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How much carbon does a forest contain?
Trees in a forest, alongside the fungi, animals and plants that live there in, capture atmospheric carbon dioxide and store it inside their tissues and in the soil as humus.
It is possible to estimate the amount of carbon stored in some portion (say 100 square meters) of a climax forest?
This should depend on the specific biome, for example Eucaliptus and Pine forests seem to contain less organic matter than broad-leaved tree forests in temperate regions.
PS: A slightly more speculative aspect of this topic is to evaluate weather reforestation can contribute to lower the amount of carbon dioxide in the atmosphere.

There are some well established methods for this. For example, estimating forest C stocks and fluxes is done for national C accounts which are used by the Intergovernmental Panel on Climate Change (IPCC) for global reporting.
The usual method is to measure the diameter of all trees in a defined area (a plot, e.g. like you suggest of 100 square meters), then use allometric equations to estimate either the volume or biomass of each tree, then convert this to C (which is simply 50% of the total dry biomass). This gives you the C stock of all trees in your plot, which can then be scaled up to the entire forest if you wish (you would need lots of plots to make a credible estimate).
Allometric equations vary between tree species due to their differences in shape and wood density. However the general proportion of C varies little between species, it is always close to 50% of biomass. It is better to use allometric equations specific to the tree species you are measuring but if none are available you can use a generic equations:

For live tree biomass, diameters of a sample of trees are measured and converted to biomass and carbon estimates using allometric biomass regression equations. Such equations exist for many forest types; some are species-specific, whereas others, particularly in the tropics, are more generic in nature (e.g., Alves et al., 1997; Brown, 1997; Schroeder et al., 1997). Cutting and weighing a sufficient number of trees to represent the size and species distribution in a forest to generate local allometric regression equations with high precision, particularly in complex tropical forests, is extremely time-consuming and costly and may be beyond the means of most projects. The advantage of using generic equations, stratified by ecological zones (e.g., dry, moist, and wet; see Brown, 1997), is that they tend to be based on a larger number of trees (Brown, 1997) and span a larger range of diameters; these factors increase the precision of the equations. A disadvantage is that the generic equations may not accurately reflect the true biomass of trees in the project.

If you already have wood volume data, which is often available for production forests, you can use a Biomass Expansion Factor to convert volume to biomass, and then to C.
Another method is to use lidar (laser scanning) to generate a 3D model of the trees in your plot and then calculate their volume -> biomass -> C.
Since trees are the easiest component of the forest to measure, there are methods to estimate the other C pools (litter, soil, roots, dead wood) because it is generally too difficult and time consuming to measure these. E.g. dead wood is generally 5-40% the C of live trees, but ideally you would use an estimate based on a  similar forest type.
You specifically mention climax forest - though the method is the same for all forests it is likely to be less accurate for climax forests because they tend to be more variable in tree size and most allometrics have been developed for smaller trees (e.g. in plantations) and are usually not as accurate for larger trees. To improve accuracy you would need to cut down some trees and measure all of their components to derive your own allometrics.
BTW eucalypt and conifer forests in temperate regions have the highest C stocks per unit of land area of any forests.

Thanks! I would discard the last sentence on Eucalyptus. The paper seems to refer to a single species, the E. regnans  (which can be as massive as some Sequoia, and has a lot of wood). Many Eucalyptus forests do not favour undergrowth and burn easily/regularly, thus store less biomass than others.

My comment was in response to your statement: "Eucaliptus [sic] and Pine forests seem to contain less organic matter than broad-leaved tree forests in temperate regions." This may be true as an average or total for all temperate eucalypt and pine forests, though I don't have those figures. Nevertheless, it is a relevant fact that the most carbon dense forests are certain temperate eucalypt and conifer forests.

This question is very broad and this would require a lot of calculations, I will focus on the carbon dioxide in the trees, hopefully some other users can add details in respect to the organism and their carbon dioxide storage.
I found an article(R.Jandl et al.,(2007)) which did some calculations, this site does a really good job in explaning these calculations so I will cite that:

As trees photosynthesise they use carbon dioxide (CO2) from the
  atmosphere with water from rain or irrigation and nutrients from the
  soil to form carbohydrates, which make up the tree’s biomass, but how
  much carbon is made by a tree in this process? Researchers at
  Ecometrica have worked it out! The amount of carbon stored by a tree
  depends on its size, which in turn is influenced by factors, such as
  species, local environmental conditions and the way it is managed. In
  an attempt to find a simple answer to this question, researchers at
  Ecometrica have broken down approximately how much carbon is stored in
  each element of a typical tree (the branches, the leaves, the stem and
  the roots) by percentage for a quick and simple calculation.
They used standard forestry practices to estimate the amount of carbon
  contained within the stem, branches, roots and leaves of a mature
  sycamore (Acer pseudoplatanus), found near their office in Edinburgh,
  with a diameter of 52 cm and a stem height of 12 m.
First they measured the various parts of the tree and, from these
  measurements; they calculated their volumes, which were then used to
  calculate the biomass (mass of living matter in plant tissues):  The
  radius of the stem at 1.3 m above the ground (r1 = 26 cm) and at the
  top of the stem (r2 = 20 cm), and The height of the stem (h = 12 m)
  They used known relationships between the biomass of the stem and the
  biomass of roots, branches and leaves to estimate the total biomass of
  the tree: Stem volume was estimated using the equation for the volume
  of a truncated cone:

which gave an estimated stem volume of 2.0 m3 The wood density of sycamore is approximately 620 kg/m3, so using the equation:
Mass = Density × Volume  the stem biomass was 1243 kg, or
  approximately 1.2 tonnes  The biomass of the roots, branches and
  leaves of a sycamore tree are known to be around 26%, 11%, and 1% of
  the total biomass, respectively. These proportions were used to
  estimate the total biomass of the tree without having to dig up roots
  or cut down branches.  In summary, the sycamore tree had a stem with a
  biomass of 1.2 tonnes, roots of 0.5 tonnes, branches of 0.2 tonnes and
  leaves of 0.02 tonnes, giving a total biomass of 2 tonnes.
The carbon content of woody matter (stem, branches and roots) and that
  of leaves is approximately 50% of  their biomass. Multiplying the
  total biomass by the proportion of that biomass which is carbon gives
  an estimate of the total amount of carbon stored in the tree, which in
  this case was exactly 1 tonne! Each tonne of carbon equals to
  approximately 3.67 tonnes of CO2.

Then the further calulations really depends on the density of the trees in the forest (if you know the exact number let me know). There are a lot of atricles which gave some numbers the range is based on these articles somewhere around 30-400(and some even 1200 trees). I used the data from this article, which measured the optimal density for growing. I assumed that the climax forest is just naturally so I just picked 400 trees per acre (this is just guessing offcourse and I just generalized this for all trees, but I saw 400 in an other article):

Then we can just do some simple math for the carbon dioxide for the trees:

total CO2 for the trees = 400 x 3.67 = 1468 tonnes

Let me know if someone can find the tree density of a climax forest

Great answer! I'd be happy to up vote, but I can't do that yet. I was thinking of an alternative approach, involving the notion of biomass. The more the biomass in a forest, or crop filed, the more the carbon stored. Probably, it is possible to estimate the carbon stored in a  Kg of generic biomass, and then check the how much biomass a forest has!

In a climax forest the stand density (number of trees) would be much less than 400 trees/acre. The trees would be larger though, with much more than 1 tonne of C each. Total aboveground C in trees would likely be 300-500 t/ha (1100-1835 t CO2). A hectare is 2.47 acres, so around 450-750 t CO2 per acre. Plus more for understorey plants, dead wood, roots, soil, etc.

It is certainly possible to make an estimate, and other answer have already elaborated on the methods used. As to the underlying question, how much this contributes to store carbon: Lewis et al have published a study (in Nature) estimating the amount of carbon stored over long time periods in African tropical forests. They combined this with other publications and estimated that 1.3 Pg C yr-1 is stored in the tropical forests of our planet.


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How does reversibility of lactic acid fermentation work?
For the production of lactic acid we need pyruvate from glycolysis.
This process is known as lactic acid fermentation. One of the features of this process is reversibility. How does this reversibility work?

The enzyme catalysing this reaction in mammals is lactate dehydrogenase of which there are two major isoforms: LDHA and LDHB. The general reaction scheme can be shown as:

In muscles LDHA reduces pyruvate to lactate consuming one NADH. This gets rid of the electrons which would normally go through the respiratory chain. The lactic acid is then transported to the liver where it is turned back into pyruvate by LDHA producing one NADH. This is know as the Cori cycle.
Both enzymes however are very similar and can catalyse the reaction into either direction, they are just slightly different in structure which make them have a greater affinity for pyruvate or lactate.

You need to add the H+ to the left hand side of your equation.

Thanks for the comments, I adjusted the text and figures

source: Stack Exchange

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Gaps in FASTA formatted genome?
I'm just getting interested in genetic structure and I decided to find a FASTA formatted genome (human) and I found one here. However, I'm confused. I know that A can only match up to T and C to G but it appears as though T is matching up to T, A to A, C to A, and etc. How is this possible? Can there be gaps where T,A ,C ,or G is connected to nothing? Small part of genome: ATTTAGAAATGACTAACAATTATGTAGGTTTATTTCTCTCAGTATAGAATGTTCATATAGAATT

Your question is based on a misunderstanding. You have a single strand, lets assume it's the red sequence in the image. The linear sequence along this strand is not limited by base-pairing rules.
The base-pairing rules (A-T, G-C) apply to the complimentary strand, given in blue in the image.

It's convention to only give the sequence for one strand because the base-pairing rules allow us to infer the complimentary sequence.

