text:
How could you measure the rate of light reactivity/ photosynthesis of a cell in a lab setting?
For a lab I must take Volvox protist cells and expose them to specific wavelengths of light. How would I know they're even reacting? The assignment I've been given does not explain what I should even be looking for. I know that they do photosynthesis, so I was thinking of looking for signs of photosynthesis occurring, but I have no idea how to tell if even that is happening.

What are the inputs and outputs of photosynthesis? How could you detect a change in one of these? How might the appearance of, say, one of the products product appear in the watery environment of Volvox?


text:
How does genetical variability works on bacteria?
I'm very Lay in biology, but I was studying the subject and the following problem emerged:
It's known that all bacteria are unicellular beings, and their reproduction it's asexual. Besides of that the indiscriminate use of antibiotics leads to the development of more severe infections, because of a process of natural selection and survival of the most resistant. How do we explain this process considering that asexual reproduction doesn't generate genetic variability, besides mutation? Why do we have this differences, if asexual reproduction generates clones?

Have you heard about plasmid

The question is based on the false assumption that sexual reproduction creates genetic variance. If we neglect epistasis, then on average segregation and recombination do not increase genetic variance within the population.
All 3 of the following processes present in some bacteria lineages do increase the amount of genetic variance:

conjugation
transduction
transformation

You should have a look at the wikipedia articles.

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text:
How conscious are mammals that mating leads to pregnancy and offspring?
Does a pregnant female mammal know that its pregnancy is the consequence of a previous mating? Or are humans the only mammals which are conscious of it?

Some animals present potential mates with nesting sites; the female chooses the mate based of the suitability of the site. Many females are attracted to mates by specific characteristics before they mate (a present of food to demonstrate hunting prowess, etc.) Some females protect their litters from non-paternal males, but allow the patenal male access. Does this mean anything in terms of consciousness of the result of mating or is it all sub-cortical? We'd have to have some method of communicating with animals to know. Otherwise we risk projecting our beliefs onto the animals.

Within mammals there is a huge diversity in any trait, including cognition. A dolphin can make concepts connections that a shrew certainly can't. Are you interested to any mammal?

I have trouble citing the exact source now as it's in one of my books at home, has 'sex' in the title (Sex in History), and I'm at work and can't Google that. But needless to say, the book made mention of studies of isolated, modern human tribes where it was evident that the people of the tribe had not made the connection between pro-creation and child-birth. Rather, intercourse was often tied to specific rituals that had a side effect of birth.
So there are a few things that one can extrapolate from this:

Pre-historic humans may have often not been aware that sex led to procreation
From that one can extrapolate further that no animals have this awareness either, as we are the most intellectual species on the planet

Further, the evolutionary development of sex points to this too. The ultimate cause of child-bearing is propagation, but the proximate cause of child-bearing is pleasure. Before life could be aware of the connection, there needed to be a reason to have sex, and so we would have developed in a way that encouraged pro-creation for no other reason than we liked doing it. Eventually we were bound to connect the dots, but we're oriented for this behavior regardless.

"The Trobriand Islanders, and some Australians, are reported to be unaware of the causal connection between sexual intercourse and procreation; they are said to believe that spirit-children enter the wombs of women on appropriate occasions, and that sexual intercourse alone is not a determinant of birth." --"Primitive Mentality" essay by Ananda Kentish Coomaraswamy. (By "primitive," the author means, of course, "original.").

This really cast doubts on (or is casted doubt on by) the concept of paternity. In species where the father expends significant effort for the offspring, I am wondering how this can be motivated without a sense of ownership of the offspring. If such a sense exists, I wonder how it can come about without knowing that the offspring it is born of the father as much as of the mother

It is completely feasible for paternalistic behavior to exist without being 'conscious' of the connection between mating and pregnancy, but without going further into that in a comment, I'll just say that parental behavior across the animal kingdom is incredibly diverse.

Wow, I've asked a question about this on another stack exchange. Please if you find the book, I would be very grateful if you gave an answer. See my question here.

For that an animal would have to know the concept of mating and pregnancy. It’s not called the sex “drive” because it requires consciousness in order to mate or become pregnant. It’s pretty automatic and subconscious. As any couple that actually tries to become pregnant but can’t can probably attest to.
So unless you need to communicate a concept to somebody else you may as well not have a concept. Like those human cultures that only have three numbers. One two and many.

