Is Protein-to-DNA ratio a good estimate of cell size?

So after discussing my concerns with my professor, I have found out that I overlooked the simple fact that the DNA concentration is not measured based on a single cell of tissue type.

Protein-to-DNA ratio is directly proportional to cell size and the reason why liver cells has the highest DNA concentration at 57.6 ug/ml is because they have a smaller cellular size compared to the other two. So a single ml of liver homogenate is going to present with a significantly higher cell count and thus, a higher DNA concentration. This is also why a single ml of heart muscle DNA concentration is only 8.6 ug/ml due to there much larger cellular size.

This finding can be confirmed from calculating the Protein:DNA ratio as the liver homogenate with its smaller cellular size is only 0.184 and the heart homogenate with its larger cellular size is the highest at 0.548.

Thank you everyone for trying to help me with this problem!


Is there any possibility of interspecies sexual reproduction in animals like hybridizing plants?

The answer is : A big NO.

Naturally, there is no way possible to create a species like vinayagar. Humans and elephants are totally different, they belong to totally different orders. And success rate of inter-species reproduction is rare for even species from same family but from different genus.


Spread of a benign virus in a population over time

To many, many decimal places, the percentage of II in the population is 100%.

To answer this you need to make some assumptions about mating structure. I assume mating is panmictic here for simplicity. Ditto sex ratio, but I'm assuming equal number M/F (and equal risk of environmental infection). Finally, I’m assuming NI and II are at equal risk of soil-borne infection (and infections to II are simply wasted), rather than the environmental reservoir somehow seeking out a fixed proportion of NIs, which I think is probably what you meant. I’m also applying the soil-acquired infection to generation 0 here (so they have a chance to become infected before they mate). Finally, II and NI are more traditionally called $I$ (for infectious) and $S$ (for susceptible) in this type of model, so I've followed that convention below.

Unless I’m missing something the population size makes no difference: the chance of a child acquiring infection does not depend on the number of children, and the background rate of environmental infection is proportional to population size, so it all cancels out. I'll therefore stick to proportions from here on, which means $I$ and $S$ are proportions below, not absolute numbers.

Each generation, the proportion of matings between two $I$s is $I^2$, between two $S$s is $I^2$, and between an S and an I is $2·S·I$. So the proportion of Is in the next generation is $I^2 + 2·I·S$. Or, more simply, $1-S^2$.

So:

$S(0) = \frac{3,999,850}{4,000,000} = 0.9999625$
$S(1) = S(0)^2$
$S(2) = S(1)^2$, which is ${S(0)^2}^2$

More generally,
$S(n) = {S(0)^2}^n$

So at generation 600:

$S(600) = {S(0)^2}^{600}$

$2^{600}$ is a very large number. So it shouldn’t be too surprising that everyone is infected by this point.

We can mess around (technical term) with the equation:

$S(n) = {S(0)^2}^n$

...to solve for (for example) how many generations it takes for 50% of the population to be infected:

$$\begin{alignat}{1}
0.5 &= {0.9999625^2}^n \\
\log(0.5) &= \log(0.9999625)\times2^n\\
\frac{\log(0.5)}{\log(0.9999625)} &= 2^n\\
\log_2\left(\frac{\log(0.5)}{\log(0.9999625)}\right) &= n
\end{alignat}$$

So 50% of your global population is infected by generation 15, only 300 years into the simulation.

  however a few NI persons will still pair with NI mates--for a while

The probability of anyone ($S$, or $I$) mating with an $I$ individual is directly proportional to the $I$ proportion of the population, so the chance of this happening just keeps going down faster and faster.


3D models of adult male brain in the Blender software? Any open-sourced version for research?

There is a model of an adult, male, real human brain here:
http://brainder.org/download/brain-for-blender/

It can be imported into Blender or any other 3D application that can read Wavefront OBJ or Stanford PLY formats.


Are alpha-ketoglutarate and glutamate involved in all transamination reactions?

The major transaminases such as the aspartate transaminase and alanine transaminase involve the glutamate α-ketoglutarate interconversion. Even the GABA aminotransferase employs glutamate/α-ketoglutarate. It seems that all transaminases use glutamate/α-ketoglutarate; in fact most of them do.

These are a few that don't:

Beta-alanine--pyruvate transaminase.
Tryptophan--phenylpyruvate transaminase.
Pyridoxamine--pyruvate transaminase.
Aminolevulinate aminotransferase.
Serine--pyruvate transaminase.
Aspartate--prephenate aminotransferase.

And a few more (see here). Most of these are present in plants.


What is the specific use of a capsule in E.coli?

According to wikipedia, the capsule contains tightly packed polysaccharides that preform several functions including keeping bacteriophages out, blocking recognition by macrophages, and holding water during dessication. Given the wide diversity of bacteria with capsules, it's probably been around for a long time, which implies it isn't going away any time soon.

If the capsule prevents the E. coli from being taken up by macrophages, then yes, it could allow the bacteria to harm us more effectively. This is one form of a virulence factor.

With proper conditions we probably could develop a bacteria with little to no capsule. We have developed L-form bacteria, which don't have peptidoglycan cell walls. It would seem to me that the cell wall is more important than the capsule, but L-form bacteria are very fragile. I don't know what advantage would be gained by producing capsule free bacteria. There would probably be more to gain from making bacteria with different capsules, perhaps carrying proteins that recognize certain substances and produce a signal, allowing the bacteria to be used as a biosensor, or to accumulate toxic compounds for bioremediation.

references: http://en.wikipedia.org/wiki/Bacterial_capsule http://en.wikipedia.org/wiki/L-form_bacteria


How can frogs tolerate freezing while humans cannot?

Generally frogs are cold blooded animals (more specifically ectothermic or poikilothermic) . Wood frogs can maintain their body temperature by production of cryoprotectants which a human body cannot produce from normal metabolic processes. Such molecules depress the freezing point of tissue and avoid ice formation. Here is a scientific report on the physiology of wood frogs and what helps them survive at freezing temperatures. There are also other mechanisms which cold blooded animals use to survive such conditions.

Now for the human part. Humans are warm blooded (more specifically endothermic). We always try to maintain their body temperature (our normal body temperature is $37^{o}$). That is why we cannot tolerate freezing temperatures, because our physiology does not have a means to avoid cell damage at that temperature. The company which you mentioned uses vitrification methods which uses various artificial cryoprotectants (which wood frog makes naturally).

There is research going on in this direction already. Researchers are using extremophiles and their metabolic products in cosmetics and medicine (like this, this and this).


How did palaeontologists discover the age of the Tyrannosaurus rex named Sue?

Dinosaur bones contain rings, similar to a tree, that can be counted to determine age. SUE was 28 when she died, making her the most geriatric Tyrannosaurus yet found. Her bones show signs of wear and even disease, including arthritis.
Paleontologists can make micron slices of bone and view the rings through polarized light, even on a microscope at 5-10x, similar to geologist mineral ID's.
https://mistralmtn.blogspot.fr/2013/03/bone-growth-rings.html

Wiki: Growth lines may be deposited in synchrony with endogenous biorhythms. For example, captive crocodilians exposed to constant temperature, diet, and photoperiod, still exhibit the periodic and cyclical skeletal growth banding of their wild counterparts.[4] Consequently, it is assumed by many paleontologists that the growth lines of dinosaurs reflect annual rhythms, and that they may be used to determine individual ages. However, in the large and long bones of many dinosaurian taxa, resorption of internal and external bone proceeds even as new cortical bone continues to be deposited, so that growth lines deposited early in development may need to be inferred.
http://tbrnewsmedia.com/wp-content/uploads/2015/05/Dinosaur-Growth-Rate-w.jpg


Small flying insects gathering around the pot flowers

Looks like some sort of fungus gnat though I won't make any attempt to ID a particular species. Note that fungus gnat describes a very wide range of species over 6 families, though yours looks most like the flies from the family Sciaridae (Wikipedia notes there are ~600 species in Europe).

Fungus gnats feed on organisms decomposing soil, which are most present when the soil is moist, especially if overwatered. The damage you will experience, if any, would be to the roots, rather than visible on the leaves, though you will see wilting if the damage becomes significant.

You say things are dry, however, the important place is the soil. You will deter, though probably not completely eliminate, the fungus gnats if you let the soil dry between waterings (in my personal experience with fungus gnats this approach was sufficient). Some specific parasitic nematodes are also used for pest control of fungus gnats, if they are available in your area.


Gluteraldehyde interacts with amino groups to block the dynamic movements that biology requires.

Yes the corpses of the fixed bacteria can be counted and bio-films will be intact but the bacteria will be fixed in place.

Biofilms that are fixed with gluteraldehyde may shrink when prepared for imaging due to the effects of dehydration.


DNA extraction kit for microbial mats, rocks, and soil in a remote area

Those are some pretty tough samples to get high-quality DNA from, even in a lab. Your best option is probably to place samples in a nucleic acid preservation buffer and carry them out for extraction later.
That said, there are some potential solutions. Akonni has some kits that don't use any centrifugation and they claim they'll work on soil and stool, so they might be good enough for your applications. They kind of seem like they're based on the same principle as this kit-free protocol (this protocol is for Plasmid DNA, but I'm sure it could be adapted for Genomic DNA with a little R&D on your part). In either case you'd probably want to look into a portable bead-beater to disrupt/lyse your samples. This will shorten your DNA fragments through shearing, but it's probably necessary to get good extractions from any of these materials.
A few companies also make portable centrifuges that run on 12V car plug adapters, assuming you'll have a vehicle somewhere within walking distance. That could open your options up to using a Powersoil kit or even something like a phenol-chloroform extraction, which you might not need a bead-beater for. (Note: you absolutely would need a properly fit-tested, full-face respirator with the appropriate chemical filters to do phenol-chloroform work without a proper fume hood, plus a way to haul out your waste).
If it were me, I'd still probably use a preservation buffer and do the extractions and analysis back at the lab.