If I got your question correctly, then you are referring to the base pairing of the genome. Here you have been misled as to how base pairing is presented. ATTT does not refer to a base pair between A,T and T,T but rather the sequence of letters in the sense strand of the human genome. What you see here are more stacking interactions than base pairing between bases. Whenever navigating databases please remember that whatever genome you are viewing, you will always be presented with the sense strand of that genome. To get the base paired strand or anti-sense strand of that particular genome, you need to a reverse complement that particular sequence of letters.

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Can the calcification response of a marine organisms, at different pH conditions, be assessed by the calcium magnesium ratio?
Can the calcification response of a marine organisms, at different pH conditions, be assessed by the calcium magnesium ratio?
the calcium magnesium ratio is a proxy  of calcification?


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How is TB harmful in HIV patients?
The mycobacterium of TB doesn't secrete any toxins. The cause of disease in the immunocompetent is the collateral damage due to the immune response against disseminated infection. But then, when HIV patients are immunocompromised, why should TB do any harm to them? There is an absence of the typical granuloma in HIV cases.

That meant the fever, blood-coughs, pain etc in tuberculosis-patient just due to secondary infection? nothing damage that bacteria do?

@always confused I  mean that. I meant that the immune response is doing more damage than the pathogen per se. For example in cholera, it is the bacteria that secretes a toxin which does the harm. In TB, theres nothing like that. It is immune cells destroying surrounding tissue.

Mycobacterium tuberculosis is the bacterial species which causes tuberculosis. Many people in the world (~1/3 of the population) have an M tb infection. However, an immunocompetent host is able to prevent the bacteria from causing disease (tuberculosis). In the case of an HIV patient, there is no immunity, and thus the bacteria is free to cause disease.

You still have innate immunity, which is the biggest perpetrator of immune-mediated tissue damage, IMO, when supplied with constant stimulation.

This is an interesting an useful question about host-pathogen interactions. For a general reference (for both hosts with and without a competent CD4+ T-cell response) see Cecil Medicine, Ch.332, and Murray Medical Microbiology, Ch. 28. There is also a decent review in Lancet Infectious Disease that discusses the pathophysiology in immunocompromised hosts.
Overview / tl;dr
Tuberculous mycobacteria may not secrete any toxins or replicate quickly, but they are clever and persistent. Without an effective immune response, they will eventually overwhelm the lungs, spread to other organs, and kill the host through organ failure and/or embolization.  In these cases, infection is universally fatal if not treated. This is what happens in HIV patients with a low CD4+ T-cell count.
In hosts with a competent CD4+ T-cell response, infection is sometimes fully resolved and sometimes held at bay for many years without major organ damage.  In other cases, the immune system's methods are too powerful for the infected organ. Tissue damage in these cases is the direct result of prolonged activation of large fused groups of macrophages. Importantly, this is not an overactive immune response, it just happens to be too much for the local organ. You cannot treat TB by shutting down this immune response. If you block TNF-$\alpha$, for example (a major player in the cross talk between CD4+ T cells and macrophages), you end up with disseminated TB. The solution here is elimination of the pathogen with direct anti-mycobacterial treatment.
Initial Infection
In either an immunocompetent or immunocompromised host, tuberculous mycobacteria enter, e.g., alveolar macrophages through phagocytosis and, initially, prevent fusion of the phagosome with lysosomes, while allowing fusion with other vesicles. This allows the bacilli to live, access nutrients, and replicate within the macrophage.
Immunocompetent host
In the immunocompetent host, the interaction between the infected macrophage and CD4+ helper T cells leads to formation of an activated macrophage and either elimination of the mycobacteria or compartmentalization of the infection. Either of these outcomes are generally good for the host. Clearance of a pathogenic bacteria is obviously good. Latency in a walled off compartment is a close second.
The typical disease syndrome of pulmonary tuberculosis involves a brief, often unremarkable respiratory infection, followed by a long period of clinical latency. In many cases where the primary infection isn't fully cleared, latency may be lifelong, only to be discovered incidentally at autopsy. The brief illness followed by clinical latency corresponds to the infection of alveolar macrophages with an immune response that successfully walls off the infection.
In a host with generally capable CD4+ T cell / macrophage cross talk, if disease develops, it typically occurs after years or even decades of latency, through reactivation. Reactivation may be the result of a temporary failure of the compartmentalization strategy, with short term or partial immunosuppression due to age, some other illness or drug. It is sometimes the result of re-exposure. In severe cases, the result is a massive and damaging, but relatively slow immune response. This is not toxic shock syndrome or gram-negative sepsis. It occurs over month to years, with night sweats and weight loss. Fever may or may not be present. Tb is a slow burn. The OP is correct here, that the tissue damage seen in these cases (caseous necrosis, cavitary lesions, sometimes followed by hemorrhage), as well as the night sweats and weight loss, are all caused by the immune response, not directly by any toxin produced by the mycobacterium.
This lung (image from wikimedia commons) was chewed up by giant, angry macrophages, spurred on by CD4+ T-cells:

Immunocompromised host
This lung (image from a public slide set through the University of Utah), on the other hand, was not chewed up by giant angry macrophages, but was lethally infected with M. tuberculosis all the same:

In an immunocompromised host, the clinical syndrome is different. For an HIV patient with a low CD4+ T cell count, alveolar macrophages are not sufficiently activated. There are no large cavitary lesions, but they are also unable to clear or quarantine the replicating bacilli. This results in disseminated tuberculosis, sometimes with spread through the bloodstream to the brain, kidney, and bone, and devastating illness that is universally fatal without treatment. Death may result from organ failure (e.g., of the lung), infectious or non-infectious embolism.
Interestingly, in an AIDS patient with disseminated TB, when you combine TB treatment with HAART (highly active antiretroviral therapy), you can sometimes see a paradoxical worsening of symptoms. This is called immune reconstitution inflammatory syndrome, or IRIS. It may look like worsening TB, with fever and worsening lung function. The solution for TB-IRIS is not immunosuppression, but supportive care and, again, direct treatment with antimycobacterial therapy. Here again, the problem isn't an overactive immune response, it is the pathogen.

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What theories exist as to how self-replicating molecules organised into the first cells?
When I was a biology student in the early 90's, what I learned and read seemed to indicate a gap in theories around the origins of life. There was, of course, no real evidence about how the first self-replicating macromolecules came about, but there were plenty of reasonable theories. One that particularly stuck in my head was Graham Cairns-Smith's idea that replication began with effective competition for space between slow-growing crystal structures, for example.
Once you have something which loosely resembles a cell then, of course, we can invoke our understanding of Darwinian evolution to explain how those early cells differentiated and developed into the diversity of life we see today. But as a student there seemed a paucity of ideas as to how we could have got from macromolecules to cells. This isn't a small step: it requires our macromolecules to be localised, enclosed in a membrane and to begin to work with each other to form basic metabolic chains.
I left academia after a few years of bench work but I was struck again by this question the other day and wondered whether there were any theories or evidence about this transition that had arisen in the meantime? A quick search on Google didn't turn up anything but the same vague platitudes about enclosures of self-replicating RNA, with little explanation of how this might have happened. It also found this question on Biology SE - How did the first self replicating organism come into existence? - but that deals with initial abiogenisis, not early cells.
Are there any more up to date ideas?
EDIT: Clarification was requested. The linked question - and information elsewhere - tend to focus on the broad question of abiogenisis and seek evidence. I'm asking about a very specific step of the process, that between replicating molecules and the first cell-like structures. I am also aware evidence is unlikely, and I'm asking for plausible theory.
Not entirely sure why this isn't clear, or why I'm getting close votes.

Can you please clarify why the post  How did the first self replicating organism come into existence? does not answer your question and esp. what you mean by "initial abiogenisis" and "early cells" and the difference between these notions?

@Remi.b edited as requested


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Is it possible to rank standardized beta coefficients in general linear mixed model?
I have an experimental treatment at 15 sites and would like to build models to associate usage rates of 4 species with a set of 6 explanatory variables. In the end, I would like to rank the importance of these variable for each species.
Ordinarily, I would simply fit the models and then standardize the beta coefficient by dividing by the standard error and ordering by absolute value.
However, in this case, I need to model a random effect of site and my response variable must be modeled as zero-inflated Poisson, which takes me outside of the realm in which I've seen this comparative analysis performed.
Is there an analogous procedure to ranking standardized beta coefficients for generalized linear mixed models?
Much thanks in advance!
Is it possible to rank standardized beta coefficients in generalized linear mixed models?

I think this is probably a better fit for stats.SE. The nature of the variables won't matter to them there, only the structure of the data and models.

@kmm , that is a good point. I thought I would ask here first since this is a fairly common issue in ecological modelling (as judging from the conversations I've had with folks in my university cohort) that I suspect either someone has already dealt with, or others in the biological community, would benefit from.

I'm voting to close this question as off-topic because it belongs to stat.SE.

If I understand you correctly, you should be able to standardize the explanatory variables (zero mean, unit sd) before the analysis (at least if the explanatory variables are continuous). Then the effect sizes can be compared between predictors that have different scales.

Also, the "importance" of variables is a bit ambiguous. A variable can have a large effect size (top-ranked coefficient), but without a fair amount of variation in that variable it might not have a large effect in practice. On the other hand, a variable with a smaller effect size but a larger variation between sites can explain more of the variance in the response.


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How we can localize sound vertically (up-down) and front-to-back?
It is quite simple to understand the concept of lateral localization of sound. It depends upon the loudness and time (and wave phase) difference between 2 ears.
But how can we detect front-back localization (if someone is calling me from my front/back direction) and up-down localization (such as an aeroplane's sound is coming from upper place and a car's whistle is coming from lower-direction of the balcony I'm standing). How does that happen? Or doesn't localization happen at all under these conditions? Is it just an illusion just because we are already aware about the possible source (such as since it is aeroplane's sound then it might coming from upward place, or I can see my friend is talking by standing my front so the sound must coming from front... etc.)
I've searched wikipedia and other sites, but I found nothing that explained the matter sufficiently.