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How do ion channels transport only specific ions?
Ion channels, such as $Na^+$ channels and $K^+$ channels, are higly specific for ion permeability. But how do these channels achieve and maintain this specificity? Like how does a $K^+$ channel transport only $K^+$ ions (same for other channels like $Na^+$, $Ca^{2+}$, $Cl^-$, etc. channel)?

I am restricting the answer to only $Na^+$ and $K^+$ channels, assuming similar mechanism for other channels. In these 2 channels, such high level of specificity is achieved because of two main differences between $Na^+$ and $K^+$:

difference in size of $Na^+$ and $K^+$ ions.
difference in chemical properties of $Na^+$ and $K^+$ ions.

Lets discuss these points one-by-one:

Difference in ionic size: the ionic size of $Na^+$ ion is 0.96$\overset{\circ}{A}$ while that of $K^+$ ion is 1.33$\overset{\circ}{A}$. How this size difference of 0.38$\overset {\circ}{A} $ is exploited by channels will be discussed in later section.

source

Difference in chemical properties: the property we are concerned here with is hydration enthalpy. $Na^+$ ion has hydration enthalpy than $K^+$ ion, meaning $Na^+$ has higher tendency to remain bounded by water molecules than $K^+$. How this enthalpy difference is exploited by channels will be discussed in next section.
source

I will discuss different methods used by these channels one at a time.

$Na^+$ channels: $Na^+$ channels are less studied than $K^+$ channels, but some of the mechanisms used are known and explained below:

$Na^+$ ions pass through channels in partially hydrated form1, and these channels have 2 rings of selection filters2 in mammals.
The first (outer) ring contains amino acids EEDD (or EEMD)3 while second (inner) ring contains amino acids DEKA4. How these amino acids bind to specifically $Na^+$ ions is not completely known yet, but it is hypothesized that the inner ring, being more conserved, is more important as a filter than the outer ring. Also, it has been shown that by changing the amino acid K in DEKA makes the channel more permeable to $K^+$ and $Ca^{2+}$ ions, and by changing sequence from DEKA to EEEE makes the channel more selective towards $Ca^{2+}$ ions5.
$K^+$ ion, in hydrated form, cannot pass through inner filter due to larger size and presence of negatively charged D and E of DEKA, whereas $Na^+$ easily passes through due to smaller size and higher hydration enthalpy6.

Negative charge in channel is such that it mimics the hydration shell (regular octahedron) of $Na^+$ from side
source (1) source (2)

$K^+$ channels: $K^+$ channels have been studied more intensively, so their mechanism is much more understood. The main points to ponder are:

The filter of $K^+$ channel contains amino acids TVGYG 7 and is present in the narrowest region of the channel.
To pass this channel, $K^+$ ion needs to be completely dehydrated i.e. without any water molecule bound to it. The amino acids in the filter replace water molecules with polar oxygen atoms. On the other hand, $Na^+$ cannot get rid of water molecules so easily and hence, its passage through the channel is thermodynamically unfavorable8, partly also because dehydrated $Na^+$ is so small that it cannot even bind with all of the polar oxygen atoms of amino acids.
Here nature shows some clever techniques. The amino acids, TVGYG, having their electronegative carbonyl oxygen atoms aligned toward the center of the filter pore, form a square anti-prism similar to a water-solvating shell around each potassium binding site. The distance between the carbonyl oxygens and potassium ions in the binding sites of the selectivity filter is the same as between water oxygens in the first hydration shell and a potassium ion in water solution, providing an energetically-favorable route for de-solvation of the ions9.

This is how the passage of a $K^+$ ion through $K^+$ channel looks like:
source
The carbonyl oxygens mimic this configuration as this is how a $K^+$ looks in hydrated form (square antiprism):source
P.S. as more deep studies are made, more mechanisms may be revealed. Also, above mentioned points are just theories and not conclusive proofs.
References:

Hille, B. The permeability of the sodium channel to organic cations in myelinated nerve. J. Gen. Physiol. 58, 599–619 (1971).
Guy HR, Seetharamulu P. Molecular-Model of the Action-Potential Sodium-Channel. Proc Natl Acad Sci USA. 1986;83:508–512.
McNulty, M. M., Edgerton, G. B., Shah, R. D., Hanck, D. A., Fozzard, H. A. and Lipkind, G. M. (2007), Charge at the lidocaine binding site residue Phe-1759 affects permeation in human cardiac voltage-gated sodium channels. The Journal of Physiology, 581: 741–755. doi:10.1113/jphysiol.2007.130161
Favre I., Moczydlowski E. & Schild L. On the structural basis for ionic selectivity among Na+, K+, and Ca2+ in the voltage-gated sodium channel. Biophys J 71, 3110–3125 (1996).
Calcium channel characteristics conferred on the sodium channel by single mutations.
Heinemann SH, Terlau H, Stühmer W, Imoto K, Numa S 1992 Apr 2;356(6368):441-3.
Mechanism of Ion Permeation and Selectivity in a Voltage Gated Sodium Channel. Ben Corry and Michael Thomas
Chemistry of ion coordination and hydration revealed by a $K^+$ channel–Fab complex at 2.0 Å resolution, Yufeng Zhou, João H. Morais-Cabral, Amelia Kaufman & Roderick MacKinnon
Mechanism of potassium channel selectivity revealed by $Na^+$ and $Li^+$ binding sites within the KcsA pore.
Ameer N. Thompson, Ilsoo Kim, Timothy D. Panosian, Tina M. Iverson, Toby W. Allen, and Crina M. Nimigean
A comparison between two prokaryotic potassium channels (KirBac1.1 and KcsA) in a molecular dynamics (MD) simulation study; Mikko Hellgrena, Lars Sandberg, Olle Edholm, 1 March 2006


text:
Agglutination test of cats

Is the blood test result for the P1 cat is logical?
Because, it shows that even the card containing no antibody, has undergone aggluntination!


text:
Evidence that Attention Deficit Hyperactivity Disorder (ADHD) is caused by too much cellular ATP?
The question is pretty simple — it's just a theory that I remember my biology teacher mentioned long ago and for years now I've wondered about it without ever asking.
Some people with attention deficit hyperactivity disorder (ADHD) report "energy bursts" with the feeling of needing to explode while sitting still. Further, they report that movement, like vibrating the legs, can help suppress this feeling.
Is there any reason to think that symptoms like these might come from too much ATP inside cells?

That's an interesting hypothesis - however, I am not aware of any evidence that this is the case. Importantly, there can be a lot of difference between cellular access to energy, like ATP, and the perception of "energy" or liveliness.
Here is a paper that actually suggests the opposite: that ADHD could be caused by a neuronal energy deficiency because of differences in astrocyte responses to catecholamines (astrocytes are non-neuronal cells in the brain that, among other functions, regulate metabolism in the brain including access to glucose). Importantly, though, this remains just a hypothesis, not a well-established theory.
ADHD is thought to impact the parts of the brain that are important for attentional control, inhibiting responses, and motivation. Based on that perspective, an alternative explanation for the symptoms you describe is that a sensation occurs that doesn't really require a behavorial response, and for a neurotypical individual this sensation is quickly suppressed (attentional control by not focusing on this sensation, inhibiting your response to shake your leg) without any real conscious effort. Instead, with ADHD, it is difficult to direct focus away from that sensation and mental resources need to be directed towards trying to hold still. The relief from moving around comes from letting the activity progress and not trying to suppress it any more, not because there was a literal excess of energy in the sense of ATP.

References:
Barkley, R. A. (1997). Behavioral inhibition, sustained attention, and executive functions: constructing a unifying theory of ADHD. Psychological bulletin, 121(1), 65.
Todd, R. D., & Botteron, K. N. (2001). Is attention-deficit/hyperactivity disorder an energy deficiency syndrome?. Biological Psychiatry, 50(3), 151-158.