Classification of equilibrium points is done on the basis of the eigenvalues.

If the two eigenvalues have no real parts, it is a hyperbolic fixed point and represents undamped oscillation.
If both have a negative real part, it is a stable fixed point. If any of the eigenvalues has an imaginary part then it represents damped oscillations (in that case the equilibrium point is called a focus).
If one or both eigenvalue have a positive real part, it is an unstable fixed point.
If one eigenvalue has a positive real part and the other a negative real part, it is a saddle point.*

You sketch the trajectories of the equilibria by starting a tiny distance away from the point (where it is not in equilibrium) and trace the quiver plot. Drawing trajectories around unstable points is tricky and you have to plot the function in negative time i.e. instead of plotting f(x1,x2,t), you plot -f(x1,x2,t).  This page has representative trajectories for the different types of equilibrium points.  This page has a more thorough explanation, generalized to multiple dimensions.

*This classification appears to be slightly variable (more or less categories), on the basis of the two links I found.  I think the one I list is the simplest version, but any classification should suffice.  They are all based on the same principles. You can refer to some books on non-linear dynamics:

Nonlinear Systems by Hassan Khalil
Nonlinear Dynamics and Chaos by Steven Strogatz


A classic standard textbook that I've used a lot myself (earlier editions) is Begon, Harper & Townsend. This book is very broad and comprehensive, but I know that some students dislike it's back-and-forth discussion style (fewer definite answers). I see this as a strength though.

Another good choice, that is much shorter, is Gotelli's A Primer of Ecology. This one has a slight theoretical leaning (many standard mathematical models), but can work well in a  introductory course. I don't have the book in front of me, but, looking at your list of topics, I suspect that A Primer... might be weak in some of them (e.g. climax, succession).


Does blood carry metallic nanoparticles?

It is very unlikely to have metallic nanoparticles in blood under normal circumstances.

Reasoning:

There are specific proteins that strongly bind metal ions: transferrin and ferritin for iron,  zinc transporters (Zrt) for zinc, metallothioneins as a catch all for most heavy metal ions etc.  These tend to be intracellular so most of the metal would be bound inside cells.  Any particles would be endocytosed and oxidized to the ionic form (probably in peroxisomes), then the metal would be bound to proteins.
Metal nanoparticles as well as free ions (of metals with more than one oxidation state) have considerable catalytic activity which is non-specific (and therefore quite toxic).  They can serve as a redox catalyst as well as generate ROS from oxygen.  That's probably why metal-binding proteins have evolved.
Lastly, iron in particular is a limiting nutrient for many pathogens.  Extracellular iron is very tightly controlled as part of non-specific pathogen defenses.  There is only exactly as little iron in blood plasma (bound to transferrin) as absolutely necessary to move it to the cells that take it up.  It's unlikely there would be any free iron, because there wouldn't be any fast, specific way to take it up the way the transferrin receptor does.


Microtubules are made up by $\alpha$- and $\beta$-tubulin units, the wiki page for this will link you to a short section on microtubule dynamics, which is the basis of how the growth & shrinking of microtubules is controlled:

Microtubules grow (by addition of $\alpha\beta$-units) and shrink (by dissociation of these units) primarily at the '+ end', which is the one in the cell periphery not at the centriole. Actually both of these reactions (growing/polymerisation and shrinking/de-polymerisation) usually happen at the same time but with different speeds. These speeds depend on whether GDP or GTP is bound by the $\beta$-tubulin at the + end, the (relative) concentration of GTP-bound free monomers and other structural proteins. Except for the GTP/GDP bound state in the mircotubule all of these factors can be controlled (or altered) by the cell through various mechanisms (some are listed on the 2nd wiki page I linked; I may add some specific ones if I have more time).


This one is most probably a longhorn beetle (Cerambycidae). The long elytrae (protective forewings) and the long curved antennae are quite typical.

Yours looks a bit like this one: https://en.wikipedia.org/wiki/Rosalia_longicorn
It is probably a different species, though.


Why do cats meow but lions and tigers roar?

They have different vocal cords, differently-shaped pharynx. I would imagine that is all that explains the difference in sound. As to mewing versus roaring, the vocalizations you reference are not applied to similar sithations.  I wonder if there are videos of baby lions mewing or making similar sounds to get their monther's attention?


Why do pink rain lilies flower only after rains, and not from being watered?

It looks like sustained or consistent moisture might be (at least part of) the phenological cue for flowering:

The wikipedia article mentions that consistent humidity will induce flowering in at least some species and cites Fernández-Alonso & Groenendijk (2004), which says:

  It generally flowers after the rainy periods, but in humid pastures and under cultivation conditions, colonies show staggered flowering during the whole year.

There's a reference in Lange et al. 2013 to Zephyranthes flowering after "watering of at least 10 h[ours]", but I'm not able to find the original citation in the google books preview (which is given at "Nitsch 1965").

Edit: I tracked down Nitsch 1965, who cites 2 sources on the topic. He reports Kerling 1949 as showing that Zephyranthes rosea after a certain period of development goes into dormancy, which is broken when two conditions are met: low temperature and high water, which must be extended over at least 10 hrs. He adds that Holdsworth (1961) presents evidence showing that Zephyranthes citrina and Z. tubispatha are primarily triggered by soil moisture.

Fernández-Alonso, J. L. & J. P. Groenendijk (2004). A new species of Zephyranthes Herb. s. l. (Amaryllidaceae, Hippeastreae), with notes on the genus in Colombia. Rev. Acad. Colomb. Cienc. 28: 177-186

Holdsworth, M. (1961) The flowering of rain flowers. Journal of the West African Science Association 7︰28-36.

Kerling, L.C.P (1949) The gregarious flowering of Zephyranthes rosea Lindl. Annals of the Botanic. Gardens. Buitenzorg 51: 1-41

Nitsch, J. P. (1965). Physiology of flower and fruit development. pp 1537-1647 in Encyclopedia of Plant Physiology Vol XV Part 1, W. Ruhland (ed.)

O. L. Lange, P. S. Nobel, C. B. Osmond, H. Ziegler (2013). Physiological Plant Ecology III: Responses to the Chemical and Biological Environment. Springer.


Punnet Square for Genotype Probabilities

Our germ cells are haploid, while our somatic cells are diploid. The diploid cells of a child result from the fusion of a paternal haploid germ cell and a maternal haploid germ cell. When these germ cells are generated during meiosis, the paired diploid chromosomes of each parent (which they in turn received one of from each parent) are randomly segregated such that for a given chromosomal pair there is an approximately equal chance of a given germ cell containing either member of the pair independent of the what other chromosomes it receives.

In the case of a single gene with a single copy on both the maternal and paternal chromosomes, the Punnet Square accurately estimates the probably of inheriting each possible genotype. (50% chance of getting one of two alleles from dad * 50% chance of getting one of two alleles from mom). In the case of multiple genes on different chromosomes, the 50% chance of any given allele still holds, as all the genes segregate independently. The accuracy of the Punnet Square fails when genes are sufficiently close to each other on the same chromosome. Genes distant from each other on the same chromosome still segregrate independently due to a high level of recombination events between chromosomes in meiosis I, but genes in close physical proximity no longer segregate independently. The closer two genes are physically the more they tend to co-segregate. This tendency is reported empirically as a "distance" in centiMorgans and is related to physical distance in base pairs (kB or mB) but is not completely proportional to physical distance due to the existence of recombination "hot spots."

It's important to note that is accurately predicts genotypic ratios, but not necessarily phenotype. Phenotypes can be less than 100% penetrant, can cause embryonic lethal, epistasis, etc. Such that the observed phenotypic ratio does not match the predicted ratio. (For example, if YY was known to be 100% embryonic lethality, live births -> observed phenotypes instead be expected at 1/3 of each of the remaining genotypes. If Y was instead phenotypically dominant (one copy of Y determines phenotype), then 75% of children would be expected to be phenotypically Y (genotypically, the Y phenotypic children would be expected to distribute evenly between YO, YY, BY).


RNA is shortlived and need not undergo repair. A "mutated" RNA will degrade and will be replaced by the correct RNA.

Even though RNAs are shortlived compared to DNA (which does not really undergo turnover), some RNAs are stable and have low turnover. Nonetheless RNA would be present in multiple copies it is improbable that all of them would have undergone mutation.

Moreover RNA with certain mutated codons e.g. non-sense mutations are cleared off by the exosome.

Thanks to har-wradim for pointing out about RNA repair mechanisms. There are few reports that say that methylations in the RNA can be corrected by the enzymes AlkB (in E.coli) and its eukaryotic homologue hABH3. These enzymes were known to repair methyl lesions in the DNA (1-methyladenine and 3-methylcytosine), but it was subsequently shown that they can act on RNA as well [1,2].

However there seems to be no mechanism for repairing deamination damage; this study has demonstrated an artificially designed system which is capable of targeted RNA deamination (but there is no system yet that can fix a deaminated base in RNA).

This article comments that AlkB is tightly regulated because if uncontrolled it can demethylate functional methylations too. Overexpression of AlkB is actually toxic to the cells unless they are under alkylation stress by agents such as EMS/MMS (Ethyl/Methyl MethaneSulphonate).

But IMO RNA repair is not as essential as DNA repair because of aforementioned reasons.


Can epigenetic structures carry a trait?

Yes, epigenetic changes does affect the phenotype. This is here the whole interest behind epigenetic. Environmental variation (incl. parental care) affect epigenetics which in turn affect the phenotype (incl. behaviour) of an individual. It is pretty much clear from the wikipedia definition of epigenetics

  Epigenetics studies stably heritable traits (or "phenotypes") that cannot be explained by changes in DNA sequence.