Localization along the azimuth (horizontal left-right axis) is mediated by various processes: 1) First, there is the head shadow effect, which means that sounds from the left reach the right ear (AD) in an attenuated state relative to the left ear (AS) due to the presence of bone and other tissues. This difference is picked up by the superior olive (SO). This mainly aids in the localization of high frequency sounds, as low frequencies simply tend to go around the head, rather than traverse it. As mentioned by others, there is a time delay between the two ears, referred to as the 2) inter-aural time delay (ITD). Given the speed of sound this adds up to delays in the microsecond range, yet the SO is still able to detect such minute differences to aid in sound localization. There is also a 3) Phase difference between sound waves reaching AD and AS when sound comes from the left or right are also picked up registered. This cue is important for low frequencies (Mather, 2006).
Localization in the vertical plane (elevation) is less well investigated. As far as I know it is the shape of the outer ear (pinna) that transforms the frequency characteristic of incoming sound. In terms of directional hearing it is thought that sounds coming from above lead to a different head transfer function than sounds from below. This means that localization can only be accomplished when the sound has a particular familiar characteristic that is slightly disturbed in the frequency domain when encountered at different angles of elevation (Hofman & Van Opstal, 2003).
Front-back localization is thought to be mediated by processes similarly to elevation cues. Spectral modifications work like filters and are derived from the reflections of sound caused by the shape and size of the head, neck, shoulders, torso, and especially, by the pinnae (Zhang & Hartmann, 2010).

References
- Hofman & Van Opstal, Exp Brain Res (2003); 148: 458–70
- Mather, Foundations of Perception, Psychology Press (2006)
- Zhang & Hartmann, Hear Res; 260(1-2): 30

The Wikipedia article is quite good.
In brief, as you state, the wave phase can be used only to localise sounds in the plane of the ears. To have an approximation of the position in the median plane (above-below/front-back), we use asymmetries that distort the sound differently at different frequencies.
In humans, it seems that these asymmetries and their processing are not genetically programmed but evolved by each listener.
This is different in owls, although different species have each a specific asymmetry. https://en.wikipedia.org/wiki/Sound_localization_in_owls

The geometry of the head + external and internal ear makes an angle-dependent spectral filter. For rich sound which timbre is known we can characterize the spectral filtering, and thus the location (probably as well for moving sound).
Contrarily, it has been shown that pure sounds produce illusions of localisation (e.g. changing the frequency changes the perceived angle).
Moreover, we have some a priori expectations, e.g. high pitch sound being more likely above.

thank you for a response. I'll take time to understand the process.


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Recommendations for an exemplary presentation of statistics related to preclinical drug studies and cellular chemistry?
I am reading Nature's recommendations for collecting and presenting statistics, but would like to also read a few exemplary articles with good charts and data presentation to learn what it looks like when done well. Would be grateful for recommendations -- thanks!


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Lethal gene and population genetics
In the European population, about 1 in 2500 people suffers from Cystic Fibrosis, a genetically determined (descared), autosomal disease. Healthy parents have a child suffering from Cystic Fibrosis. The woman remarries a healthy man. What is the chance of a child from this second marriage suffering from Cystic Fibrosis ?
My attempt
http://i.imgur.com/4mhU3Qh.jpg
But the answer given is 1/100

Welcome to Biology.SE! Images are not searchable and are problematic for people with visual impairment. Please, always type everything when asking a question on a SE site.

Genetics of Cystic fibrosis
Cystic fibrosis is caused by an autosomal recessive allele. We therefore know that the frequency of the homozygote recessive allele is $P_{aa} = \frac{1}{2500}$, where $a$ denotes the recessive allele and $A$ will denote the dominant allele.
Solving the problem
The probability of the second child (from a second husband) has cystic fibrosis is the probability that a second husband is heterozygous ($P_{aA}$) times the probability that this father will transmit the recessive allele $a$ ($\frac{1}{2}$) times the probability that the mother transits the recessive allele $a$ ($\frac{1}{2}$, note that we know the mother is heterozygous as she is healthy but already had a child that suffers from cystic fibrosis).
So the answer is $p_{Aa} \frac{1}{2} \frac{1}{2} = p_{Aa} \frac{1}{4}$, we only need to calculate $p_{Aa}$. Let $x$ denote the frequency of the recessive $a$ allele, then $P_{Aa} = 2 x (1-x)$ at Hardy Weinberg equilibrium. As we know $p_{aa}=\frac{1}{2500}=x^2$, it results that $x=\sqrt{\frac{1}{2500}} = \frac{1}{50}=0.02$. Therefore, $p_{Aa}=2 x (1-x) = 0.0392$. The final answer is  $p_{Aa} \frac{1}{4} = \frac{0.0392}{4} = 0.0098 ≈ \frac{1}{100}$.
What you did wrong
You were pretty close to the right answer. In your calculations you multiplied the frequency of the recessive allele $a$ (which I called $x$) by $\frac{1}{4}$ but you should have multiplied the frequency of heterozygote genotypes (which I called $p_{Aa}=2 x (1-x)$) by $\frac{1}{4}$.

@Rajdeepdhingra Thanks for letting me know if it answered your question. If you think the question is answered, you can check the answer (top-left of the answer).


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Why does underwinding create topological strain of DNA?
I am currently studying the supercoiling of DNA. I understand why overwinding would create additional strain for two attached strands of DNA, but I really don't get why underwinding would create strain and thus supercoiling. If anything it seems that the strands would just separate and strain would be relieved from any DNA helix. If someone would care to explain, that would be great!

Take a look.

The double helical structure of DNA with ~10.5 bp/turn is thermodynamically favorable. Any perturbation from this results in strain. Thus, if DNA is under wound, it is favourable for it to adopt a negative supercoil to return to ~10.5 bp/turn.
That said, negative supercoiling and DNA melting are in fact in some kind of equilibrium. This is important for processes such as transcription and replication which require ssDNA.

it is favourable for it to adopt a negative supercoil to return to ~10.5 bp/turn - can you cite a reference, in support of this?

@SanjuktaGhosh Do you disagree with that statement or do you just want further reading?

I want to know if it does (decrease the bp/turn), how does it achieve it.

@SanjuktaGhosh At the end of this answer, there's a video which shows the interconversion between twist and writhe, if that's what you're asking: http://biology.stackexchange.com/a/56721/6307

No I'm not talking about that.I'm asking that how does negative supercoil decrease the length of the twists of its associated region as you mention in your answer.

Good question! I didn't know the answer either, but I think I have a good idea after thinking of DNA as a normal rope.
This answer helped me put it into perspective: https://physics.stackexchange.com/questions/30871/what-prevents-a-natural-fibers-rope-from-untwisting-when-it-is-elongated
As well as the video linked to in this answer: What is positive and negative supercoiling?
Basically, imagine you have two long strings, then you twist them around each other (DNA helix structure), each twist is called a coil.
Now tie each end to opposing hooks (imagine the hooks located on each side of a doorframe at equal height) without allowing your two strings to untwist.
Once your double stranded rope is secure (the hooks it's tied to represent a point opposite the unwinding site on the circular DNA), pull the two intwined strings further and further apart from each other at the middle of the rope. (This is what underwinding does)
Because each end is secured, it can't untwist, so it supercoils. By pulling the strings apart in the middle, you didn't untwist the coils, you just pushed them closer together, squishing them 'tighter' (stressed) on each side.


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Visibility of a cell membrane under microscopic Imaging
When we see any cell under a microscope the membrane surrounding the cell is opaque. But then if the cell membrane surrounds the cell in all the three dimensions how come we can see through the cell membrane and have a look at the organelles inside if the membrane is also covering the cell from the top and not just at the boundries on the object plane.

A little simplified: a glass (say a glass of water) is clear, yet if you look at it level with the water level, the sides are dark, as is the top of the water. Swiveling the glass doesn't change anything; the glass and water are very clear, but where there is an increase in the sheer amount of clear matter in the same plane, it appears darker. Same principle.

If you can see the cell's insides, the cell membrane is, obviously, not nontransparent

The membrane(and associated proteins) isn't actually opaque, it is just "more opaque" or "less translucent" than the cytosol: when you look through the microscope, you are utilizing this contrast to detect the edges.
In the center of the cell you observe, you see the membrane straight-on, and light is only affected by 1-2 layers of membrane. On the edge, you are viewing through the membrane somewhat "sideways" , so there is effectively more "thickness" of membrane. Maybe not an exact replica of the situation, but one that might be easier to visualize, is earth's atmosphere viewed from space. You can see the "blueness" of the atmosphere at the edges, but when you look straight down at the ground you see clouds, oceans, landmasses not tinted as blue.

I'm not sure if this answers my question. What I think of a cell is a three dimensional object surrounded by a cell membrane. Now if on looking at a cell 2 of microscope I can see the cytosol then it probably means that the cell membrane that should have been between the microscope and the cytosol is transparent but then how come at the same time I see the cell membrane in the same image as a dark boundary surrounding the cytosol.

In the center of the cell you observe, you see the membrane straight-on, and light is only affected by 1-2 layers of membrane. On the edge, you are viewing through the membrane somewhat "sideways" , so there is effectively more "thickness" of membrane. Maybe not an exact replica of the situation, but one that might be easier to visualize, is earth's atmosphere viewed from space. You can see the "blueness" of the atmosphere at the edges, but when you look straight down at the ground you see clouds, oceans, landmasses not tinted as blue.


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Actively Harmful mutations
Usually harmful mutations are those which disrupt a vital function, what you might call "passively" harmful. What about a mutation that makes a protein, which is not just useless, but actually toxic to its host?  Are there any known examples?