I have no expertise in ADHD whatsoever, but basic biochemistry shows that this is not possible. A cell can't really have "too much ATP", and ATP does not by itself change how cells behave.
ATP is just a carrier of energy, an intermediate that stores energy extracted from nutrients like glucose and delivers it to energy-demanding processes like neurons firing action potentials ("work"). The amount of ATP stored in any cell is very small compared to the rate of production and consumption, so ATP is a short-lived molecule --- a cell's ATP store turns over (is consumed and renewed) in a few minutes. Therefore the amount of ATP does not really matter for energy metabolism; it is the rate of ATP production / consumption that matters.
Now, the rate of ATP metabolism is controlled by the demand for energy (how much work has to be done), not by how much nutrients are available. When cells need to do work --- for example, you start to run and muscles begin to contract --- the rate of ATP consumption increases. In response, the rate of ATP synthesis is increased by "burning" (oxidizing) nutrients more quickly, so that the system balances. Similarly, when a neuron starts to fire action potentials, its ATP consumption increases, and in response the cell generates more ATP by burning sugar. In contrast, ATP turnover cannot be increased by having too much nutrients. If this was true, cells would start doing work randomly as soon as they encounter nutrients, regardless of whether its needed or not, just to dispose of the generated ATP. Think about your legs starting to kick wildly as soon as you have a meal ...
In summary, the need to do work causes ATP turnover, not the other way around. Of course, having too little nutrients available does limit the amount of work that cells do, but that's a different question. Also, there are many signaling / hormonal mechanisms that alters behavior in response to nutrients. Eating a meal triggers reward centers in the brain, for example (hence, "comfort food"). But these systems are not directly related to ATP metabolism.


text:
What is the species name of this plant?
Rubbing the leaves between your fingers feel strong, pleasant aroma of citrus.
The leaves are not fuzzy and are about 2 cm long.

In Germany.

Please provide your location too.

Are the leaves fuzzy? I can't tell...  Also please add dimensions of leaves and any pictures of flowers if present.  A comment about where you got the plant could help, too.

The leaves are not fuzzy, about 2 centimeters in length. In Germany.

Where exactly did you find it? Assuming you found it growing in the wild. Please be as specific as possible, location/habitat.

One acquaintance gave. It is grown in pots in the room. He said that can eat.

He said that can eat. -what do you mean?

Can use as spice.


text:
During the process of plasmid isolation, how can we be sure that only plasmid DNA has been isolated and there is no chromosomal DNA?
We separate the membrane and all other cell components, but how is it that only plasmid DNA is isolated and not chromosomal DNA?

It comes down to the size of genomic DNA (relatively huge) compared to that of plasmid DNA (rather small).
Cell lysis for plasmid extraction involves an alkaline buffer that includes sodium hydroxide and SDS. Both plasmid and genomic DNA denature in this condition. When the alkaline reaction is neutralized with potassium acetate, the fairly short plasmid DNA can quickly re-anneal, while the much longer and more complex genomic DNA tends to become tangled up with itself, which prevents sister strands from properly aligning and often results in protein-DNA binding interactions.
DNA bound to protein will then get pulled down during centrifugation, while soluble plasmid DNA remains in solution.
Qiagen and BiteSize Bio both offer some more description of the process:
https://www.qiagen.com/us/resources/technologies/plasmid-resource-center/key%20steps%20in%20the%20plasmid%20purification%20protocols/
http://bitesizebio.com/1660/plasmid-v-genomic-dna-extractionthe-difference/

It's also important to note that plasmids are cccDNA (covalently closed circular) which means that the two strands will be catenated upon denaturation. Basically, even though the strands are separated, they are still linked together.


text:
toxin determination and treatment of wild water
I am writing an article on the treatment of wild water from a wilderness survival angle. I have come across the term "toxin" and am finding it hard to produce a determination and treatment strategy.
It is first difficult to advise if a water source contains toxins, other than the presence of algal blooms. For example, a lake had blue-green algae. I understand that the associated toxin is produced by the cyanobacteria, but not the bacteria itself.
Pathogen treatment would be boiling or if available, chemicals such as iodine, chlorine or chlorine dioxide. Chemically contaminated water would require distilling.
I don't know if I can treat water containing toxins at all without distilling it or if there are different strategies for different toxins.


text:
Do other animals suffer from myopia or hypermetropia?
Mammals have eyes similar to humas and many other animals like octopuses have a lens in the eye. So do they have such eye defects? If yes, how do they overcome it? Do they feel selection pressure against them in such cases?

This article in Washington Post https://www.washingtonpost.com/national/health-science/animals-eyesight-has-evolved-to-suit-the-differing-needs-of-different-species/2013/03/18/4aaae76c-8b15-11e2-9838-d62f083ba93f_story.html?utm_term=.fb5b97c12f17 addresses your questions

do they have such eye defects?