The term "phenotype" (or "phenotypic") is actually present 3 times is the first small paragraph of the wikipedia article.

For example, you can read here on wikipedia an example of a study showing that maternal care affect epigenetic variations which in turn affects stress level later in life as measured by HPA.


Why is sex hurtful for some animals but pleasurable for others?

There are various selection pressures that may lead to sex being more or less harmful. I don't think there is an easy way to summarize these selection pressures other than just going through load of examples. Here is an attempt to give you some notions of why can sex be pleasurable and/or painful. Note that I do not consider myself particularly knowledgeable in this field.
Why could it be pleasurable
We tend to seek for positive experiences. If we like sex, we have more sex. If we have more sex, we are more likely to have more offspring. Hence, the trait "liking having sex" is positively correlated with "fitness".
Why could it be harmful
Dick pics
In many species, the penis has spikes and stuff and is most definitely hurting the females. Here is a Drosophila penis

And here are penises of two dragonfly species

Here is a feline penis

By the way, according to wikipedia (could not find peer reviewed paper on the subject so take this with a grain of salt), some humans still have on remnants of those barbs you can still see on many feline penises left from our ancestor. They are called hirsuties coronae glandis. Here is a perfectly healthy (but I would tend to consider quite extreme) example of hirsuties coronae glandis

Some theory
There is a lot to say here and I only want to say a few words and hopefully you will go get more information by yourself.
So why do these species evolve these fancy and scary "armed" penises. In many species, it is a small investment for a male to make a baby (just mate and the job is done) but a big investment for the female (producing the egg, eventually even parental care, ...). Because the sex-ratio is always (assuming no group selection) pushed toward 0.5 (see this post and Fisher's principle), it happens that males end up with lots of free time looking for females (see Why are female not competitive for reproduction like males? and Bateman's principle). You might also want to read about sexual conflict.
Why would such penis evolve?
The reason vary among species. Here is a non-exclusive, non-exhaustive list of reasons:

In some species (e.g. nudibranch, damselflies)The goal is to remove the sperm from an eventual previous male so as to reduce sperm competition (Cordero-Riviera, 2016).

In some species, the goal is to damage the female reproductive track so that she will not subsequently mate with other males hence reducing sperm competition ().

In some species, the male can even leave toxic products in the female (Chapman et al., 1995).

In some species, females get severly harrassed by males for mating and rape is not unusual (e.g Drosophila). Some penile barbs and spikes can be used to get the female stuck in place. To avoid that the female can escape before the sperm has been delivered ()! That being said, in some circumstance such use of spiky penis might be beneficial to the female too. This non-peer reviewed article may bring some light.

In some species, the male can pierce through the female abdomen to deliver its sperm. This is called traumatic insemination.

In a classical experiment, Rice 1996 shows that there is an arm race between males and females. Race in which males increases their negative impact on female's reproductive organs and females protect themselves from it. The paper is free, is short, easy to read and has a pretty amazing experimental design. It is worth having a look at it.
Feeding the babies via the mother
I just want to point with other examples that sex does not have to be romantic in many species. In some species, the female eats the male after sex or even while having sex. To what I have heard (; please be cautious with this information), in some mantis prey, the male does not even release his sperm before the female has cut the male's head off. Why would the male do that?
A male that let himself get eaten by the females ensures that the female has lots of energy for taking care of her babies. Hence a male may increase his fitness by sacrificing himself to his partner.


For ligation of a linear molecule to occur, the two ends must come together at the active site of the DNA ligase. In a simple molecular cloning experiment the aim is usually to avoid recircularisation of a cut plasmid vector, and instead to get a new fragment of DNA inserted into the vector. However because the ends of the linearised circular plasmid are tethered together (by being ends of the same molecule) they are more likely to encounter each other than they are to encounter the end of an incoming fragment. This is usually overcome, in part, by increasing the relative concentration of the target fragment.

If you are aiming to recircularise a long fragment then the opposite effect will come into play: the ends of individual long molecules will be much more independent and so the end of another molecule will be likely to compete successfully for ligation. In theory this effect could be overcome by reducing the DNA concentration, but I assume that this is impractical for other reasons.


How accurate is facial reconstruction in forensics?

okkkk. I did a big project on this... and here's some of my research... let's hope it answers your question

Facial reconstruction (also known as craniofacial identification) is a method used in the forensic field.  Many people view facial reconstruction as an art instead of science.  Art is commonly portrayed as the expression or application of human creative skill and imagination, typically in a visual form such as painting or sculpture, producing works to be appreciated primarily for their beauty or emotional power.  Science is thought of as the intellectual and practical activity encompassing the systematic study of the structure and behavior of the physical and natural world through observation and experiment.  But where do science and art blur the lines?

WHAT CAN WE TELL FROM THE SKULL:

The skull provides clues to personal appearance. The brow ridge, the distance between the eye orbits (sockets), the shape of the nasal chamber, the shape and projection of the nasal bones, the chin's form, and the overall profile of the facial bones all influence facial features in life. Using these bones, artists and forensic anthropologists work together to reconstruct facial appearance through the process of forensic facial reconstruction.  There are many ways of telling both the approximate age, and the approximate ethnic background of the victim.  To find age, you can pay attention to the cranial suture (or the place where the cranium fuses to other bones of the skull), the size of the skull can help, as well as the teeth and the formation of the bottom jaw.  When looking for the birth gender of the victim, scientists often pay attention to the brow ridge, eye sockets, mandible, and the slant of the jaw.  Sometimes, it is impossible to tell by looking at the skull what birth gender the victim was.  In cases like this, people look to the pelvis to tell if the human has given birth, and if not, males do not have a ventral arc.  It is often very difficult to find the race of a victim if they are mixed race, or if the skull is very worn out.  However, to find the ethnic background scientists will look at the shape of the skull, the nazel root, and the space between eye orbits.

WHAT ARE THE PROCESSES OF FACIAL RECONSTRUCTION AND ARE THEY ACCURATE:

Facial reconstruction is an exacting process. The finished product approximates the actual appearance, because the skull does not reflect the details of soft tissues-eye, hair, and skin color; facial hair; the shape of the lips; or how much fat tissue covers the bone. Yet, facial reconstruction can put a name on an unidentified body in a modern forensic case, or, in an archaeological investigation, a face on history.

Today, many forensic facial reconstruction techniques are in use, including two-dimensional (drawn), three-dimensional manual and three-dimensional computer-based.  In the manual techniques, including two dimensional a cast of the skull is required, so the facial markers do not become an anomaly when analyzing the skull.  Although all of these methods are used, it is most common that a trained sculptor, who is familiar with facial anatomy, works with a forensic anthropologist and uses clay to build the facial features. The forensic anthropologist interprets skeletal features such as the subject's age, sex, and ancestry, and anatomical characteristics such as facial asymmetry, evidence of injuries (a broken nose, for example), and loss of teeth before death.

Facial reconstruction is used when the victims dental records fail to identify them, and there is no dna to pull from the body.  The process of reconstruction starts with making a mold of the unknown skull with the jaw attached and false eyes in place.  Depth markers are placed on 21 different “landmark” areas of the mold of the skull to approximate the facial tissue thickness that lay on the skull.  These tissue thicknesses are approximated from averages of other people of the same age, sex, and race as the skull is assumed to be.  Facial muscles are placed on the mold next and then the face is built up with clay to within a millimeter of the depth markers as tissue.  The nose and eye setting are very difficult to estimate due to the enormous amount of variation possible, mathematical models are used to make the approximations, the mouth is assumed to be the same width as the distance between the pupils. In facial reconstruction the eyes, nose, and mouth are mostly guess work.  Characteristics such as birthmarks, wrinkles, scars, and such are guesses at best and cannot actually be determined from the skull.  Facial reconstruction is accurate because it has been using mathematics, and calculations as such, in order to determine spaces, amounts, as well as the shapes of the face themselves.

WHY IS FACIAL RECONSTRUCTION IMPORTANT:

Facial recognition, as well as facial reconstruction is very important in the forensic field.  Both have a very important role in catching murderers, and investigating crime.  Without having a facial reconstruction, often times, you cannot identify victims.  Assuming the body is historical and for museum purposes, then without an identity it becomes very difficult to fill in large gaps of information, and time that can be crucial to history.  Also, if you can’t identify a murder victim then scientists could only look into cause of death.  Learning the identity of a deceased victim is as important to crime investigations as learning the identity of the suspect. When human remains are found, then the top priority is often to find the identity of the victim.  Police often also will look for an identity out of respect, for both the victim and the victim’s loved ones if any.  Facial reconstruction has been used ever since 1890.  Before 1890, people mostly used few facial indicators such as the shape of the frontal bone, and the remains of flesh to help identify the victim.  Facial reconstructions, can also show what injuries were sustained previous to death.

WHAT CAN WE LEARN FROM FACIAL RECONSTRUCTIONS:

Our skeleton is an extensive record of our lives. The food we eat, the rate at which we grow as a child, the injuries we sustain, whether we have given birth; all can be determined from our bones. Experts can determine sex, age, and ethnicity, relatively easily from the skeleton, with the skull and pelvis playing pivotal roles in this analysis. Later this week, we’ll be taking a more detailed look at how to determine sex and ethnicity from a skull.Teeth can reveal information about diet and a comparison between dental records of the deceased and the recovered skull is often the primary method of identification.  By looking at the scull (or any bones in fact,) you can tell childhood injuries from injuries that might have been fatal.  You can also look at bone density and other factors to tell if the victim was suffering from any diseases.  People look for the sagittal suture – the squiggly line that runs the length of the skull – If it is fully fused, the remains are likely to be of someone older than 35. After that professionals look for a second line at the front of the skull -- the coronal suture – which fully fuses by age 40. Teeth are also looked at. If they're worn down it could be a sign of a poor diet. If they're well-maintained and/or have good dental work such as fillings, they were able to afford proper dental care—another clue as to the identity of your skeleton. Oftentimes professionals consult a scientist who specializes in teeth, known as an odontologist. They can determine how old a person was at death, what kind of health they were in and what kind of diet they had.