There are definitely examples! For one, you might consider sickle-cell anemia to fall into this category.
The mutation that causes this disease leads to abnormal strands of hemoglobin that distort the shape of red blood cells, to the point that those cells can directly disrupt blood flow.
Interestingly, carriers of the sickle-cell trait actually have some protection against malaria, which explains the high incidence of the allele despite the dangerous consequences of the disease.
You can find many other examples in the category of autosomal dominant disorders (though note that sickle-cell is considered recessive, though carriers can still have some negative effects). Because these disorders only require one copy of a gene to cause illness, there is often some toxicity of the mutated protein, whereas in what you refer to as "passively" harmful mutations, one healthy copy can often compensate, fully or partially. Of course these are general statements and there will always be exceptions, but I hope thinking about it this way can guide your curiousity!


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Are there enzymes for every given reaction?
This is a question that's been bugging me, and I haven't been able to find a definite answer anywhere.
We know there are thousands of enzymes (proteins, let's ignore catalytic RNA for now) that catalyze many different reactions, and they do this because they have the correct shape to fit the substrates.
Theoretically, given some reaction, can an enzyme be created to catalyze that reaction? Or is there some reaction that it's not possible to catalyze with an enzyme? Can any given shape be created out of polypeptide chains? If not, what determines the shapes that it's possible to create?

This will probably be a difficult question to answer definitively without some hand-waving or redefining the question; I can't imagine proving the negative result that no enzyme is possible for a given reaction, except for some cases where the reaction is just thermodynamically impossible outside of incredible conditions (for an extreme example, what about hydrogen fusion: the reaction exists, but the conditions necessary are outside the tolerance of protein-based catalysts).
As @tomd pointed out in a comment, enzymes do not change equilibrium, so enzymes are only possible for reactions that are thermodynamically favorable. However, some enzymes couple reactions that are thermodynamically unfavorable with highly favorable reactions to produce a net thermodynamically favorable reaction, which greatly increases the number of reactions that can theoretically be catalyzed.
As for whether any shape can be created out of polypeptides: given the diversity of amino acids and the structural effects of the tertiary structure of proteins, there is a near limitless array of combinations which exceeds human comprehension, but not a truly mathematically infinite number. There are interesting projects such as this one that seek to harnessed underutilized computing power to iterate all of these possibilities to search for useful drugs and explain the causes of disease.

Are there enzymes for every reaction? The short answer is, "No" - there are reactions that occur within the human biology that do not require enzymes. One example of this is the formation of advanced glycation end products (also known as "AGEs"). These are biological molecules like lipids or proteins that become glycated through exposure to high glucose concentrations, like those observed in diabetes or insulin resistance. The high concentrations of glucose allow non-enzymatic mediated covalent attachment of glucose molecules to the macromolecule. See this review for a more in depth discussion of AGEs as well as other references that discuss them.

The question "Can any given shape be created out of polypeptide chains" is rather tricky, but let's unpack it. A protein has a fold - or topology - that determines its overall shape, but can be considered as a framework on which to hang active residues.
There are 'only' 1,200-1,400 known folds, depending on the classification scheme (CATH, SCOP) which seems quite limited. However, if we take just one of those folds - the TIM barrel - and alter the loops you can get a diverse set of structures. That paper does not discuss enzymatic function, of course.
So for small molecules, it's difficult to see any reason why you can't arrange active sites any way you like. The only theoretical difficulty is that you have to fold proteins before they can be active. It might be possible that some complicated arrangement of active site residues would prevent the whole protein from folding - although that's just speculation.
More complicated might be reactions on macromolecules. For example, there are enzymes that bind to DNA, polysaccharides, and other proteins. These longer molecules are still possible for enzymes to bind to - it generally just requires a long surface. Some of the more complex actions include that performed by topoisomerases or chaperones or whatever vaults do.
By moving from tertiary to quaternary structure, it seems like enzymes can do nearly anything that's chemically possible.


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Can we digest food as well as herbivores
I heard some guy say that we can't digest plant food as well as herbivores. Which seems weird to me seeing as how humans can survive without any nutrient deficiencies besides b12 on only plants but we would pretty much just die of nutrient deficiencies on a carnivore diet. Can someone show me how we can't digest plant food as well as herbivores?

Hi and welcome to Bio.SE! This is an interesting question, but it remains quite broad at the moment. Could you narrow down which plant food you mean. For example, we can eat onions but they are somewhat toxic to horses, yet most grasses would probably cause us to vomit whilst cows can't get enough of the stuff! More context is key to making this an answerable question.

Humans do not have microflora that can hydrolyze cellulose, but plant-eating herbivores do. One advantage of that though is that the cellulose helps move food through your gut and aids digestion. Herbivores have fermentation chambers in their alimentary canals that contain mutualistic bacteria and protists that can break down the cellulose for them; some of the microorganisms also use some of the sugars from the digested cellulose to produce nutrients vital to the animal, such as vitamins and amino acids. Also, herbivores have longer alimentary canals relative to their body size, due to the fact that plant matter is harder to digest because of the cell walls.
Here is an excerpt on herbivore teeth structure, taken from Campbell Biology, 10th Edition.

"Herbivores, such as horse and deer, usually have premolars and molars with broad ridged surfaces that grind through tough plant material. The incisors and canines are generally modified for biting off pieces of vegetation. In some herbivores, canines are absent" (Reece et al. 906).

References:

Reece, Urry, Cain, Wasserman, Minorsky, and Jackson. Campbell Biology. 10th ed. N.p.: Pearson, 2014. Print.


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Production of $CO_2$ basal metabolism test

Can the production of $CO_2$ be used as a type of basal metabolism test? Explain.

The answer to this is obviously yes, but I don't know how to explain it. Would the following be a good explanation?

The faster your metabolism the more cellular respiration your cells do, and you produce more $CO_2$, so $CO_2$ output can be used as a type of basal metabolism test.

Yep, you got it.


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Luciferase promoter vector over p-AcGFP1-C1 vector
AcGFP1 vector can emit light by itself, whereas in case of Luc vector a substrate is needed for the reaction. Nevertheless, Luc is said to be more specific or better than AcGFP1. Why is this so called? What are the advantages of Luc vectors over AcGFP1?

You are confusing luminescence and fluorescence. GFP does not emit light. The abbreviation stands for Green Fluorescent Protein. You need to shine a blue light source at it and it will fluoresce green. The problem is that many organisms have background fluorescence, a cell without any GFP can often have a little bit of fluorescence by itself or contain pigments that mask the signal.
Luciferase assays depend on a chemical reaction which oxidises a molecule (luciferin in the case of firefly luciferase) and photons are emitted.  This is much more sensitive than fluorescence but is also a lot more expensive and usually (but not always) requires cell lysis. It is very rare for a cell to emit light by itself so the background will be a lot lower allowing you to see smaller difference.
There are many reasons to choose one over the other in an assay, if you share a bit more on how you intend to use the reporter you can get a more detailed answer.

The vector to use will depend on what you want to do.
The possible problems with GFP are :

The lost of function of the fusion protein (you add 238 amino acids to your protein, that's a rather big change !). There are vectors allowing fusion in C- or N- ter of your protein to try to avoid that.
The GFP may separate from its fusion protein, making observations or immunoprecipitations useless.
With a high expression vector, you may have a saturation of fluorescence in your cells so quantification would be difficult.

With luciferase assay, you add the substrate so your quantifications can be made as soon as the reaction start and luminometers are sensitive enought to detect very low Luc activity or use very few cells.
BUT
GFP vectors allows you to do in vivo assays (quantification, intracellular localisation, cell sorting...) while Luc assays needs the lysis of your cells.
So, depending of your goal it will be better to use one system or the other.


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How does the brain alter/inhibit muscle reflexes?
I can find lots of information on how stretch-reflexes/reciprocal-inhibition/autogenic-inhibition work but from them all it's unclear how exactly the brain interfaces/controls/disables such automatic muscle reflexes when it needs to?
Can it alter the weighting of inhibition in antagonistic muscles?  As well as 'set the length' for a stretch reflex to target?  Or does it somehow control both 'with one value'.  Where and how exactly does it interject into the feedback loops?
I am trying to understand it more from a programmers pseudocode or equation point of view rather then get lost in meandering biological terms I have seen everywhere that gloss over this point.

how exactly the brain interfaces/controls/disables such automatic muscle reflexes when it needs to?

A: At multiple places within a hierarchical system:
In a  simplified way, the Motor cortex is the executor of movement via projections to the brain stem and spinal cord, this is accomplished via excitatory signals to a muscle, the agonist, and inhibitory signals to the antagonist, so in one sense, spinal interneurons would be the answer, since they interface with the motor cortex and alpha motor neurons at the muscle site.
There are also feedback loops all over the motor hierarchy, premotor and supplementary motor cortex regions for instance help plan the movement direction, we don't seem to code a target in the strict sense, but rather a movement direction and then correct via sensory feedback.
The cerebellum projects to premotor, motor cortex and the brainstem, and receives projections from premotor areas, it is involved in stopping and timing movement,the brakes for action if you will.
The circuitry of the Basal Ganglia  which loops with premotor and projects to the motor provides the go, no go and graded modulation via inhibition to the motor cortex, which in turn affect less spinal interneurons, so in another sense this circuitry would be responsible.

Can it alter the weighting of inhibition in antagonistic muscles?

Yes, via spinal interneurons (Henshaw cells, Ia inhibitory interneurons and Ib inhibitory interneurons)

As well as 'set the length' for a stretch reflex to target?

Yes, via a the motor,basal ganglia,cerebellum motor hierarchy, although as mentioned, there is no target but rather a direction vector and feedback that tells you when to stop the movement, i.e. you reached your target. ( Higher cognitive areas do seem to have a representation of the target though).

Or does it somehow control both 'with one value'.

Depends on the interneuron, but basically they serve as information relays ( they also convey sensory information )

Where and how exactly does it interject into the feedback loops?

As mentioned there are multiple feedback loops, the brain is not a unit, but a system and as such I would rephrase the question as which subsystems, brain regions, neuronal tracts and neurons create feedback loops in the motor system.

