to close this question as off-topic because it's not about biology it's about history, and not very interesting history either. Why should you care whether it was HindIII or EcoRI for goodness sake!

I don't understand what can be wrong in getting a doubt cleared? The question (in the title which still stands unedited) was the main question behind this post. NCERT (a book back from my school) did not mention the Type II part to keep things simple. It lingered in my mind (as why an enzyme which is II yet the first) and definitely it was my silly mistake to not have observed the Type II thing even while reading it after so many years. My question wasn't which one's the 1st enzyme? But why HindII the first one?  @David

I call them as I see them. (Friendly tip: best to try to avoid Indian English "doubt" on International forums — use "question" instead.)

if the strain is Rd then instead of Hind,HinR should have been written, what is the answer

The explanation here is quite simple: HindI, despite having been isolated/discovered before HindII, is a type I Restriction Enzyme, not a type II:

A type I restriction enzyme from Haemophilus influenzae, Hind I, which requires adenosine 5'-triphosphate and 5-adenosyl methionine, was studied for its activity on transfecting and transforming deoxyribonucleic acid (DNA) [...] Most of the restriction enzymes from Haemophilus belong to type II restriction enzymes according to the classification system proposed by Boyer. These enzymes require only Mg2+ for their action in contrast to type I enzymes that require Mg2+, adenosine 5'-triphosphate (ATP), and S-adenosyl methionine (SAM).

(Source: Biological Properties of a Haemophilus influenzae Restriction
Enzyme, Hind I)
Thus, in fact, HindII was the first type II Restriction Enzyme isolated/discovered, as it's well documented.

PS: As a bonus, here is a table with the main differences among RE types I, II, III and IV (Source: Thermo Fisher Scientific):
Type I:

Multi-subunit protein with both restriction and methylation activities
ATP requirement
Cleavage site a variable distance from recognition site

Type II:

Specific recognition sequence
Cleavage site within or close to recognition sequence
Generates 5′ phosphate and 3′ hydroxyl termini at cleavage site
Mg2+ requirement for most

Type III:

Two-part recognition sequence in inverse orientation
Cleavage site a specific distance away from one of the recognition sequences
ATP requirement

Type IV:

Cleavage of only methylated DNA
Cleavage site approximately 30 base pairs away from recognition site


text:
Copy number regulation & CNV
I have some genes which showed copy number loss between two groups. Now I want to see the copy number regulation of those genes. I really don't know about this concept. Can anyone please tell me clearly about this like why we need to check regulation of copy number loss genes? And any idea how to do this?
Thank you

It might be helpful if you showed us what sort of data you are looking at since copy number variations and gene expression can each be detected in similar but distinct ways.
Generally speaking, both gene expression and CNVs are detected by counting the number of reads that map to a given genomic region. The difference is that CNVs are detected using DNA sequencing while gene expression is detected using RNA sequencing. This is an important distinction because CNVs are a more stable genomic feature than gene expression. Reviewing the Central Dogma might help if this is confusing.
In the context of your problem, the main thing to understand is that CNVs can exert an influence on gene expression but gene expression cannot exert an influence on CNVs. Having fewer copies of a gene means that the process of transcribing RNA to express it cannot proceed as quickly as normal. So in an organism with gene X showing copy number loss, it makes sense to expect diminished expression of gene X than in organisms whose genome includes more copies of that gene X. If you're asking for an undergraduate class, chances are this is all you're expected to understand about "copy number regulation": the maximum transcription rate of a gene is dependent on how many copies of that gene are available for transcription.
Gene regulation becomes important for understanding how an organism with fewer than normal copies of gene X in its DNA might have the same amount of gene X RNA expressed as an organism with a normal number of copies of gene X. Suppose that some molecule, M, is necessary for expression of X but degrades after a short time. The cell will send M to the nucleus whenever it needs X to be expressed and the number of X transcripts produced per molecule of M will be dependent on the number of X copies available for transcription. If M is abundant and can be continually sent to the nucleus, then the cell with fewer copies of X can theoretically produce as much X as the cell with a normal number of X copies although it'll take a bit longer. If instead M is a finite resource within the cell, then the amount of X expressed in cells with fewer copies of the gene should be consistently lower than cells with more copies.
Of course if M happens to be produced by a gene exhibiting copy number gain/loss then that could also play an important role in how much X RNA transcripts you ultimately detect (even in the event that X actually has a neutral copy number). Hope this helps.