Baby's bones begin to grow in the womb. At birth, the skeleton is partially formed. Many bones are still in "parts." The ends (epiphyses) and bony shafts (diaphyses) of long bones form separately in the womb. At birth, the ends of the long bones are mainly cartilage, with centers of bone beginning to form inside. As a child grows, the shafts get longer, and bone gradually replaces the cartilage epiphyses. Through the growing years, a layer of cartilage (the growth plate) separates each epiphyses from the bone shaft.  By paying attention to this, it is easier to tell age, and follow growth patterns to have a successful reconstruction.

Between 17 and 25 years, normal growth stops. The development and union of separate bone parts is complete. At this point, you and your skeleton are as tall as you are going to get - with many fewer bone parts than you started with.  The bones that enclose the brain grow together during childhood along lines called cranial sutures. During adulthood, bone "remodeling" may gradually erase these lines, at variable rates. Closure of cranial sutures gives general information about a person's age. It is best used with additional indicators to estimate age, or when other age indicators are unavailable.

WHAT ARE THE LIMITATIONS:

It is very hard to estimate a person’s weight and represent that with facial markers.  Since a chart of average thickness of soft tissue is used to estimate the way a person looked, if you were on the skinnier side, your head might appear a lot more overweight than usual and or skinnier.  To help determine weight, scientists look at the rest of the remains for a height.  Facial reconstruction relies on the relationships between the facial features, subcutaneous soft tissues and underlying bony structure of the skull. If there is no clue for potential identity because of impossibility to compare questioned remains with possible familiar material, in such cases one of the last chances is to recreate ante mortem appearance by face reconstruction. Many of the soft tissue thickness values are significantly different from those reported for comparable groups, suggesting that individuals from different geographical areas have unique facial features thus requiring population-specific values. This literature review attempts to throw some light on the important aspects that has to be taken into consideration while setting norms of soft tissue thickness among various populations.

Studying the unknown skeletal remains mostly becomes the only way to find out more information about individual characteristics, which could lead to identification of potential victim. If there is no clue for potential identity the most precise comparative techniques fail, because of impossibility to compare questioned remains with possible familiar material. In such cases one of the last options is to recreate ante mortem appearance by face reconstruction. Following the first introduction of reconstruction in the late 19th century, other techniques have been developed including radiography, 3D statistical model, ultrasound, MRI, CT and Cone Beam Computed Tomography (CBCT).  Facial contours were traditionally considered to be the result of positioning of underlying hard tissue followed by the soft tissue. However, current trend shows a paradigm shift from the conventional hard tissue analysis to also include both hard- and soft-tissue analysis.

IS FACIAL RECONSTRUCTION AN INTERDISCIPLINARY ART:

The skull is made up of 22 bones, 14 of those are facial and eight are cranial bones; it is a complex structure, and small variations during development and growth, together with soft tissue differences, create the enormous facial variation seen in the human population.  Artists have long been interested in the direct anatomical relationship between the skull and facial appearance.

Artist, Gaetano Guilio Zumbo (1656-1701), used facial reconstruction as an art because he believed that math and science are both forms of art.  His work can be found in the Wax Anatomical Collection at La Specola Museum, Florence, became famous for his macabre scenes depicting various stages of decomposition of the human body.  One of his most famous pieces is the head of a dead man, with facial muscles recreated in wax over a real skull.
This is the earliest surviving anatomical wax model created for didactic purposes and exhibits extraordinary anatomical precision alongside an artistic sense of horror and decay. Although we assume that Zumbo was less concerned with facial appearance than anatomical detail, he pioneered the development of scientific art and this work ranks as one of the finest examples of three-dimensional facial reconstruction.

By definition, an interdisciplinary art is relating to more than one branch of knowledge.  Facial reconstruction is often categorized as both a science and a mathematical equation.  Both science, math and art are human attempts to understand and describe the world around us. The subjects and methods have different traditions, and the intended audiences are different, think the motivations and goals, specifically for this purpose is fundamentally the same.


Tree census data for Sweden/Scandinavia?

I would definatley look at data from Swedish National Forest Inventory (Riksskogstaxeringen). They have time series data of multiple variables (DBH, size classes, species, dead wood etc) from plots all over the country. Extrapolations based on these data should produce reasonable estimates of total tree count, and probably the most accurate one that can be obtained at the moment. As an example, this report (in swedish) includes graphs on trees/km$^2$ for different species and areas (page 17 ff), but this is only based on areas that can support productive forestry.


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

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

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

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

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

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

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

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


In a tumor, why hypoxic regions have access to glucose?

I think this is a difficult question for which the answer is not clear --- to my knowledge there is little data on metabolism in solid tumors, and no clear consensus in the scientific community. So I'm not going to attempt to give a definitive answer, but here's at least a few thoughts / opinions.

Why transformed cells engage in aerobic glycolysis, or the "Warburg effect", is a question people have been trying to answer for nearly a hundred years now. There are dozens of hypotheses, but none of them is broadly accepted. One popular hypothesis laid out by Gilles & Gatenby says that transformed cells from solid tumors are glycolytic because they have been selected for anaerobic metabolism in a hypoxic environment, and this selection is somehow irreversible, so that the cells stay glycolytic even after being extracted from the tumor and cultured in aerobic conditions. I think this hypothesis is the origin of the idea of hypoxic and yet glycolytic tumors.

In a way the Gilles & Gatenby hypothesis is a clever idea --- it rests on the well-accepted fact that most cells become glycolytic in hypoxia, and rhymes with the concept of selection for survival in tumors. But the problem with the argument (as you have realized) is that the tumor environment would have to be low in oxygen and at the same time high in glucose. I agree with you that it is unlikely that such an environment could arise due to lack of blood supply, since oxygen diffuses more easily through tissues (and cells) than glucose does. Moreover, considering the high demand for glucose by glycolytic cells, glucose should become limiting long before oxygen runs out. So one can argue that poorly vascularized tumors should be mainly oxidative, not glycolytic!

To my knowledge, there is no data demonstrating existence of (regions of) solid tumors with low oxygen and high glucose. There is of course ample evidence that many solid tumors consume large amounts of glucose, and also many studies showing hypoxic regions in tumors. But most likely these are different types of tumors, or different regions. In an environment with neither oxygen nor glucose, cells will simply die --- which is exactly what happens in the necrotic cores of larger solid tumors.

The best source of further information is probably the tumor physiology literature. This review is a good starting point.

Finally, another issue with Gilles & Gatenby's hypothesis is that aerobic glycolysis can easily be demonstrated in cells that have never been in a tumor. For example, in vitro transformation can increase glycolysis, and normal lymphocytes induce rapid glycolysis when activated by receptor stimulation. So there is no need to assume that glycolytic tumors are hypoxic.


this is a chart of the light activation of the light sensitive cells in the human eye.

see that little blip up on the tail end of the red cone, that minor ranges means the extreme blue end of the spectrum activates blue cones but also has a chance to activate red cones. That is why you can sometimes see magenta tinges in bluest of blue light. There is also a sensitive issue as blue cones are the least sensitive of our cones so it requires a stronger blue light source to activate it than the equivalent light on other cones, since red is more sensitive a strong blue and a weak red source will blend to about equal as far as our eyes are concerned so at the bluest end of the spectrum, where the blue activation is at its weakest it does not take much to activate the blue and red "blip" equally meaning all sources at that extreme end blend into magenta.

Also magenta itself is not actually part of the spectrum, it can be produced in two ways, the first I discussed above, hitting the far end of that little blip perfectly. The second and most common requires light from two disparate and different parts of the spectrum in other words not a single wavelength. It is blue light and red light without green light, it is not a real color but an artifact of how our eyes see light. Your cones can't tell how they are activated just that they are. Yellow and cyan (and every other common human color)on the other hand can be produced by a single wavelength, which may or may not activate multiple types of cones.
You can find more information here


If you zoom in on the image, you can see that it is not just composed of black vertical lines, but also has pixels with different gray tones in the white areas. When you move your head sideways, you perceive the gray tones more.

If you were to remove the black lines, you could see the face clearly. Initially I thought that by blurring the gray shapes when your head moved, they became more visible as they seemed larger. On reflection though I think that actually what's happening is that the high contrast between the black lines and the mostly white background causes your perception to adjust so it doesn't easily see the mid tones. This is because we have a low dynamic range in our vision (relative to absolute brightness, but compared to camera CCDs we have a high dynamic range) - we have to adjust the light sensitivity to compensate for the overall brightness of the image. This is called brightness adaptation. There's a good free textbook for further reading about this at Utah U's Webvision.

When you move your head, the black and white lines blur together which makes the overall brightness appear to be the average brightness of the black and white. So against that background your light sensitivity increases and the areas where the pixel tone is different from the average - the gray pixels of the face - start to stand out.

By reducing the brightness you can see the faint image in the background much more clearly...


The link you give doesn't mention limbs sticking out of the body wall, but only vestigial hind limb elements. Many whales do retain pelves and femora, as this page at the Bergen Museum shows. Given the variation in limb development across vertebrates, it would not be surprising to find more distal elements (but I would be very surprised if they extended past the body wall).


Yes, pepsin does digest plant proteins also. Pepsin is a protein and its job is to cut other proteins (also known as polypeptides) into smaller pieces. Proteins are made of amino acids and there are 20 amino acids found in proteins. Pepsin cuts the bond between two amino acids to break the protein into smaller pieces. When pepsin encounters a tryptophan (Trp), tyrosine (Tyr), and/or phenylalanine (Phe), it cuts the bond between that amino acid and the one next one, as shown below.

image source

Proteins from plants contain these amino acids so pepsin can cleave plant proteins.