I am trying to understand it more from a programmers pseudocode

I am a software developer myself, so let me try switching hats, this is one scheme:
If all you want is to control agonist/antagonists, tie up 2 or more variables together such that when one goes up, the other goes down, and presumably change 2 effectors ( virtual or real ) and their position relative to each other,
If you want specific control, you would then need to send 2 channels of information and modulate both variables, if you just send one to either one, the other will respond based on the above configuration.

Thank you so much for your helpful insight.  So I think a basic simulation model might best have a ‘brain’ supplying 3 parameters per muscle: a target length (or angle), an error correction rate, and a reciprocal inhibition weight - assuming every muscle is antagonistically paired.  All error corrections could be computed first, then brain weighted reciprocal inhibition could happen between antagonistic pairs using something probably a little more complex then a straight inverse linear modulation - I guess partially due to muscle strength varying depending on length.


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Is the sex of siblings mutually independent?
I am studying probability, and one of the lectures I came across (Skip to 52:00) states that the sex of siblings is not mutually independent and that there is some correlation.
Can anyone tell me why? And if so, where is the evidence?

There is at least one paper that claims this:

A test for heritability of the sex ratio in human genealogical data is reported here, with the finding that there is significant heritability of the parental sex ratio by male, but not female offspring.

--Trends in Population Sex Ratios May be Explained by Changes in the Frequencies of Polymorphic Alleles of a Sex Ratio Gene. Corry Gellatly, Evolutionary Biology 36:190-200, 2009 DOI: 10.1007/s11692-008-9046-3.
In other words (simplistically) some families are more prone to have male offspring, which implies that the probability of male offspring is not independent.  However, this is a hypothesis, not a proven fact, and I think it's not a very strong hypothesis.
A non-scholarly, but apparently careful, discussion is here:

The odds of having a girl seem decrease after having each boy, but only very slightly. Even after 3 boys, you are only 6.4% more likely to have a 4th boy than a girl.

What are the odds of having another boy or girl?

Has anyone just simplistically looked at how the sex of your first born impacts on your likelihood to have further offspring of the same sex?

I updated the answer to point to a non-peer-reviewed site that looked at that.


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Help ID this plant, quite possibly a weed
I found this plant near my South Indian home in Kerala, India. Most probably it could be some sort of weed. Anyhoo, is this plant of any medical or commercial value? Is it a remedy for something?

It has a white tap root with little veins off the main root
It has a really small yellow flower
It's leaves are similar to that of a clover, except for that it has three to five leaves

Merci d'avance!
(P.S. Forgive me if this is some very common plant that I should know about, I'm in 7th grade.)

So long since I've heard weed for this other meaning..

I presume it is Cleome viscosa, the Asian spiderflower.

It is commonly found in rainy season.

Medicinal uses:

The crushed leaves have been investigated as a treatment on stored seeds of cowpea, to prevent weevil infestation.
The leaves are use as external application to wounds and ulcers. The seed are anrhelmintic and carminative Juice of leaves is used as remedy against discharge of puss from the ear.

Identified by the following features-

Palmate leaves

Colour of flower especially the brown part at the base

Herbaceous habit

References:

Wikipedia
Flowersofindia.net


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Is it possible to have undamaged healthy cell, that is dead?
I am trying to clarify my understanding of how unicellular organisms are alive, given my existing background (computational modelling, unrelated to biology). During my thoughts on subject I have came to a conclusion that any unicellular organism, given it's undamaged, and has enough resources (so it does not undergo autolysis), must be always alive.
Is my conclusion true? In other words, is it possible to have completely undamaged cell that appears healthy, but yet is dead? And by "dead cell" I mean a cell that does not move, does not consume any resources, does not respond to any external stimulus an alive cell would respond to, does not divide, etc.

Would a frozen cell meet your definition?

Your definition of "dead cell" seems to include dormant cells and spores, which, technically, are not dead organisms. So you might want to reconsider your definition: cell death is something irreversible, while dormancy and sporulate state are not.  Anyway the notion of "healthy dead cell" seems a bit oxymoric...

@toriningen, Flo makes a very good point. Assuming you are committed to your definition of "dead cell", changing "dead" to "quiescent" would be advisable. healthy =/= dead

There is a great bit on the podcast "The Infinite Monkey Cage" wherein Brian Cox recurrently asks "When is a strawberry dead?"
If you think about it, it is a difficult question: when a berry is growing on a plant, it is easy to say it is living because the cells are actively dividing and functioning. But when the berry reaches maturity, the autosomal cells no longer divide. This is called Programmed Cell Death or apoptosis. This is a physiological process. However, one could still argue the strawberry is alive in the sense that the seeds are still viable and can actively produce new strawberry plants. These cells are quiescent. What though, if a strawberry is crushed to smithereens or a disease infects all of the cells? In this case the "death" of the cell has ceased function as in apoptosis, but this is externally mediated. This type of non-programmed cell dysfunction is called necrosis.
So, in direct answer to your question, you must taken into account the mechanism (internal or external) for cessation of function and the permanency. Internal and permanent = apoptosis. Internal and temporary = quiescent. External and permanent = necrosis. External and temporary = ...maybe injury?
To be clear, I've used a multicellular plant as an example (because it is easier to relate to than yeast), but the principles are the same for unicellular organisms.
@Flo made the good suggestion to add references for those interested:
Buttner et al. (2006) Why yeast cells can undergo apoptosis: death in times of peace, love, and war. Journal of Cell Biology
Gordeeva et al. (2004) Apoptpsis in unicellular organisms: mechanisms and evolution. Biochemistry

OP was mentioning unicellular organisms. I'm not sure they are concerned by apoptosis. Do you have a reference for apoptosis among unicellular organisms?

@Flo Yes, it is still defined as apoptosis in unicellular organisms. I've added a reference and a note for clarity.

Dead means either at physically decaying stage or at least no longer able to react whatever the future changes of its environment (contrarily to dormancy).
To be in such state, an apparently healty cell would need to have had his epigenetic "program" stuck in some dead-lock bug (I don't know if this exist). I wouldn't say that this states his then an "healty" state.
Now maybe what you do seek for is dormancy state. But since it's waiting for some environmental signal, you could assimilate this to "lacking of a resource".

What do you mean by "epigenetic 'program'"? Why would such a phenomenon need to be epigenetic rather than genetic?

Because the whole expression mechanism is involved. (comprising how DNA locations are packed or exposed to transcription. + the various expression factors).

I can imagine a scenario, as you've proposed, in which a genetic mutation creates downstream effects that disallowed a cell to react to a environmental stimuli, while still preserving pathways for all other homeostatic functions (so, essentially "healthy"). In this case, the issue would be strictly genetic and digital, and not epigenetic.

Then if it is maintaining homeostasy, what would you call it "dead" ?

I only said it would have all mechanisms for homeostatic function, not necessarily in homeostasis, nor actively maintaining homeostasis. In this case I would call it quiescent. See my answer above in which I propose four, more exact alternatives to "dead."


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Why don't plants get hot under sunlight?
I've read that efficiency of photosynthesis is only like 5%, and it operates on visible light spectrum, not infrared (which is heat radiation). Which means light should either be absorbed and increase plant temperature, or reflected, and heat what's around the plant. But when you get near or touch plants under sunlight, they are at ambient temperature. In contrast, if you touch a metal plate, ceramic tile, rubber, plastic, asphalt, concrete, sand etc, that's exposed to strong sunlight, they are very hot, either because they reflect heat onto you (sand), or because they absorb heat and their temperature is high (asphalt). But with plants, it seems like neither happens, and it stays cool. How does that work?

This seems like more of a physics question than a biological one..

Not really, the physics part is well outlined in the question. Radiation (light) must either be reflected or absorbed, and this will result in a heating of the plant or the surroundings, unless the energy is transformed. My question is, what biological mechanisms do plants use to transform energy and avoid excessive temperatures.

@MattDMo I disagree, I'm pretty sure plants use specific mechanisms to avoid getting too hot, which would hinder their normal metabolism.

Take a look at the Temperature paragraph from this reference:
Ecophysiology

Plants can avoid overheating by minimising the amount of sunlight absorbed and by enhancing the cooling effects of wind and transpiration.

They seem to have several ways to counter the heat as we do with transpiration, wind etc.
This article is more complicated but as really useful informations on the effects of wind on the plant's temperature:
Leaves in the lowest and highest winds: temperature, force and shape

that makes sense, the reference linked is also very useful.

Plants 'transpire' a lot. If you look at false-colour photographs, vegetation lights up as dark-red, and not green, because the radiate a lot of near-infrared light: heat. @Southbob

You mix several things.

logic: if the plant converts some of the radiation into energy rather than heat + reflection, then it's normal that it heats less than some other object with same amount of reflection.
physics: the feeling of cold/hot object is related to his thermal conductivity more than its temperature. That's why walking on wood/wool doesn't feel the same than on steel.
physics+bio: plants are mostly made of water, and thus evaporate, which cool them down. Steel doesn't.

You misunderstood the question. I acknowledge that energy has to be transformed, what i asked is what is the mechanism used to convert, and how much is converted.


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Sheep vs. Furry animals

Why can't we take the fur of a fox without killing or skinning it just like the sheep , what's the biological or chemical structure or even the trait which is on a sheep's body that separates wool from its skin
Why can't we apply the bioclip technology on furry animals too ?

Not knowing anything about the fur trade, I would suspect it is mainly a matter of quantity of fur. Imagine taking only the fur (without the skin) of a fox. What could you want a do with it? The hairs are maybe 1cm long only. You need to take the skin to keep the hair together. With sheep, we are often not interested in the fur as we can process their massive amount of wool.

@Remi.b, see my answer. Quantity isn't a limiting factor, cow fur must be an abundant resource given the number of cows that get slaughtered. Also, sheep only have wool, no fur.