Yes, eye defect is not specific to humans of course. Cases of eye defect are very common in animals. It is most often witnessed in domestic animals and they are the ones we observe the most (see The physiology of domestic animals)
Eye defects have typically been observed in tree shrews, monkeys (incl. macaques), cats, dogs, horses, rats, elephant and a Cape buffalo.
You should have a look at the wikipedia article Myopia in animals

howw do they overcome it?

They don't wear glasses obviously!
Humans uses the sense of vision a lot. Many animals uses smell (and taste), hearing or touch much more than humans do. For such non-visual animal, having a slight eye defect is not too big of a deal.

Do they feel selection pressure against them in such cases?

That is a bit of an awkward question. Nobody can feel a selection pressure on themselves. A selection pressure is a fitness differential associated with genotypes. A selection pressure is therefore defined at the population level. There is no such thing as a fitness pressure against a single individual.
Let me rephrase this last question to something that makes more sense. I am not sure I will address the specific question that was of interest to you though.

Are non-humans animals that have an eye defect aware that they have an eye defect?

It is unlikely that any animal would have the cognitive abilities to notice that they see more poorly than another animal of the same species. Doing so, would at least require having the ToM and only few species do.

To add on to your point about awareness of eye defects - I'd argue that even theory of mind isn't really sufficient - plenty of humans think they see just fine until someone puts glasses on them for the first time.

I agree. This is why I wrote "would already require" in the sense of "would at least require". I now edited the post now


text:
Using anatomical terms for human organs and parts of plants
I know how to apply anatomical directional terms (e.g., dorsal/ventral, anterior/posterior, etc.) for animals as a whole (bipeds and quadrupeds).
Recently, I've been studying plant physiology, and I came to know that the upper surface of a leaf is the ventral surface and the lower surface of the leaf is the dorsal surface. I cannot understand how these terms are applied to plants and leaves.
I've also seen anatomical directional terms being used for body organs such as the brain.
I want to know how anatomical terms are applied for parts of plants and body organs.

Wonderful question. Yes in biology there are various terms to indicate  directionality and frame-of-reference for a phenomenon (such as transport) or a picture (eg. a section)

First, for reference, see here for a discussion about the difference in directional terms between bipeds and quadrupeds as well as a fairly complete explanation of word meanings/etymology.

The etymological meanings of the various anatomical directional terms should help explain their usage in body organs. For example:
Ventral -> "belly" side
Dorsal -> "back" side
Anterior -> "before" or "toward the front"
Posterior -> "after" or coming after (opposite to) the anterior

For body organs (or other body parts):
This SE question addresses hands and feet, while this page from Bryn Mawr College directly demonstrates the usage of anatomical positional terms of the brain:

Rostral/ Anterior --->   Head or front end
Caudal/ Posterior --->  Tail or hind end
Dorsal  --->    Back or top side
Ventral --->    Belly or bottom side

Anatomical positional terminology for brains is consistent across organisms. Here is another picture demonstrating anatomical positional terminology of this organ from Santa Monica college:

For plants, see "Plant Identification Terminology: An Illustrated Glossary" (Harris & Harris, 2001):

Dorsal. Pertaining to the back or outward surface of an organ in relation to the axis, as in the lower surface of a leaf; abaxial. Figure 407.
Ventral. Pertaining to the front or inward surface of an organ in relation to the axis, as in the upper surface of a leaf; adaxial. Figure 1428.

Therefore, dorsal/ventral are determined relative to the axis of where the leaf connects to the stem (ie., the axil). Because of this, in my experience terms such as abaxial and adaxial would be preferred when referring to plants.

So, back and bottom are opposite terms. Aren't they?

@MrAP well that depends on which context you're talking about. In some instances (e.g., quadrupeds)  they are opposite and in other instances (e.g., bipedal anatomy) they are orthogonal. In plants, neither appears to be the case b/c from a whole plant perspective, "back" and "bottom" would be synonymous when referring to a leaf. However, just like when we refer to the dorsum of a human foot, using dorsal (i.e., "back") when referring to a leaf uses a different point of reference (POR) than the whole plant -- dorsal still means "back", but in the case of a leaf, the POR is the leaf axil.