Absolutely a serious part of research - quantum mechanics defines chemical structure and reactivity. Whenever you see a headline like 'Scientists find quantum effects important in protein activity, weird huh?', read it as 'Scientists find pragmatic classical approximations inadequate in describing protein activity'.

In protein structure, for example, classical molecular dynamics/mechanics are important in generating computationally tractable problems, however they represent a tacit and streamlined parameterisation of underlying quantum mechanics. QM protein structures are usually too gnarly to compute (at least historically speaking), except in regions of interest like an active site, where a model fine-tuned for sequences of amino acids will probably fail badly anyway. As a concrete example, the group that I'm in is in part interested in computationally modelling the active site of plant photosystem II, which contains a cluster of spin-coupled manganese atoms. To glean any useful understanding of how this cluster functions via a computational model, an explicit quantum mechanical level of theory that takes into account electron exchange and correlation must be used. This requirement can probably be extended to any metalloenzyme.

And this isn't touching upon the resonance hole transfer that oxidises the active site, the Davydov solitons that manifest in protein alpha helices, or indeed the quantum electrodynamical origins of the Van der Waals interaction that causes everything to tend to stick to everything else.

Hope this is interesting :D

(note: I am not involved with PetaChem, I just think it's freaking awesome.)


Why does hair grow after trimming but remains at a constant length after a while?

Hair grows from the follicle; there is no way for the follicle to determine if the hair tip is trimmed or not. This is unlike plant shoot/root growth that happens at the tip. Also there is no signaling from tip to follicle.

Hair growth has four stages: Anagen (Initiation), Catagen, Telogen (resting) and Exogen (falling off). Initially the primary follicle is formed during development of the skin, after that the hair growth continues in a cycle. In other words the old hair shaft is replaced by a new one. The period of the cycle (or how fast it happens determines the final hair length); the faster is the cycle the shorter will be the hair (you may note that certain people have a very short head hair even when they do not trim). This is because the old shaft doesn't get time to grow before it is shed and replaced by the new one.

From: Stenn & Paus (2001)

From the same source

  Because there is a limit to the time a follicle stays in anagen, there
  is also a limit to the length of its product, the hair shaft. The
  anagen phase has been divided into six subphases (64, 359). Except for
  the last subphase, anagen VI (the duration of which dictates the shaft
  length), the length of the anagen subphases I–V does not differ
  substantially between follicles from different regions (490, 565).
  […]
   Because the actual length of a hair follicle does not appear to
  dictate the length of its shaft (rather the duration of anagen
  determines hair shaft length), it is tempting to speculate that the
  subcutis offers optimal growth conditions…
  […]Although influenced by environment (light, temperature, and
  nutrition) and systemic (endocrinological factors) parameters, it is
  generally believed that there is considerable innate local control of
  hair shedding; each fiber grows to a specific length, for a specific
  period of time, before being shed


Why does ATP contain ribose rather than deoxyribose?

Short answer:

The pentose ring does not participate chemically in the energy transfer reactions involving hydrolysis of ATP to ADP.

Enzymes that catalyse these reactions would tend to be specific for ATP (rather than dATP) because they bind the whole molecule and this would most likely include the 2'-OH of the ribose ring. dATP would therefore bind less well or not at all. (There may also be an advantage for evolving such specifity so that dATP could not compete for the active sites.)

The reason that evolution produced ATP as the energy transfer molecule rather than dATP is purely a matter for speculation. One might argue that it is an extra energy expense to reduce the ribose ring, although I prefer a more mundane answer. That is that if one assume RNA genomes (and enzymes) predated DNA genomes evolutionarily, then molecules involved in energy metabolism that contain ribose — not just ATP, but NAD and coenzyme A — arose at that time. When the genomes switched to DNA there was no selective advantage in changing ATP (and NAD) as well, and such an advantage would have been required as the enzyme systems that used these small molecules would by then have been already established.


Species identification: 2.5mm (3/32" or 1.5/8") brownish ant in highrise apartment

According to the pest control expert, the ants are likely pharaoh ants.  It matches the description on the Wikipedia page in all respects:

Colour
Size
Pervasiveness in indoor environments throughout the world

He is treating the problem in my unit and a neighbour's unit using Maxforce Quantum.  It could take some time :( .

This is not conducive to a fitness regime of pushups, situps, leg lifts, and side planks (all on the ground, of course).  It doesn't help that my apartment largely has wall-to-wall carpeting coloured with a brown and white texture.  Spraying down the vicinity with vinegar is unlikely to help, as the ants have clearly demonstrated a lack of repulsion from vinegar droplets.


What is the meaning of Dimer Catastrophe?

A "plasmid dimer" is defined as a plasmid that has two origins of replication instead of the usual one origin of replication. This can happen if two copies of the same dimer undergo recombination resulting in one plasmid with two origins and one with zero. I hadn't seen this term before, but it seems to be the meaning with which it's used in this paper and a few others I saw.

The "dimer catastrophe" hypothesized in this paper refers to the idea that over time this would lead to a reduction in overall plasmid copy number (and thus an increased probability of plasmid loss), since dimers may be more likely to replicate than monomers (due to having more origins of replication).

For what it's worth, I also found the paper you linked a bit hard to understand, but I found this one more explanatory (your mileage may vary): Multicopy plasmid stability: Revisiting the dimer catastrophe.


Why does IUCN classify pistachio as a "Near Threatened" species?

Short answer: They were talking about the wild species.
Using the presentation by a Farm Advisor and a Pomologist, Pistachio Cultivars as a rough indication of the state of the species, we see that the commercial crop does not have much diversity.

Probably 97% or more of the pistachio acreage in California is planted to the Pistacia vera female cultivar called ‘Kerman’ and a P. vera male called
‘Peters’.

The presentation mentions that other geographic regions prefer other cultivars. But generally, the the entire commercial population of pistachio seems to be limited to a few tens of cultivars.
The IUCN Red List that I cited in the question is rather poor on the details. However, the publication, Geneflow '06, included a report on Uzbekistan's pistachio:

Saving Central Asia’s pistachio diversity
For three millennia, pistachio trees were used in metallurgy and mining in Central Asia due to their accessibility and the highly calorific charcoal they produce. The result was a major depopulation of wild pistachio in the region. During the Stone Age, pistachio trees in Central Asia covered approximately 2 million hectares, compared with only 300 000 hectares today.
The loss of wild pistachio diversity in Central Asia has major implications for pistachio growers in the region and beyond. Most of the pistachio gene pool is to be found here, where it is needed to underpin the continued availability of the tasty nut.

All the reasons they cited as factors for threatening the species likely refers to the wild trees.


Is it possible to cultivate cheek epithelial cells in a non-CO2 incubator?

L-15 media does not require a CO2 atmosphere and according to Sigma-Aldrich this media is suitable for primary explants of adult human tissues.


Does sympathetic nervous system acts bilaterally for pupil dilation or other two sided organs?

Yes, they do. At least in the case of pupils. In fact, the absense of simultaneous regulation of the diameter of the pupil is used as a medical test for the evaluation of brain damage.


I'm going to take a stab at this. If your plant is not particularly aromatic, I feel pretty confident it is Lycopus uniflorus.  There are good descriptions here and here.  In particular, the description of the flowers at the Minnesota site, as having 2 purple-stemmed exserted stamens seems to match your flowers.  Apparently this species should have a tuber (should you end up digging yours up), while Lycopus virginicus which is probably a good second guess does not have tubers (see the differential description at the bottom of the Minnesota page).

Updated and Revised Answer

With additional pictures of now more mature flowers, which are clearly lilac in color, and the info that the leaves are strongly minty smelling, we'll revise the answer to Mentha arvensis, which fits all the available info. More here.


As Sudachi has commented it has been pruned, probably over many years, to take on this form. It is not natural shape.

I would say that it is not possible to identify the exact species of tree without a close up of the leaves. From zooming in it looks like it could be a Lawson Cypress (Chamaecyparis lawsoniana) although it could be a Leyland Cypress (x Cupressocyparis leylandii), or a number of other possibilities.

One way to investigate this further if you want to know for certain, apart from posting a close up of the foliage which may help, would be to find some specimens of cypresses that you can find the name of. Perhaps in a garden centre or an arboretum, then compare the smell of the foliage when you pinch and crush it between your fingers. Different species have a characteristic smell that is a useful method for identification.


How does Serotonergic (5-HT2A mediated) Psychedelia work?

Brenton, the linked pdf is called "Multiple receptors contribute to the behavioral effects of
indoleamine hallucinogens". It goes into detail on a a few basic behavioral responses.  I don't know what your background is so if you need help understanding parts point them out to me and I'll give it a go.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3110631/pdf/nihms267079.pdf

https://docs.google.com/file/d/0B0JUrCVOms3MdzdlYmh0SnBmOHc/edit (I'm hosting the pdf on my Google Drive if you aren't able to see the link hosted by the NIH).


Why do epithelial cells arrest in response to serum?

TGF-beta would be a good candidate. To cite:
"TGF-β inhibits G1/S progression in a variety of eukaryotic cell types. Among these, untransformed epithelial cells are particularly sensitive to the growth inhibition by TGF-β."
http://genesdev.cshlp.org/content/14/24/3093.full

Fetal bovine serum (FBS) contains a high level of latent TGF-β. Human serum as well has high level of TGF-beta (20-50ng/ml)

It is also possible that growth arrest is part of the induction of terminal differentiation by serum factor(s) such as TGFb.
"Type beta transforming growth factor is the primary differentiation-inducing serum factor for normal human bronchial epithelial cells."
http://www.ncbi.nlm.nih.gov/pubmed/2871553

Edit: got more reputation, so now I can post more than two links. Here is a review on TGFb signalling: http://genesdev.cshlp.org/content/14/6/627.full

Also a link to serum levels of TGFb:
http://www.ncbi.nlm.nih.gov/pubmed/16845225


Animal with "advantageous" trait in a environment where the trait is never utilized (high cold tolerance in mild climate) - natural selection occur?