Sheep wool is like cutting long curly human hairs: they stick together due to the length and curliness.
For foxes, chita, rabbit, lions, etc, the hair are really short and parallel: it's like cutting your eyebrows: they won't stick together. That why you (used to) find them as carpet, kept with the skin.

@user27247 It does not seem very strategic to chose an answer that has received two down votes (and one up vote) and lack any sort of reference while Michael_A's answer has received 7 up votes and is much more complete.

May you allow the OP to make his own choice, without "politics" or "strategy" considerations, about what is the answer he found clear ? I'm scientist, but I also do science popularization. I agree  Michael_A's answer is detailed and very interesting... for readers having some scientific background. More importantly, how interesting it is, it doesn't answer the question (getting the hair without killing or skinning the animal).

@Fabrice NEYRET I'm not concerned by the OP exercising his/her voting right, even if I think it's a strange call. To be clear, I have answered the final question. Read the final sentence, you could shear a fox and produce a fabric but the fabric would likely be poor and there's no reason to do so. I have even provided, linked, evidence for my answer by giving a specific example where a fur is bioclipped/shorn and used like a wool.

Fur, wool, and hair are all made of keratins.
To the best of my knowledge wool and fur are separated arbitrarily, based on the properties of the fibres. This arbitrary division allows rabbits to have fur but selective breeding has produced angora rabbits, which have wool. The opposite should be possible, with time you could breed a sheep that has fur.
Length; Wool grows continuously and animals are clipped when the fibres are long. Fur often has a maximum length.
Structure: The structure of the keratin in the wool makes the fibres kinked (crimped). These kinks aid the production of fabrics. I believe the cuticular scales also aid in the production of fabrics.

Fur doesn't have kinks, so even if it's long enough to weave the fabric is likely to lack durability.
Some furs are used in textiles rather than pelts. Possum fur is 'plucked' and woven into fabrics with wool. The resulting fabric is slightly less durable. However, possum fur is hollow and smooth so possum fur fabrics are very soft and warm. The clothing is very good to to wear.
However, fur is generally inferior to wool for textiles and it took a couple of decades to develop techniques to produce textiles from possum fur. This happened because of odd ecological and economic drivers. Possums are are a major pest species in New Zealand where they contribute to the decline of native birds and insects. Millions of possums are killed every year in New Zealand. The market for possum skins is very small. This is why so much effort was put into producing a fabric from possum fur.
So you could shear a fox and produce a fabric but the fabric would likely be poor and there's no reason to do so.


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Is human mtDNA unique in its single origin?
Other than Humans, is there another primate who has a traceable “original Eve mtDNA”?

can you give some more background information on what your talking about? Can you define "original Eve mtDNA"?

I was referring to Prof. Sykes book the Seven Daughter of Eve referred to by another as Original Eve mtDNA!  My question was simple, is there a comparable circumstance in other primates?

You can trace back any piece of DNA (from any life form) to a single ancestor called LUCA (Last Universal Common Ancestor), so the short answer is 'yes'. But be careful in your interpretation.
If you look backward in time, you can see that lineages merge (siblings merge first, then cousins merge, etc...) and you necessarily end up with a single individual. In absence of recombination (which is the case for mtDNA), you can always trace back a piece of DNA this way and always find a single ancestor. The age of this common ancestor depends mainly on the population size and demographic history of the lineage. Typically, in a panmictic diploid population of constant size $N$, the expected time to the MRCA (Most Recent Common Ancestor) of the population is $2N$ generations.
So yes, you can find an "original Eve mtDNA" in any species. But please by "original" don't think this ancestor must have represented any novelty or anything of interest and do not make the mistake to think that before this ancestor no one had mtDNA.
The second paragraph is an extremely vulgarized explanation of coalescent theory. You should have a look at an intro to coalescent theory (wikipedia article here) but you might well need an intro to evolutionary biology first. Understanding Evolution might be a good way to go.

Good answer. +1 Maybe, to further clarify things for the OP, one could add three things about what the 'original Eve mtDNA' carrier was not. (i) She was not the only female alive at that time. (ii) She was not the ancestor of all genes in the gene pool. (iii) She was not necessarily a member of the species.

Very important add-up to avoid misconception. Thank you

I was referring to Prof. Sykes book the Seven Daughter of Eve referred to by another as Original Eve mtDNA!  My question was simple, is there a comparable circumstance in other primates?

And I was thinking the answer was pretty easy as well. Please let us know what is unclear to you in my answer. Side note: please do not post the same comment twice.

Thanks, I am not academically trained.  What had confused me was that Prof. Sykes and others, currently seem to find this "Clan Mothers" evidence surprising.  However, if this is common in all life...my curiosity is satisfied.

I never heard of the concept of "Clan Mothers". If you want to question Sykes's claim you'll need to give more info about the concept he's using (give us some background) and probably quote him. You might need an intro level in evolutionary biology though before being able to do so (if you don't yet).

Sorry, I have asked my question poorly and confused it with the genealogy term. “The clan mothers were not the only people alive at the time, of course, but they were the only ones to have direct maternal descendants living right through to the present day. . They show how everyone alive on the planet today can trace their maternal ancestry back to just one woman.
Sykes wrote, and maps the migrations of the worlds populations  haplogroups.
My question is, how would this compare to chimpanzee populations?  Do all species inherently have an common core sequence in their mtDNA?

Well, yes this quote will be true for any piece of non-recombining DNA in any lineage (which includes mtDNA in chimps). The answer still hold. You should really read about coalescent theory to get a better understanding of this general subject.


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Cytokine responsiveness
Why is it that cytokine responsiveness is less in progenitor cells than their ancestors(stem cells)?
What will be the benefit of such reduction in responsiveness?

Maybe this is well-known, but I hadn't heard of it before. This sounds like a a rule that is far more complex in practice than in this question. Can you point out a citation/textbook in which you found this comment?

@AJK it's present in G.K. Pal physiology 2nd edition, pg.no-59

Could you add the quote to your question? I can't access that textbook.

@AJK it's present in the form of a table.

My answer assumes you are asking about in-vivo effects of cytokine responsiveness.
It has to do with the regulation of the differentiation process. Cytokine responsiveness depends on other factors like cell-cell signaling. To be sure that the differentiation occurs in the right place, the progenitor cells need a signal feedback from the surrounding context (the actual tissue where the cells will differentiate). If the feedback matches, they differentiate.
Stem cells on the contrary, are physically distant from that context, so they lack all the feebacks needed and do not respond to cytokines stimulation as the progenitors do.
Here's some literature about it:

Developmental changes in progenitor cell responsiveness to cytokines.
Mechanisms regulating lineage diversity during mammalian cerebral cortical neurogenesis and gliogenesis.
Signal transduction pathways involved in the lineage-differentiation of NSCs: can the knowledge gained from blood be used in the brain?
Enhanced responsiveness of committed macrophage precursors to macrophage-type colony-stimulating factor (CSF-1) induced in vitro by interferons alpha + beta 1.

However, note that the whole process is still largely unclear and it may vary for different cell types, so consider my answer as a generalization of the concept.


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immunity to Malaria
What is "immunity to the disease" in the following sentence?

In some regions, the parasites are resistant to certain antimalarial drugs, particularly chloroquine.
  People continually infected gradually develop immunity to Malaria.

where does that come from? can you give a reference? Is the text "People continually infected develop immunity to Malaria" directly from a source? Is there supposed to be some punctuation somewhere?

When there is one existing subclinical infection, it prevents another new superinfection. This is called premunity and is rather very important for malaria inendemic areas. Just thought of mentioning. Its different from the immunity you're talking of though.

I would think it is not immunity to the Plasmodium, but rather something like a system-free infection. They don't get the symptoms of Malaria any more, but they are still infected.

They might build up slowly an immune response to the manifestation of symptoms of malaria that arise when the microorganism is present in the blood, from what I remember. But can't get rid of it since it hides when not in the blood (cycles in the liver if I remember correctly.


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Where can I find trees preserved for hundreds of years?
I assume there are climate conditions that cause trees to be preserved, since there are fossilized trees, however, it may be extremely rare to find a tree in a nascent state of fossilization.
Is it possible to easily find trees that have been preserved for 200-300 years? By a tree, I actually just mean a preserved stump.

Full trees will be hard to find, but a search for "petrified forest" might help you out.

Are you looking specifically for those in the wild? I'm sure there are museums and natural history collections that have specimens. There aren't going to be petrified/fossilized trees only a few hundred years old. Those processes take far longer.

swamps and bogs are a good place, anywhere the log will be perpetually submerged in oxygen poor water.

Yes, this occurs fairly regularly in Alaska and British Columbia (and probably other places with low-elevation glaciers that interact with forested zones) where climactic oscillations have led to rapid advance and recession of glacial extent.
In Glacier Bay, Alaska, for instance, there are a number of interglacial stumps (you can see a few sites marked on this map). These stumps represent a forest that was established in the ice-free interim period between the Last Glacial Maximum (10,000-15,000 ya) and the "Little Ice-Age" (~500 ya). Thus, these trees have been preserved under the ice for a few hundred years and have only been uncovered recently (<100 ya). Many of the glaciers in Southeast Alaska are receding, so new stumps are being exposed every day.


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What happens if a speciation event causes the new species to evolve out its clade's defining trait?
If a speciation event occurs to a member of the strepsirrhine clade in such a way that its rhinarium is selected out, would it stay a strepsirrhine?

Yes, it would. A clade is defined as an ancestor and all of its descendants regardless of whether they look alike or not. Now, it is of course up to us (humans) to decide what we want to call strepsirrhine. If we decide that the new species that has no rhinarium is not a strepsirrhine, then strepsirrhine will stop being the name of a clade but will be the name for a paraphyletic group (and we would probably need a new name for the current clade of strepsirrhine).
You can get more information about phylogeny in this post and much more info in an intro class to evolutionary biology such as Understanding Evolution for example.