This is why word etymology is so important. :p

So, ventral refers to the belly side and dorsal refers to the side opposite to the belly side which is always the back side but ventral may not always be the bottom side. Right?

So, overall, the trick to understanding all of this is threefold. First, understand that each of these words has etymological meaning/background -- e.g., "ventral" originated from terminology referring to the belly side and "dorsal" originated from terminology referring to the "back." The second part of these concepts is understanding that these terms are applied in different fashions (i.e., using different points of reference). Further this is not always done appropriately based on the etymological meaning of the words themselves...

Given all that, sometimes ventral/dorsal are parallel to the ground (i.e., indicating "up"/"down" relative to the ground, respectively ) and other times they are orthogonal (i.e., indicating anterior/posterior). In cases such as the hand (facing palm forward in anatomical position) when the body is supine or plant leaves (point of reference is the leaf axil), the terms ventral/dorsal appear to be backwards (as in dorsal is "down" not "up" relative to the ground). Again, this is because of point of reference. Regardless of changing POR, these terms retain their etymological meaning.

Again, ventral and dorsal should be avoided when talking about plants because in such cases we are extensding these terms beyond their original etymological meaning. Terms such as abaxial and adaxial are more appropriate because they literally directly refer to the plant part that is important: the leaf axil on the stem.

Dorsal and Ventral is very much confusing term as well as very casual term (and unscientific enough... Because we cannot compare our ventre or front with plants'). Unfortunately this casual terms widely used.
I usually avoid the term "dorsal" / "ventral"  and "upper" / "lower" since there are available and better synonym Adaxial and Abaxial.

Fig-1. Adaxial and abaxial surfaces of leaf shown on the same leaf-drawing provided in another answer.

P.S.
The term "dorsal" and "ventral" have another (quite opposite)  usage in case of thalloid bryophytes such as Riccia and Anthoceros. and there are also use of terms "upper" and "lower" surface;  in case of those bryophyte thalli; "ventral" or front-side is the "lower" side (towards ground) ; and "dorsal" or back-side means the "upper" side.... and that is exactly opposite of leaves' terminology.

example:
  Diagram from the textbook, College Botany , Vol-2, by Ganguly & Kar, New Central Book Agency...

The diagram (its Fig. C) describes the lower (ground-touching), rhizoid-containing surface as Ventral surface.
Diagram from another textbook, Botany for degree-students- bryophyta, by B.R. Vashishta, A.K Sinha and Adarsh Kumar; S-chand publications

The side where "dorsal groove"  has been pointed; is its upper surface.

$$\begin{array}{c|c|c}\hline
\bbox[coral]{\textbf{term}} & \bbox[yellowgreen]{\textbf{usage in an angiosperm leaf}} & \bbox[yellowgreen]{\textbf{usage in thalloid bryophyte}}\\\hline
\text{VENTRAL} & \text{Upper side, Adaxial side}& \text{Lower side}\\\hline
\text{DORSAL} & \text{Lower side, Abaxial side}& \text{Upper side}\\\hline
\end{array}$$
So a thalloid bryophyte's  "dorsal"  or "back" (which is upward) side is not comparable to an angiosperm leaf's "dorsal" or "back" (which is downward) (best to say "abaxial") side.
Similarly a thalloid bryophytes "ventral" or "front" (which is lower or ground-touching) side is not comparable with an angiosperm leaf's  "ventral" or front" (which is upward) (better to say adaxial) side.

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text:
Why are X-linked illnesses less common in females if females have X-chromosome inactivation anyway?
I have read this post but am still slightly confused about this. Do tissues in the human body not all develop from the same cell(s) in the embryo? If so, I do not see how the cell 'mosaic' would be grainy enough to mask the fact that half of the female's cells are not working properly. For example, all liver cells come from the same cell in the embryo which has an inactivated X. In that case, there is a 50% chance that the females liver is dysfunctional. So I would predict that some females would exhibit X-linked disorers even if they are heterozygous, but I haven't heard of this being the case...

think of a given organ in your body (if you're a female) like a calico cat's pattern