Recipe for selection

There is selection on a specific phenotypic trait if and only if

There is variance for this trait in the population
This variance is, in part at least, explained by genetic variance
The trait covaries with fitness

The first two points can be reduced to a single point by stating "The trait has some non-zero heritability in the population". For more information about heritability, please have a look at Why is a heritability coefficient not an index of how “genetic” something is?.

This recipe is often called Lewontin recipe.

Applying the recipe to your case

So, in the model you consider, some individuals are cold tolerant and some aren't, so the first point is checked!

We will assume that the difference in cold tolerance is caused by genetic differences. Second point is checked.

Does the trait covary with fitness? As you defined that, in the environment considered, being cold tolerant does not have any impact on fitness, then no, there is no covariance between the trait and fitness. The third point is not checked and therefore, there is no selection happening.

Are you sure there is no cost to being cold tolerant?

Note, btw, that it is not rare to observe (or at least to assume) that some adaptation such as cold tolerance would come at a comparable cost when the environment is warm enough.

For example, increased cold tolerance might be mediated via anti-freeze proteins. The production of such proteins might be costly for the individual. In such case, we would have a covariance between fitness and the trait (cold tolerant individuals would have lower fitness that individuals that are not cold tolerant) and hence selection should act as to reduce the frequency of individuals that are cold tolerant in the population (always assuming an environment that is warm).

What else could cause the frequency of cold tolerance to evolve?

In absence of selection, the frequency of cold tolerance individuals might still evolve in the population. Things like genetic drift, selection at linked site or selection at correlated trait or migration can typically affect this frequency.


I would guess that it's a noctule (Nyctalus noctula) also.  The Bat Conservation Trust has a nice UK section with fact sheets for the 18 different species of bats found there.  It seems you can rule out the long eared bats by the photo and the pipistrelle because you didn't mention it flying eratically.  The fact that it was out so early seems to narrow it down to either the noctule, which is usually the first to appear, or the leislers (Nyctalus leisleri) which appears shortly after the noctule.  A distinguishing feature of the noctule is a mushroom shaped tragus, and for the leislers is long fur around the shoulder and back.  Although this is a great photo, it's going to be hard to make a definitive determination without knowing size and some of the other finer details.  Photos of the noctule and leislers can be found on the linked data sheets and the link to the UK section can help you determine if there are any other possible candidates I missed.


Why do some animals have 8 Limbs (e.g. Spiders, Octopuses)?

No, there is nothing special about eight legs. You have species with two legs (humans), four legs (most mammals), six legs (insects), eight legs (spiders), ten legs (lobsters), and many more legs (millipedes, centipedes).


Principle of 16 S rRNA technique for bacteria identification

There are several reasons some of which are fairly obvious:

The most obvious reason is that PCR only works with DNA, because it uses DNA-dependent DNA-polymerase. One can argue that you can use an RNA-dependent RNA-polymerase, but it has several drawbacks, mainly the cost and synthesis accuracy (Lauring et al., 2013, Nature). Since RNA-polymerase itself has higher error rates than DNA-polymerase (Berg et al., Biochemestry 5th edition, 2002) RNA transcripts might already have some variation from the original gene and using a low-fidelity polymerase in PCR will only lead to exponential error accumulation, which reduces identification resolution.
RNA is less stable in aqueous solutions due to the additional -OH group at the 2' position in the ribose, hence RNA extraction and storage is more complicated and expensive in most cases.
In community studies DNA and RNA have different biological implications, hence metagenomics and metatranscriptomics are different fields.


About artificially induced processes that would normally cause a cell to self-destruct

In some cases yes — when there is a mutation in apoptotic regulators such as Bcl2 family of proteins. In other cases it is difficult to identify and only identification is that those cells are growing rapidly; in other words failure to undergo apoptosis is not the cause but the effect of the cancerous transformation (as in case of p53, Ras, Myc mutations etc).


This is a Gerbera, which belongs to the daisy family (Asteraceae). Compare:

There are various species.

  The domesticated cultivars are mostly a result of a cross between Gerbera jamesonii and another South African species Gerbera viridifolia.[5] The cross is known as Gerbera hybrida. Thousands of cultivars exist.

(from Wikipedia)


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

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


Alcohol effect on heart and vascular system

The actual mechanism through which alcohol increases blood pressure is poorly understood (1,2). However, there is a mountain of evidence that shows that there is a strong correlation between alcohol intake and hypertension (small, infrequent amounts may have positive effects whereas excessive consumption has very negative effects (3)).

Back to the underlying mechanisms however, there is a good paper by Kazim Husain, Rais A Ansari, and Leon Ferder, which presents all the possible mechanisms that may contribute to alcohol-induced hypertension. The core ideas are as follows:

Mechanisms of alcohol-induced hypertension. CNS: Central nervous system; SNS: Sympathetic nervous system; RASAS: Renin-angiotensin system and aldosterone system.
Image taken from: Husain et al - 2014 - Alcohol-induced hypertension: Mechanism and prevention

Central nervous system in alcohol-induced hypertension

  [..] greater effect [of] alcohol on systolic blood pressure compared with
  diastolic blood pressure may indicate an imbalance between central
  nervous system factors influencing cardiac output and the peripheral
  vascular effects of alcohol

Baroreceptors in alcohol-induced hypertension

  Alcohol diminishes the baro (presso) reflex by interacting with receptors in the brain stem, i.e. nucleus tractus solitarii and rostral ventrolateral medulla.

Sympathetic nervous system in alcohol-induced hypertension

  Several studies reported increased sympathetic nervous system activation and discharge of sympathetic amines after alcohol consumption.

Renin-angiotensin-aldosterone system in alcohol-induced hypertension

  The serum levels of vasoactive substances such as renin-aldosterone have been reported to be affected by alcohol ingestion in vivo or ethanol in vitro.

Cortisol in alcohol-induced hypertension

  Certain studies have implicated the role of cortisol in alcohol-induced rise in blood pressure. Potter et al have reported a significant rise in plasma cortisol levels following alcohol consumption and a drop in plasma cortisol levels when alcohol intake was discontinued.

Increased intracellular calcium and vascular reactivity in alcohol-induced hypertension

  Rats treated with ethanol showed constriction of blood vessels due to greater shifts in the binding of the calcium ion (Ca2+) in arterial and arteriolar smooth muscle cells causes increased sensitivity to endogenous vasoconstrictors.

Endothelium and oxidative stress in alcohol-induced hypertension

  Imbalance of specific endogenous vasoconstrictor such as angiotensin II, endothelin-1 and nor-epinephrine and vasodilator nitric oxide (NO) may also play an important role in alcohol-induced hypertension. Alcohol stimulates the release of endothelin 1 and 2 from vascular endothelium in a dose dependent manner. Alcohol also increases the angiotensin II levels in the blood and vessels. Endothelin 1 and 2 as well as angiotensin II are known to be potent vasoconstrictors of the blood vessels.

References:

Husain et al - 2014 - Alcohol-induced hypertension: Mechanism and prevention
Saunders et al 1981 - Alcohol-induced hypertension
Grønbæk et al - 2009 - The positive and negative health effects of alcohol‐ and the public health implications


There's no single common mechanism for intracellular communication, and some of the mechanisms (and some parts of some of the mechanisms) are known in much greater detail than other. For each of the processes you mention, we at least know that they proceed via very different mechanisms.

ATP distribution, for example, proceeds mostly by simple diffusion. ATP is a small molecule and is able to diffuse fast enough that it can move from one end of a cell to another in about ~20 ms on average [1].

Our picture of how ATP actually gets taken up by the various organelles is much murkier. For the case of the endoplasmic reticulum (ER), there is evidence that ATP is brought in via an ATP/ADP antiporter [2]. Transporting ATP via an ATP/ADP antiporter would have the effect of keeping the ratio of ATP/ADP stable in both the cytosol and the ER. It is reasonable to assume that similar mechanisms control ATP transport across other organelle membranes, but you'd have to dig into the literature to find out details.

References

1: Diffusion coefficients of ATP and creatine phosphate in isolated muscle: pulsed gradient 31P NMR of small biological samples

2: Transport and transporters in the endoplasmic reticulum


The sensory and motor components are  required (GP and vagus respectively). Similar to the corneal reflex and cranial nerve 5 and 7, if a lesion exists in either the sensory or motor component there will be a defect. In your case, there is no motor innervation on the left due to the lack of the vagus nerve so there is no vagus nerve response.


Why is it important to study chromatin to understand cancer?

Most cancers involve, in addition to genetic changes, a whole suite of epigenetic changes that orchestrate changes in transcriptional profiles. Additionally, multiple epigenetic modifiers (Eg - EZH2) are associated with worse prognoses.
There is also the fact that chromatin modification machinery is very highly mutated in cancers; examples include EP300 - a histone acetyltransferase, and members of the SWI/SNF nucleosome remodelling complex. The study of epigenetic factors needed for the continued transcription of oncogenes like Myc has also led to the formulation of potential therapeutic strategies (Check out some of the literature on inhibiting Brd4 to silence Myc in certain settings).


This is a treehopper (an insect in the family Membracidae).
As Arthur J Frost mentioned in his comment above, it will be difficult to ID this specimen more specifically given the angle, lack of further info, and my personal lack of knowledge of Indian fauna.
However, you can view an at-least similar looking species by viewing Oxyrachis tarandus, which is found in India (see here and Sharma & Pati (2011)1).
You can find photos of O. tarandus here, with one copied below for reference.