text:
Could someone help me identify this insect?
Does anyone know what this insect is? I put a rubber ball on my lawn, and within seconds a bunch of these insects (maybe 15 or 20) landed on it. I took a look around and saw that there were lots of them flying low near the grass or sitting on the grass (they were not as obvious on the lawn as on an orange ball :).
Location: Massachusetts (USA).

Could you provide an estimated size of your specimen?

Looks like a Bibio, sometimes referred to as "March flies" and one species in particular known as "St Mark's Fly". Yours seems unlikely to be that one because it is found in England and it seems like nowhere else.
Most likely I think yours is a Bibio vestitus from the picture below (unfortunately I wasn't able to find multiple sources corroborating this, though, so take it with some caution), and although I had trouble finding definitive distribution data, it looks like the one in your picture has the copper-colored legs, and in addition the first image below claims to be from Massachusetts. There are many many species of Bibio though so I can't be certain of species.

Bibio vestitus
Reference

This is certainly some species of fly (order Diptera) and appears to be a species of march fly (Bibionidae)

 Bibio anglicus
Bibionidae (march flies) characteristics [Source]:

Dark colored
Eyes usually meet along the top of the head
Front legs often have strong spines on the tibia
Often with dark spots or “stigma” on the wings.
Wing patterns (from Wikipedia):

The wings have two basal cells (posterior basal wing cell and basal wing cell), but are without a discoidal wing cell. R4+5 is simple or branched; at most, only three branches of R developed. The leading edge wing veins are stronger than the weak veins of the trailing edge.

The march flies are known to hover close to the ground like you saw [Source].
Although IDing to species is difficult with the low quality of the photo, I would think that Hardy et al 1958 would be a good start for you to use:

Hardy, D.E. et al., 1958. Guide of the insects of Connecticut PartVI. The Diptera or true flies of Connecticut Sixth Fascicle: March flies and gall midges. Bibionidae, Itonididae (Cecidomiidae). Conn. Geol. Nat. Hist. Surv. Bull. 87, 218 pp., 15 pl., 29 figs.

Your specimen is likely in the genus Bibio (march flies or St. Mark's flies).
You can tell it's not a robber fly (family Asilidae) because the eyes of your specimen come together at the top of the head (like most march fly species [Source]), while according to here

All robber flies have a characteristic divot on top of the head, which is located between their especially prominent compound eyes.


text:
What determines when twining plants twine?
Some climbing plants, such as clematis and honeysuckle use their leaves like tendrils. Others, like Aristolochia use their stems. The young leaves of these plants are able to twist around slender objects. Twining stems twist around whatever they touch, be it a pole, branch, wire or chair leg. The stems will wind clockwise or counterclockwise, depending on the species of plant.
AFAIK, plants can't see or feel, but the way they climb clearly shows they have some way of knowing when to twine. How does this work?

Thigmotropism
This is a special case of tropism, called thigmotropism. In botany, tropism is a modified growth in response of an environmental stimulus. The most famous tropisms are:

Phototropism: plant growth in response to a light stimulus
Gravitropism: plant growth in response to gravity

In the case of thigmotropism, the growth is modified in response to touch (from the greek θιγμός). Curiously, this phenomenon was studied by Darwin in his late life: Darwin, C. (1865), On the Movements and Habits of Climbing Plants.. Journal of the Linnean Society of London, Botany, 9: 1–118. doi:10.1111/j.1095-8339.1865.tb00011.x
The mechanism of thigmotropism can be compared to that of phototropism: in phototropism, the shaded side of the stem apex has a higher concentration of auxins compared to the sunny side and, therefore, grows more quickly, and the result is that the plant grows towards the light source (positive phototropism).
In thigmotropism, there are mechanic receptors in the epidermis which detect touch (mechanoreceptors), possibly membrane proteins. Then, after detecting touch, there is a signal transduction somehow, which "informs" the cells opposite to the touching side about the stimulus, and those cells exhibit an increased rate of growth.
The mechanism may be similar to that of phototropism, also depending on auxins. According to Scorza et al. (2011):