Barr bodies (X-chromosome inactivation) don't form in the initial fertilized embryo — it's not that one X-chromosome is inactivated, and then that same inactivation is passed down to daughter cells. Rather, X-chromosome inactivation occurs on a cell-by-cell basis in differentiated cells.  Note how the accepted answer to the question you linked mentions that different cell lineages will have different X-chromosome inactivation patterns — in other words, inactivation occurs later in the differentiation and proliferation processes than I think you might be assuming.
To use your example: the liver cells do not all derive from a pluripotent (undifferentiated) cell with one inactivated X-chromosome, but instead derive from said pluripotent cell, and then undergo X-chromosome inactivation.
Although the jury is out, scientifically speaking, on the mechanisms of selection of the X-chromosome to be inactivated, it's been postulated that some sort of decision-making may occur on this cellular level, resulting in a higher likelihood of inactivating the damaged or deleterious chromosome, if one is present.
Regardless, as the accepted answer to the question you linked mentions, the 50% of functional cells that would result from chance or random X-chromosome inactivation tends to be sufficient for the body's needs.

Let me know if this answers your question!

"the 50% of functional cells that would result from ... random X-chromosome inactivation tends to be sufficient for the body's needs." Does this mean that it is the percentage of functional cells that determines the phenotype of a female? eg if a haemophilia carrier has 50:50 normal:diseased X, they may be fine, but if they had 30:70 normal:diseased X, then they would have haemophilia? Otherwise how do you explain women also get X-linked diseases when one of their X is inactive? Inactivation means only 1 X is meaningfully functional so isn't that the same as males having has just 1 X anyway?


text:
What's the difference between morphospace expansion and packing?
I'm reading an article that talks about morphospace and niche expansion or packing.

Differences in slope above and below zero indicate dominance of
  morphospace expansion versus morphospace packing, respectively.

What do the terms mean? What's the difference?
The way I understand it is that morphospace expansion is the change in morphology from the perspective of a population, but morphospace packing is, from the perspective of the ecosystem, the process where organisms are occupying the ecosystem space entirely so that no niche are available anymore. Is that correct?
The "packing" seems to refer to the density of the different "regions" of morphospace. Or said differently, you could "pack" different morphotypes in an environment. Is this a probable explanation?
I haven't found an answer looking at the history and definitions of niche.

You're almost there--both terms concern the relationship between increases in species richness and morphological diversification. They're two opposing patterns:
Morphospace expansion indicates that a lineage is occupying new areas of morphospace with increasing species richness. (The slope is more or less relating density of morphospace occupation to speciation rate--so > 0 means new species tend to go farther away in morphospace.)
Morphospace packing indicates that a lineage is not expanding its morphospace with increasing species richness, so the existing region of morphospace that it occupies is getting more densely filled, instead of expanding.
The relationship between functional/ecological diversity and morphological diversity isn't always clear cut, though, so you have to be careful when relating the two. If you're going to use these concepts, especially if you're going to use morphological diversity as a proxy for functional diversity, it's best to state that assumption outright.
This paper includes a nice discussion of the two concepts (and is cited by the one you list): http://rspb.royalsocietypublishing.org/content/283/1822/20152013

Thanks! As a quick question, are you saying that niche expansion is the same thing as morphospace expansion and same for packing?

Not quite -- niche expanision/packing are the same base ideas, but for ecological niche instead of morphology. I'm generally pretty careful about being explicit when relating one to the other.
So, for niches:
Niche expansion = exploring/ expanding to new areas of niche (ecological diversity)-space with increasing species richness
Niche packing = filling in the existing area of occupied niche space with increasing species richness. Does that make sense?

Yes! And it would be equivalent to say that morphospace expansion is the extension of the previous (before expansion) trait distribution to new phenotypes whereas packing would be the development of of already existing phenotypes, but increasing their density. Is that ok?

Precisely! You've got it!


text:
What is the consistency of cytosol?
Imagine you somehow got a cup of pure cytosol.  What would be its consistency?  That is, how thick, how sticky, and how viscous would it be?

pure cytosol - you just want the aqueous phase of the cytosol only? so wouldn't it have to be pretty much like water with some salt in it?  the really sticky stuff is in vesicles and/or it would be excluded from the aqueous phase with whatever filtration you apply.  the cell as a whole, however, does not behave like salty water, but rather like a gel

Cytosol is actually about as viscous as water
(i.e. ~1 cP or 1 mPa/s).
From the Introduction of Bicknese et al. 1993

In fibroblasts and several types of epithelial cells, fluid-phase viscosity was 1.1-1.5 cP, not much higher than that of water (1 cP) (Periasamy et al., 1992). Recent measurements of cytoplasmic viscosity in CV1 and PtK1 cells by a novel ratiometric method supported the conclusion that fluid-phase viscosity in bulk cytoplasm is similar to that of water (Luby-Phelps et al., 1993).