 © www.NatureLoveYou.sg

 1. Sharma, A. and Pati, P.K., 2011. First report of Withania somnifera (L.) Dunal, as a new host of cowbug (Oxyrachis tarandus, Fab.) in plains of Punjab, northern India. World Applied Sciences Journal, 14(9), pp.1344-1346.


Which statement is incorrect for Rubisco?

Short answer
D

Background
A. Is correct, as it is the most abundant enzyme on land, and probably also in marine environments (Raven, 2013).

B. Is correct, as Rubisco catalyzes the carboxylation, or oxygenation reaction depending upon the molecular concentration of CO2 or O2 (Sudhakar et al., 2016).

C. Is correct, as it reveals the inefficiency of Rubisco, as CO2 and O2 compete for the active site. Fixation of O2 during photosynthesis oxidizes ribulose‐1,5‐bisphosphate into 3‐phosphoglycerate and phosphoglycolate - which is basically a waste of energy.

D. Is incorrect and hence the answer to your question: Rubsico is present in CAM plants.

E. Because of the photorespiration described under B & C, Rubisco is indeed regarded to be inefficient.

References
- Raven, New Phytologist (2013); 198(1): 1–3
- Sudhakar et al., Phenotyping Crop Plants for Physiological and Biochemical Traits, 2016


Which fish did modern tetrapods descend from?

Your question cannot be answered.
One of the effects of how incomplete the fossil record is, is that it is impossible to say if a species was a member of a direct line or a side branch. we just do not have the resolution in the vast majority of the fossil record to tell. The answer could be both, neither or one or the other and we would not be able to tell. All we can say is it is likely they were closely related to or part of our ancestral line. But the working assumption is always that you have a related sister species and not the ancestor unless you can show extremely good evidence otherwise, (which is so rare you can assume it is impossible in extinct vertebrates).
Tiktaalik and Ichthyostega only give us a rough idea of what our ancestors would have been like. It is impossible to say with any certainty if either was a direct ancestor or merely a sister species to them. This is part of the reason cladograms are constructed the way they are, so that no fossil is ever put on the direct line.
Source.
Source 2
Note: Tiktaalik probably did not live on land, more likely it was a shallow water air breather.
Also whatever species was the ancestor of tetrapods, all living tetrapods would be its descendants. One aspect of population genetics is for a specific individual in an ancestral population, past a certain point in a linage  either every descendant is your descendant or you have no descendants.


The binding constant of an antibody-antigen complex remains an empirical measurement.

There have been many efforts to solve this problem quantitatively and qualitatively over the years since the original crystal structures of an lysozyme-Fab complex there are over 400 structures at the www.rcsb.org in a search for antibody antigen complexes.

At this point the general methodology is to model the structure of the antibody-antigen complex.  Then from the complex a free energy of binding is estimated, or more reliably, variants which might bind more tightly can be modelled.

There are tools available to do this work, but they are still far from perfect.  This 2012 paper compares a new antibody-antigen crystal structure against the results of several modeling suites.  In Table 4 the authors show that the invariant parts of the structure as well as some of the hypervariable loops are really precisely modelled, but hypervariable region 3 was way off in this case (rms error of about 2 Angstroms).  Which is not precise enough to calculate actual free energy of binding.

Currently while free energies of binding and therefore estimates of binding constants are not reliably calculated from protein complex structures.  Such software is in practice used to rather compute the relative binding strength of two models (see this 2012 example).

This 2010 paper which describes SnugDock, a newer suite of software, outlines a state of the art antibody-antigen design process (emphasis added).

  One could envision a complete computational antibody engineering pipeline starting from the antibody sequence and ending with accurate predictions for optimized antibody-antigen interactions. In this paper we have been successful in reaching the second step by computational docking using computational models of the monomer antibody. The next stages may be additionally challenging. High-resolution complex structures might next be used for computational alanine scanning, computational affinity maturation or alteration of binding specificity. For antibody therapeutics, structures will help define drug mechanisms for regulatory approval, enable epitope mapping and humanize constructs. These applications require varying amounts of resolution and further testing will reveal the full utility of the SnugDock predictions.

As you can see, the method recommended is to create a series of models to try to create tighter relative binding.


Is an Eidetic Memory (or other unusual forms of memory) less susceptible to anterograde amnesia?

This question is more of a medical question than one of the underlying mechanisms of biological function.

The formation of long term memories is related to long-term potentiation. There are multiple neurotransmitters involved in this process. Ethanol primarily affects NMDA receptors. Drugs used to specifically induce anterograde amnesia, like propofol, primarily affect other others, like GABAA.

The process of memory formation relies on a variety of factors including the orchestration of multiple neurotransmitters. Anterograde amnesia can be induced by many factors and does not have a single known mechanism of action. It is not possible to conclude any single person will react identically to all inducers of anterograde amnesia. It is often the case that people have unique responses to drugs within a distribution of possible reactions.

The individual nature of responding to drugs is why side effect lists are lengthy, and usually only a few out of this list are observed in any individual.

My hypothesis is, as a regular consumer of alcohol, your liver function is elevated and responsible for your high tolerance. The cytochrome p450 family of enzymes are responsible for much of the metabolism of drugs in the body.

Liver function tests are cheap and interesting, I find. You might have some blood work done at a local lab to check out those stats as well as your cholesterol, etc., if you have an interest in such things.


What's the difference between stabilizing selection and balancing selection?

Usual meaning

Usually, Stabilizing selection is a concept that applies to a phenotypic trait while balancing selection is a concept that applies to a given locus.

Balancing selection can either be due to negative-frequency dependence selection or due to overdominance (=heterozygous advantage at a single locus).

What Darwin may have meant

Because Darwin didn't know about genes, he was necessarily not using the term balancing selection as I am using it. I can think of several more or less related pattern of selection that might fall withing the definitions for "stabilizing selection" and/or "balancing selection". Maybe he meant "frequency-dependent selection", "positive selection for an intermediate trait", "varying selection through time (temporally heterogenous environment)" and "varying selection through space (spatially heterogenous environment)". Eventually again, that might mean "positively correlated traits that undergo opposite selection pressure (or the opposite)" but that would definitely be surprising.


What modern insects are not (flying OR descended from flying ancestors)?

Silverfish, also known as Lepisma (order Zygentoma), does not fly and does not descend from flying ancestors.

It's close to Archeognatha, which don't fly either nor descend from flying ancestor.


Why is statistical mechanics relevant to RNA and protein folding?

I’m no physicist, but your statement “To my knowledge statistical mechanics and thermodynamics exist when we have an ensemble of particle such as in a liquid or a gas” is surely incorrect. The problem of protein folding is one of thermodynamics — finding the structure of lowest free energy, and the path by which it is reached from a random coil.

One of the difficulties relating to the path is that of getting ‘stuck’ in a position in the energy landscape from which the protein cannot escape. This is called ‘frustration’ and there is apparently a quantitative treatment of ‘minimal frustration’ using the statistical mechanics of spin gasses. This is mentioned in a review by Onuchic and Wolynes, available on-line, which you will probably be able to understand better than I can.


Are there differences in cell membrane cholesterol levels between cell types?

Yes, there are differences in cell membrane's cholesterol levels among different human cell types.

This table from Alberts (2002) shows the difference in cholesterol composition in a liver cell, a red blood cell and a Schwann cell/oligodendrocyte (myelin):

Table: Approximate Lipid Compositions of Different Cell Membranes

Besides that, the table shows that there is difference in the cholesterol composition among different membranes in the same cell (compare plasma membrane, mitochondrion and ER). Actually, that's a more famous difference, depicted in this figure from Lehninger (2000):

Figure: Lipid composition of the plasma membrane and organelle membranes of a rat hepatocyte. The functional specialization of each membrane type is reflected in its unique lipid composition. Cholesterol is prominent in plasma membranes but barely detectable in mitochondrial membranes.

Sources:

Alberts, B. (2002). Molecular biology of the cell. New York: Garland Science.
Lehninger, A., Nelson, D., Cox, M. (2000). Principles of biochemistry. New York: Worth.


The question of homosexuality and its role in nepotism is interesting.

According to this wiki article, less than 10% of the population is homosexual. If you consider that homosexuality makes human eusocial because homosexual do not reproduce but help their brothers and sisters to reproduce, then you would have to consider any species where a few percentage of the population produce some kind of altruism to be eusocial. Given that all phenotypic traits theoretically have social impacts, then I would bet that you might call eusocial a lot of species.

It seems wiser to me to limit the definition of eusocial when an important part (maybe 98% minimum) of the population do not reproduce but help others to reproduce. One might also want to consider some other restrictions for a the use of the word "eusocial"

Therefore, using the argument of "reproductive division" I would rather not include Homo sapiens in the list of eusocial species. But it is nothing more than a question of definition. You're free to define your words the way you want and call human eusocial but make sure your interlocutor knows your definitions.

Now, let's say we place the limit to the definition of eusociality at 1%. When more than 1% of the population does not reproduce but help their kin to reproduce, then the species is eusocial. Then, humans would seem to fit in this definition at first sight. But do homosexual in our modern society really help their kin to reproduce? In other words, do siblings of homosexual reproduce more (or have offspring that have a high fitness)? This study investigated the question (as pointed out by @oreotrephes in the comments) and they indeed found some pattern but the difference in reproduction between relatives of homosexual and non-relative of homosexual is is quite weak. But if homosexual don't reproduce and don't help their kin reproducing then, humans is definitely not a eusocial species.

Finally I want to add that individuals from lots of different species have been found to perform homosexual behaviour (see this wiki article). If you want to consider human as eusocial because some homosexuality, then you will have to consider sheeps, labradors and pigeons to be eusocial as well!


turtles will crawl onto anything to get out of the water and bask, fallen logs are common and they likely cannot tell the difference between a still alligator and a log.  It might also be possible that the turtles do know what the gator is and are hoping to tag along and pick up scraps after it strikes.