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Interleukin 6 class cytokines
Wikipedia says:

Leukemia inhibitory factor, or LIF, is an interleukin 6 class cytokine that affects cell growth by inhibiting differentiation.

So does this means that il6=LIF ? or does it implies that both il6 and LIF belong to some common class of cytokines?  If latter is true then what is the name of that class?

From the interleukin wikipedia page for IL6 :

number of other cytokines may be grouped with IL6 on the basis of sequence    similarity.[21][22][23] These include granulocyte colony-stimulating factor (GCSF) and myelomonocytic growth factor (MGF)

from the Leukemia inhibitory factor wikipedia page:

LIF derives its name from its ability to induce the terminal
  differentiation of myeloid leukemic cells, thus preventing their
  continued growth.

From this we can suggest that LIF is grouped with the IL6 because of its action on myeloid leukemic cells and specifically on their growth (MGF).


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Do symptoms of common cold infections correlate with the infectious agent?
The common cold - in summary, an acute upper respiratory tract viral infection - is one of the most frequent viral infections in humans and can be caused by about 200 viral types [Eccles (2005)]. Symptoms are thought to be caused by the immune response in the host, rather than by actual damage caused by the virus [(Hendley (1998)].
My question: is there a correlation between the symptoms observed during a common cold and the viral type that causes the infection? Of course, one can find out the cause of the infection diagnostically by taking samples and isolating DNA or setting up cultures, but that is not my question. My question is whether it is possible to predict the virus taxon causing the infection by symptoms.
My prediction from the information I have at hand is that it should, at least in tendency, be possible as different infections agents use different infection pathways that in return invoke different immune responses and, finally, symptoms [Eccles and Weber, ed. p. 107 - 147 (2009)]. However, I found a rather dated article by Tyrrell et al. (1993) that analyses infections caused by several rhinovirus strains, a coronavirus, and of the respiratory syncytial virus (virus taxa among the most common infectious agents for common colds). They conclude that the main difference between colds induced by different viruses is in duration of the incubation period, whereas patterns of symptom development were not substantially different with different viruses. So is this the current state-of-the-art?

The strains can mean the difference between mild or severe symptoms though (just think spanish flu vs H1N1). Symptoms can also be different depending on the person infected (some have headaches, some don't) since it depends alot on how your body reacts to the virus, I would think that differentiating viruses by the symptoms would be extremely hard, but severe symptoms could suggest some specific strains for example.

Not going to post as an answer because finding the literature to support it would be too time consuming. No, symptoms are inadequate to differentiate among viral agents with a few rare exceptions. There is a dearth of research because it doesn't really matter, does it? There is no treatment for the vast majority of respiratory viruses, and more importantly, the illness is for the most part mild and self-limiting. To fund research, there has to be a fairly good reason besides curiosity (like ability to treat/prevent, or infection causes significant morbidity/mortality, e.g. RSV/H1N1.)

You cannot necessarily identify the cause of a particular case of the common cold by culture or nucleic acid tests. These tests will tell you if an organism is present, not if it is causing disease, and many of these organisms are present in samples from individuals who do not have a cold.

@anongoodnurse I think the dearth of research is more the result of lack of interest than lack of a reason. The common cold is one of the most common causes of provider visits and causes substantial economic burden on a population level. The treatment is simple and appears to be effective: empathy, reassurance, and counseling about appropriate otc remedies for symptom relief.

@DeNovo - "the dearth of research is more the result of lack of interest..." There is no lack of interest (or research) in the common cold; as you said, it is a very significant societal burden. What there is no interest in is correlating the very, very common symptoms with which of the hundreds of possible viruses may be the cause.

@anongoodnurse this is true, but i'm sure you wouldn't be surprised to hear that residents fall asleep as soon as I start talking about how to approach the common cold.

@DeNovo - lol, residents fall asleep the moment they stop moving. As a resident, I fell asleep listening to a patient's heart. I've heard more embarrassing falling-asleep stories. :) That said, the common cold is bread and butter; they should be listening.


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Is this pollen?
The small round "pockets/buns" in the image. I am almost sure it is, but maybe someone knows more. Sample comes from (50.156992, 12.532546) (Google coordinates). It is a re-cultivated tailing in the Czech Republic. In the specific area we find birch trees and fir trees.

What area is that? Can you give geographic coordinates or something?

Yes. Google coordinates: 50.156992, 12.532546 . It is a re-cultivated tailing in the Czech Republic.

Looks like pollen to me, and I've spent a lot of time looking at pollen


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Why isn't direct diagnosis of infectious disease through microscopes a common thing?
I'm not sure if I am being accurate about this but from what I know about diagnostics (watching House MD etc), if a doctor has a suspicion of a pathogenic infection then he/she usually prescribes corresponding medication without doing some kind of a confirmatory test. But isn't it possible to just have a look at the blood sample under a microscope and then confirm it? I guess it can't be done for viruses because they need an electron microscope to resolve them apart but I guess normal bacterias can be identified using more commonly available microscopes.

The problem with this is that A) the infection may be local, and very few if any bacterial cells may be in circulation, and B) even if the infection is systemic, there could be as few as a couple of bacterium per million red and white blood cells, making visual confirmation impossible. More often, if the attending physician feels the need for a direct ID in order to prescribe the correct medication, a culture is taken from the site of infection or blood is drawn, and then subjected to one of any number of different automated ID systems and/or culture conditions to identify the particular type of bacteria present. This can be as simple as Gram staining to identify Gram positive vs. Gram negative bacteria (different types of antibiotics work on the two classes) all the way to a full identification (genus, species, strain) based on molecular sequencing, typically of ribosomal RNA.

Could the person who didn't like my answer offer ways of improving it, including pointing out incorrect assertions (if any) or things I may have missed?


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Definition of nucleotide-associated proteins and RNA-polymerase associated proteins
Nucleotide-associated proteins and RNA-polymerase associated proteins, I found those two terms in an article but I didn't understand what they mean exactly, is there any relation between those terms and DNA-binding proteins ?
The article : DNA supercoiling-a global transcriptional regulator for enterobacterial growth?

Could you post the article for context?

@canadianer I added the link to the article.

In short:
Nucleotide-associated proteins are DNA-binding proteins that bind DNA. RNA-polymerase associated proteins bind RNA-polymerases and are required for its functionality.
In more detail:
DNA-binding protein is a higher level term that comprises all proteins that bind to DNA. These can be seen as nucleotide-associated proteins as they interact with the nucleotides in the DNA strand, even though I did not hear people use that term very often. There are two types of binding:

Non-specific DNA-binding proteins that do not bind to specific sequences DNA sequences, e.g. structural proteins.
Specific DNA-binding proteins that bind to specific DNA sequences, e.g. transcription factors. These proteins mostly have specific DNA binding motifs like zinc fingers or helix-turn-helix motifs.

RNA-polymerase (RNAP) associated proteins are different from that. RNAP itself is a DNA-binding protein, but proteins binding to RNAP are necessary for it to be fully functional. The fully functional RNAP then is a holoenzyme. For example RNAP II requires an initiation factor called sigma in bacteria and several general transcription factors and regulatory proteins in eukaryots.

"Nucleotide-associated proteins are DNA-binding proteins that bind DNA." Written in a hurry perhaps? Is DNA the only nucleotide then? And are there a class of  DNA-binding proteins that do not bind DNA? Accepted or not, your answer needs serious revision. And although you give a host of links, none are to the two terms the poster enquires about. In the absence of such I am not prepared to accept your short definition of RNA-polymerase associated protein either.

Neither of the terms “Nucleotide-associated protein” or “RNA-polymerase associated protein” are standard in molecular biology in so far as they are not defined in the reference Gene Ontology. (In contrast, “DNA-binding” is.)
An internet search does not bring up many examples of the former usage (at least) and in those it brings up it is not defined. One can only conclude that it means exactly what it says and no more, presumably because the author has limited information about the function of the protein.(Without the original reference I cannot be sure.)
A “Nucleotide-associated protein” is therefore “a protein that in some way interacts with a nucleotide”. On may imagine that it might bind the nucleotide, but the nature of this binding is unspecified and could be reflect the fact that the protein is a kinase of some sort and ATP (or GTP etc) is a substrate. It therefore need not be a DNA-binding protein, in contrast to the statement in the accepted answer from @AlexDeLarge. In fact the term would most likely imply a mononucleotide-binding protein, i.e. a protein that bound ATP or cyclicAMP or GDP or dUDP etc. If it bound a polynucleotide, this could equally well be RNA as DNA.
Likewise, an “RNA-polymerase associated protein” is “a protein that in some way interacts with RNA-polymerase”. It is more likely that this is a protein that forms a complex with — i.e. binds to — RNA-polymerase, but the fact that the author does not use the term “binding” suggests that he is being cautious because he has no evidence for this. Perhaps both proteins are found in the same immunoprecipitate.


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Pattern in parental care behaviour from lower to higher animals?
I was studying about parental care behavior. There seems a pattern present in this behavior in case of vertebrates. The more evolutionary advanced class the animal belongs to, the greater effort an animal gives to care its off spring?
Is it a real pattern?
My current thinking is that if the pattern is indeed real, it is because the more complex an animal is, it takes more time to get fit with the environment, so it takes more effort for parents to get them ready for the environment. Am I close?

What do you mean by evolutionary complexity/advanced-ness?

What would be reasons for this particular pattern (assuming it is generally applicable to animals of "increasing complexity", which you need to define) to exist? Traits don't exist in a vacuum, they are intimately connected to one another. What's different about the development of a snake vs. a mouse vs. a deer vs. a gorilla vs. a human?


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What is the evolutionary significance of germ cell migration to gonads?
Why do germ cells have a different origin than the gonadal organs? Does it help the animals in any way?
P.S. I know it is difficult to answer whys in biology but is there any theory as why do they have different origins.