Ultrastructural studies revealed that most thigmotropic and thigmonastic movements are caused by differentially changing cell turgor within a given tissue. Auxin has emerged as a key molecule that modulates proton extrusion and thus causing changes in cell turgor by enhancing the activity of H+ATPase in cell membranes. (emphasis mine)

The actual details regarding the mechanism are not well understood, and they are way less understood than those of phototropism or gravitropism, for instance. The result, however, is that the touching side grows less that the opposite side:

If you combine thigmotropism and negative gravitropism (the growth against gravity), the result is that the climber grows up going around the support, in an upwards spiral:

A detailed explanation can be found here: Plant tropisms. 1st ed..
Sources:

Scorza, Livia Camilla Trevisan, and Marcelo Carnier Dornelas. “Plants on the Move:  Towards Common Mechanisms Governing Mechanically-Induced Plant Movements.” Plant Signaling & Behavior 6.12 (2011): 1979–1986. PMC. Web. 14 May 2017.
Gilroy, S. and Masson, P. (2008). Plant tropisms. 1st ed. Ames, Iowa: Blackwell Pub


text:
How can you gain 1 lb of bodyweight from eating less than 1 lb of food surplus?
A commonly referenced "fact" is that a caloric surplus of 3500 kcal is equivalent to a 1 lb gain in bodyweight. But I'm confused. If you get 3500 kcal worth of, say, fatty acids, which are 9 kcal per gram, then that's about 390 g, which is just under 0.86 lb. How can you gain 1 lb of bodyweight from eating a surplus of less than 1 lb? Am I missing something?

Probably water.

Also, although there are problems with the 3500kcal equals 1 pound rule, even when it works, the point isn't that eating 3500kcal adds a pound of bodyfat: rather, catabolizing 1lb of body fat equals about 3500kcal of energy.

agree with @BryanKrause above concerning water... however, the way you have phrased the "fact" mentioned above is not entirely correct, which is a common misconception - it costs some energy to store energy in the body. In other words, even though 3500 kcal is ~1 pound thermodynamically, that does not translate into exactly one pound of body weight gain. To store energy as lipid, the body "spends" some of the energy to package and store it as lipid. Thus, if you gain a pound, you've actually eaten more than 3500 calories. (Note: the 3500=1 pound is hotly debated, etc)

@VanceLAlbaugh Thanks, you explained a bit more thoroughly than I did. Also: proof that it is easier to lose a pound than to gain one! Call the daytime TV 'doctors'! (all a joke, of course...)


text:
Is a novel homozygous SNV reasonable?
I'm doing some variant discovery in a human trio (affected child, non-affected mother, non-affected father) and I have found what looks like a homozygous novel mutation. All of the aligned reads in the child have the same nucleotide in that position, but neither of the parents do.
In looking at a small handful of variants, I've seen plenty of novel heterozygous SNVs. But on first blush a novel homozygous SNV seems extremely unlikely. Two independent germline mutations at the same position on both paternal chromosomes is all but impossible, right? Are there other mechanisms by which a novel mutation would become homozygous? Or am I right to be skeptical here?

I was going to make a hilarious joke, but then I thought some modicum of tact may be prudent. Is it possible that one of the parents isn't actually a parent?

What technology are you using.  Illumina?  Sanger?  Have you "eyeballed" the variant?

A heterozygous allele can become a homozygous via homologous recombination. You can check if the region around the SNV is also homozygous.

@WYSIWYG But remember, this isn't a heterozygous allele. It's a novel allele that didn't exist in either parent. Although from the context of homologous recombination, it the novel mutation had already occurred by that point it would be considered heterozygous. But could you clarify how heterozygous alleles can become homozygous? I'm rusty with my molecular genetics, but I thought homologous recombination swaps DNA between paired chromosomes, not copy from one to the other.

@DanielStandage https://en.wikipedia.org/wiki/Gene_conversion