I image that for the gators thrashing around to dislodge the turtle has to high a risk of scaring off prey so they just put up with it.


How is epinephrine and norepinephrine different?

But little amount of epinephrine also serve as a neurotransmitter.

Iam mentioning here some of the differences I found out myself when I had the same question.

If you need further reading you can visit the site  as mentioned by @Spartacus9
https://en.wikipedia.org/wiki/Epinephrine
https://en.wikipedia.org/wiki/Norepinephrine

1)Norepinephrine is mostly made inside nerve axons and released when an action potential travels down the nerve.

Epinephrine is made from norepinephrine inside the adrenal medulla.

2)Norepinephrine acts mostly on alpha receptors.

Epinephrine is relatively non specific,stimulating both alpha,beta1,beta2,beta3 receptors more or less equally.

3)In medicine, norepinephrine is used to increase and maintain blood pressure related to cardiac arrest,spinal anaesthesia,septicaemia,etc.

Epinephrine is used in medicine to treat low blood pressure associated with septic shock and also for the emergency treatment of allergic reactions.


This is a Northern pufferfish. It is called Sphoeroides maculatus.

  Source: https://www.flickr.com/photos/vims_photos/3570935564

You can confirm this on FishBase.


Why doesn't a substance like loperamide promote analgesia?

This is more of a chemical question I think, but the gist of it is that, unlike its predecessors difenoxin (Motofen) and diphenoxylate (Lomotil), it was specifically designed by Dr. Paul Janssen and other researchers at Janssen Pharmaceutica to have limited bioavailability from the gut (it is easily first-pass metabolized through cytochromes), as well as being too lipophilic to be dissolved in water and thus administered intravenously (and thus, junkies hoping to get a "hit" from loperamide through injections will be sorely disappointed), while still retaining its ability as a μ-opioid receptor agonist to the receptors in the myenteric plexus (resulting in the slowing of peristalsis). (Difenoxin/diphenoxylate in fact is administered with small doses of atropine to discourage abuse.)

In addition, efflux mediated by P-glycoprotein in the blood-brain barrier helps retard the entry of loperamide into the CNS. The concomitant administration of a P-gp inhibitor like quinidine (a stereoisomer of quinine used as an antiarrythmic) with loperamide, however, will cause respiratory depression and other CNS effects that are characteristic of μ-opioid receptor agonists.


Chicken Genome what are the LGE 'chromosomes'?

LG stands for "linkage group". It seems the Chicken Genome Sequence group (Hillier et al., 2004) allocated several linkage groups (alleles or genes which tend to be inherited together) to the microchromosomes (tiny chromosomes typical of birds and reptiles), in this case called "linkage group E64" and "linkage group E22....". There are a load more microchromosomes which are the ones numbered 28-31 and 33-38 which haven't yet had their sequences resolved (Burt, 2007).

References:

Burt, D.W. (2007) Emergence of the Chicken as a Model Organism: Implications for Agriculture and Biology. Poultry Science. 86 (7), 1460 –1471. Available from:  [Accessed: 8 February 2012].
Hillier, L.D.W., Miller, W., Birney, E., Warren, W., Hardison, R.C., Ponting, C.P., Bork, P., Burt, D.W., Groenen, M.A.M. & Delany, M.E. (2004) Sequence and comparative analysis of the chicken genome provide unique perspectives on vertebrate evolution. Nature. 432 (7018), 695–716.


I was wondering how many SNPs there are in a single person on average

A SNP is a polymorphism in the population, it is not a thing a haplotype can carry. Each individual has a given variant for any given of the SNPs (except for cases of sequence deletion).

It is possible though to say how many SNP a diploid individual in between its two haplotypes but I doubt this is where you interest was. Ewens smapling formula gives expectation and distribution under an infinite alleles model, panmictic population and absence of selection.

Other statistics that make sense include the average number of deleterious mutations pre individual or a few other things or how many new mutations a couple transmit to their offspring,... But asking how many SNPs an individual carry on average makes little sense.

Note as @Chris said, by stating 10k SNPs in the human genome, you seem to under-estimate the number of SNPs.

EDIT

In the comments, you further

  Would it make more sense to consider a rough minimum and maximum?

The answer is no, it would not make more sense. Consider the definition of SNP by wikipedia

  A single nucleotide polymorphism, often abbreviated to SNP (pronounced snip; plural snips), is a variation in a single nucleotide that occurs at a specific position in the genome, where each variation is present to some appreciable degree within a population [My emphasis]

The term population is key here. The concept of SNPs (or of polymorphism to be more general) makes only sense if you can make comparisons. A single individual does not have any polymorphism (to the exception of the one between his two sets of chromosomes).

If we step back and think of different species it might become more intuitive. Think of the number of pairwise differences between two species. It does not make any sense to ask "how many pairwise differences is there between a blue whale?" You need to say "how many pairwise differences is there between a blue whale and a wolf". Similarly, you cannot say "How many SNPs is there 'between a single individual'" (to the exception again of the consideration of the differences between the two sets of chromosomes), you need to consider a group of individuals.


Can polystyrene sulfonate bind calcium or sodium in the gut? How?

Are you talking about Sodium Polystyrene Sulphonate (a.k.a SPS)?

If yes, then ...

Quoting from Chaitman, Dixit and Bridgeman (2016)

  Synthetic cation-exchange resins are insoluble polymers resembling a crystalline lattice. When placed in a solvent, this structure swells, allowing the exchange of ions between the reactive group on the resin (in the case of SPS, sodium) and ions dissolved in the solvent.

However, other cations like sodium and calcium ions can bind too.
As SPS moves through the intestine, sodium ions are released and exchanged for potassium ions.

References
Chaitman M, Dixit D, Bridgeman MB. Potassium-Binding Agents for the Clinical Management of Hyperkalemia. Pharmacy and Therapeutics. 2016;41(1):43-50.


What is this lightning-fast tiny spider?

Many web-dwelling spiders are lightning-quick in their own web (even if they are slow/clumsy walkers outside of their web) so that doesn't help in identification.
Hard to tell from the photo, but it appears to be Cyclosa ginnaga
A better image of the specimen would help identify.
edit after comment:
Here is a gallery of observations (currently 50 of them) of cyclosa ginnaga: https://inaturalist.ca/observations?place_id=any&subview=grid&taxon_id=360502
All those observations were made in South-East Asia or Australia.
You could also look at Cyclosa Insulana with similar range:
https://inaturalist.ca/taxa/560706-Cyclosa-insulana/browse_photos?quality_grade=any
But I think the length of abdomen in your photo more closely resembles C.ginnaga, and also the observations of C.ginnaga more consistently show a spiral in the thick webbing while C.insulana tends to be more random.
And here is a breakdown of the cyclosa genus broken down into specific species if you want to browse other possibilities:
https://inaturalist.ca/taxa/127360-Cyclosa/browse_photos?quality_grade=any&grouping=taxon_id


Figuring out if populations from two regions share the same Neanderthal haplotypes

What I am saying here is the way I would approach the problem. And as such this post is meant to give you some direction. Please do not hold me responsible if you do not get the expected results.
First off, I don't know how the Plink format works, you would do well if possible to convert that to a BED/GFF/GTF file somehow.
I looked up the file format, and most of your columns are significance scores. For a start I would use the BH FDR & p-value as a preliminary filter and later use the Bonferroni corrected p-value.
Wiki link to FDR
The wiki link should also give you an idea why I say later on move onto bonferroni.
Interesting questions asked on cross validated for FDR

Provides a vague idea on FDR
Provides a relation between p-value and FDR: Re-read the answer a few times and you'll get it.
Check out the books if you want some understanding of Statistics

Using the SNP data, I need to try to find out if they have Neanderthal haplotypes in the same parts of their genome. I've found a map of putative Neanderthal introgressed haplotypes from 1000 Genomes Project's European and East Asian genomes

I looked up the file, these are regions with an average span of 73.4kb across the entire genome. So what you want to do is map the "statistically significant" SNPs from your plink file to these regions.
If you don't know how, check out the UCSC genome browser. A detailed step by step would be too big an answer, but the overview goes something like this;

Choose your reference genome from assembly
Create two custom tracks, here you can upload your SNP data in bed format, which is the easiest to make. Link to format And add the existing haplotype population.bed file.
Go to intersection, to create an intersection between these two tracks.

This will give you an idea as to which of your haplotype regions are present in the population.
Ofcourse, it isn't that easy, because you have to make a consideration here. Do you choose to say the population is carrying that haplotype if a single SNP is present in a region which spans 73kb? That is more than the average size of a gene in Humans.
As far as the Neanderthal and Denisovan genomes are concerned. I would again point you to the UCSC genome browser where they have the Neanderthal and Denisovan assemblies and their corresponding variants mapped to the Human genome (assembly hg19). You can again get these files and see where the neanderthal/denisovan variants lie in the haplotype file using the same approach. Finally you can then use these two overlaps to find where your variants had mapped and if any ancient variants had mapped in the same region. You must also make consideration for Insertions and deletions within the genome, so the variants may not map at the same location but it will map nearby.
UPDATE

You can check out this link for retrieving allele frequencies from 1K genomes, for the overlapping variants. I never meant that you would use the bed files for finding allele frequencies. What I outlined is;

Use the haplotype population regions as a template and overlap your significant affy SNP variants on it.
Next, because the Neanderthal and Denisovan variants are mapped on the hg19 or hg18 assembly, you map back those variants to the same regions
Find the regions where an affy SNP and an ancient SNP exactly overlap

What I understand from your comment is, you have already done step one. And you want to know the allele frequencies for a particular ancient variant. You need to do step 2 and 3 before coming to allele frequencies.
Then you can look up the allele frequency of the variants which mapped exactly at a position which had an ancient variant in the 1K genome vcf files.