Germ cells are protected from mutations and other recombination events. It is therefore essential to keep them isolated. Germ cell segregation, therefore, IMO, happens very early during development. You can have a look at this post.

@WYSIWYG Germ cells are protected from mutations and recombination? I don't get this claim. They are not. Sure, most crossovers happen during meiosis but meiosis occur only at the very last step in the germ line.

@SanjuktaGhosh I am having a hard time with the semantic behind the post. Can you please help me out and explain how does the question differs (if it differs) from Why do we have specialized sexual organs??

@Remi.b I'm actually asking the reason behind germ cell migration. Why did animals evolve with such a different way of germ cell production. You know cells coming from a different region to the gonadal ridge instead of actually developing from the gonadal ridge(the future gonad). Has it got any evolutionary significance? Would it affect the animals if the PGCs developed from the gonadal rigde (post gastrulation structure though) itself? That's what I mean.

@Remi.b I am not talking about meiotic recombination. I am talking about transposon expansion and other non-meiotic recombination events. Plus, it is necessary to protect the germ cells from mutations. However, not much is known about how DNA repair mechanisms are highly efficient in germ cells. There are piRNAs to suppress transposon expansion. Overall, genomic instability is actively prevented in germ cells.

@WYSIWYG Could you suggest any e-book,website or paper from where I can learn about non-meiotic recombination? Besides how can somatic mutation affect PGCs?

@SanjuktaGhosh You can simply google recombination and you'll get resources. Non-meiotic recombination events include homologous recombination, VDJ recombination, transposon expansion etc. By somatic mutations I meant general mutations that can arise in any cell. Ignore the word "somatic" (it was a mistake).


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How do Sertoli cells protect sperms?
I was reading Developmental biology by Gilbert and stumbled upon a fact that Sertoli cells provide protection to the developing sperms with no futher explanation.
I googled it and found a few books mentioning that it protects sperms from cell mediated immunity and antisperm antibodies. Yet I found a website called fertilitypedia that said:

Sertoli cells do not only control the process of spermatogenesis, but they are also responsible for creating so called immunologically privileged area in the testicles. It means, that Sertoli cell manage to keep blood separated from seminiferous tubules through the connection between them, called tight junction. Tight junction keeps bloodborne substances from reaching germ cells, so all stages of germ cells are protected from the body immunity. Tight junction also keeps surface antigens found on developing germ cells from eluding into the bloodstream so no autoimmune reaction could happen. Since Sertoli cells form the block between the blood and lumen of seminiferous epithelium, they are also in control of the entry and exit of nutrients, hormones and other chemicals into the tubules of the testis.

I'm unable to verify this explanation from the cited sources as none contain the mentioned information.
So my question, how does it actually protect the sperms?

Have you tried Wikipedia? I know Wikipedia is far from an ideal source but that page has some references as well as links to other wiki pages that are relevant to your question such as one on the blood-testis barrier.

@BryanKrause you can write an answer if you want, then I can mark it as solved.

@BryanKrause I gave it a second thought, things written in Wikipedia, something I didn't consider at first, there are suppositions without any citation. So I think they are not good references.

Did you try my suggestion to search google scholar for reviews? This isn't a particularly controversial issue, it seems pretty well established and agreed on. The Wikipedia pages are not fully cited line by line but all the information is likely in the books and papers that are cited if you actually read them.

Found one.@BryanKrause

The Wikipedia pages on Blood-testis barrier and Sertoli cells have some information relevant to your question, with some academic references included.
You could also search for reviews on Sertoli cells on Google Scholar - several of the first returned results seem relevant, if you are able to access them.

Can you consider editing? I'm afraid but this doesn't answer the question ''How does it actually protect the sperms?''.

Doesn't your question contain that answer? Tight junctions between the Sertoli cells keep a barrier between the immune system and the developing sperm to prevent autoimmune reactions, because the sperm express antigens not found in the rest of the body.


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How many isomeres of sucrose can we use?
It appears that of sucrose (C12H22O11) there are about 512 possible structures (nine carbon atoms are asymmetric= 2^9). And only one of this 512 forms taste sweet. Now it is known that human can't use all isomeres of amino acids but how many forms of sucrose can we digest or use in the glycolysis for our energy?

How did you come up with the number 512?  To my knowledge, the variants of glucose are (1) D and L stereoisomers (2) the pyranose and furanose forms, and (3) alpha and beta stereoisomers at carbon 1.  Any combination of these can occur, so there are 222 = 8 cyclic forms. Plus the linear form, caused by the ring opening.  But then the pyranose/furanose and alpha/beta isomers interconvert spontaneously in water solution via the linear form (ring opening/closing), so the only biochemically distinct forms are D and L. I think.

This question is totally confused. Assuming the questioner means hexoses, there are 16 isomers of aldohexose. I have no idea what the sentence about "human can't use all isomers of proteins" means — possibly amino acids? And glucose is not used in the citric acid cycle. Perhaps the questioner means glycolysis. Unless the question is revised I shall vote to close it as unclear.


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How can an animal live without a head / brain?
The human body is unable to do anything if it loses its head - as the brain is separated from the body, the body immediately dies.
But why does the same not happen to other species or animals? (As they are somehow similar organisms/living things, like humans). However, when the head is cut off from a chicken, snake ( also insects, but it's different system, answered here... I mainly interested in bigger animals) ... the body continues to move. Why and how does this occur? Who manages the functionality of body, if there is no manager (brain)?

There is nothing different between animals and humans. Have you tried to google Why do headless chickens run??

@Remi.b - Have you googled "Why do headless humans run?" Of course there's a difference.

@anongoodnurse My comment was misleading. Sorry about that. I reacted to the use of the term "live" as if in animals some fake essence of life of the organism was not dependent on the presence of the head while it would be in humans.

related: https://biology.stackexchange.com/questions/79167/can-turkeys-run-around-when-their-head-is-cut-off-like-chickens-do

In general, and this is somehow speculative, the animals that you mention have more autonomy in their extremities and less control from a head, muscles have evolved autonomous responses perhaps as an evolutionary advantage, ( i.e. having a brain be in charge of reactions can add precious milliseconds ), there also seems to be a relationship in between brain size ( specific motor control areas) and this autonomy, which introduces a metabolic cost (i.e. our big heads need a lot of energy)  Further, there are other biological considerations for providing extremities with their own resources and thus to a degree be more independent, perhaps another evolutionary strategy. At the other end of this control-autonomy relationship, the head takes control of the extremities most of the time and their interdependance is greater, so if you cut it no movement will happen, although we still possess a few hard coded reflexes that work for a while provided they have enough energy left or a blood source.
To give you an example: a cat ( somewhere in the middle ) can still walk when you cut the connections from the brain /head  to the legs due to reflex actions ( the cat has to be on a treadmill though).

Some limb movements in vertebrates can occur at the level of the spinal cord (e.g. swimming behaviours in fish; coordination of alternate movement of legs in walking animals). This might support some uncoordinated movement for brief periods following complete severing of the head.
However, most (all?) vertebrates require nuclei in the brainstem to control breathing. Without an intact brainstem the body will not survive.
Decerebrate cat walking on a treadmill (but with an intact brainstem): https://www.youtube.com/watch?v=wPiLLplofYw
Chicken survives without a head (but with a brainstem): http://modernfarmer.com/2014/08/heres-chicken-can-live-without-head/

Brain is needed for lung breathing motion (at least for mammals, maybe for all vertebrates), which limit the life span without brain.
Attention: In the case of the chicken, the low stages of the brain are at the level of the "neck", so sometime cutting the head is not fully cutting the brain and some base functioning can keep working.

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


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Why does double vision when drinking happen?
Why do you see double sometimes when you're drunk?  Its weird because it seems to happen more when you try to focus.

Try to look at something when you're drinking and it barely seems to double up
Try to focus on it more than just immediately, and slowly the image seems to separate
Refocusing on new object seems to re-focus and lets you not see double

Why does this happen?
Edit:
http://www.esquire.com/news-politics/q-and-a/a5711/double-vision-causes-0509/ This seems to imply an inability to focus, however, if I try to refocus on a new object it works out

I don't think it has anything to do with alcohol. Its related with eyes and refocusing from far to near object (and vice-versa). You should change the tags.

I have experienced same thing while practicing mindfulness. When I just look at a flame I could see it as I normally do but trying to focus on it more will cause the flame to double up and yet refocusing will bring normal vision. As @another'Homosapien' said I think it has something to do with vision.


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Why do we see black when we close our eyelids?
Why do we usually see black when we close our eyelids assuming there is no strong light source outside?
I realize we never really stop seeing as long as our eyes are healthy but based on assumption I would have assumed that the back of the eyelids would be the same as the front and this could be a range of skin colors other than black.
Is it because most times not enough light is being reflected off the back to show the color?

This is easily answered by first washing your hands, then standing in front of a mirror, pulling an eyelid away from the eye, then folding it to look at the underside. Hint: it's not black.

Hah! That sounds painful and it does not answer the question the in actual text of the post which is why we see black when we close our eyelids. I will retitle the question. Sorry.

The question is actually not a question of biology but of the physics of light. Absence of light is black. Closing your eyelids prevent the light to reach your eyes, so you see black. Even if the interior of your eyelids were snow white, you would still see black.

the cone cell in the eye allows you to see different colors, and it only function in an illuminated environment, and function less in a less illuminated area.
 when your eyes is closed totally obstruct the entrance of incident ray from the outside thereby causing only the rod cell to be functioning .then the only thing you can observe is total darkness.

can you add a reference for your answer?


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Why do tendons require over 100 days to make new collagen?
{1} says:

Tendons require over 100 days to make new collagen.

Why does it take so long for tendons to make new collagen?

References:

{1} Bass, L. M. T. "Tendinopathy: why the difference between tendinitis and tendinosis matters." International Journal of Therapeutic Massage & Bodywork: Research, Education, & Practice 5.1 (2012): 14-17. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3312643/