And from the conclusion:

Apparent fluid-phase viscosity near the cell plasma membrane was 1.1 ± 0.2
  cP (fibroblast) and 1.0 ± 0.2 cP (MDCK), not significantly different from the viscosity measured in bulk cytoplasm far from the
  plasma membrane.

Interestingly, the paper cites the following studies:

In fibroblasts, fluid-phase viscosity was weakly temperature-dependent (Arrhenius activation energy 3-5 kcal/mol) and nearly independent of cell volume (Fushimi and Verkman, 1991).

Note:
cP = centipoise

A centipoise (cP) is a non-SI (non-System International) measurement unit of dynamic viscosity in the centimeter gram second (CGS) system of units. It is multiple of the CGS base viscosity unit named poise (P)
1 cP = 0.01 g/cm/s
1 cP = 1 mPa/s

Source:
Bicknese S., N. Periasamy, S. B. Shohet, and A. S. Verkman. 1993. Cytoplasmic Viscosity Near the Cell Plasma Membrane: Measurement by
Evanescent Field Frequency-Domain Microfluorimetry. Biophysical Journal 65: 1272:1282

Further Reading:

Beals et al 1999
Gyurov & Token 2011
Guthrie & Nettesheim 2012
Kalwarczyk 2011

I can't comment about the consistency of this viscosity between all cell types or between taxa. I welcome suggestions to edit if anyone finds additional or more recent info.

Nice answer - I'm not an expert in plant physiology but that's one example where I might expect to see a higher viscosity, at least in some plant tissues (I don't mean that as a criticism of your answer but just a suggestion in case no one comes along to add on).

I do not agree, all your other sources report (slightly) higher viscosities. Based on those measurements I'd say it's more comparible with blood (3-4 cP). Still fluid, just a bit less than water. However, that's only for small molecules. If you're looking at bigger probes (>5 nm) the viscosity is 20-40 cP, comparable to vegetable oil (numbers according to your Kalwarczyk source). Also, based on the protein content alone you'd also have to assume a viscosity of 5-15 cP.


text:
Is a mycelium sewage pipe possible?
Over the past few years I've seen mycelium used as a supplement for various building materials. I was wondering if mycelium could be successfully used as construction material for a sewage pipe.
Furthermore, would this sewage pipe be able to provide any filtering of waste, given the mycelium?
Sources:

mycelium packaging
mycelium plastics
mycelium bricks

Providing some reference to instances in which mycelium have been used for building materials previously would strengthen this question. Further, perhaps a quick comment about why you want to know this information -- this would help guide those providing answers to stay relevant for you.

@theforestecologist agreed — please offer examples of mycelium incorporation into construction!

I'm assuming here and here are examples of what the OP is referring to? I'd seen both of these stories about 7 or 8 months ago I think.


text:
On the selection coefficient
I'm reading  Williams' Adaptation and Natural Selection:
A Critique of Some Current Evolutionary Thought.
In this book the author talks about selection coefficients which, if I understand it correctly, can be calculated as finiteness arithmetic means (for each allele).
My question is: should this calculation be made assuming a ceteris paribus condition?

Definition of selection coefficient
A selection coefficient is a difference in fitness between two genotypes (or haplotypes). Let the two genotypes be A and B. Let's use relative fitness and say that the fitness of A is $w_A = 1$ and the fitness of B is $w_B = 1 - s$, where $s$ is the selection coefficient. As a consequence $w_A - w_B = s$.
The question of long-term fitness is unrelated to the definition of selection coefficient, as the selection coefficient is defined as a difference in fitness. A question of importance is "What measure of fitness should one use for a population where selective pressures are changing over time and/or space".
What measure of fitness should one use for a population where selective pressures are changing over time and/or space
Roughly speaking, if changes in fitness are over space, then you should use arithmetic mean fitness and if changes in fitness are over time, then you should use the geometric mean fitness but it is not quite that easy.
The real interest is whether fitnesses are correlated among generations. In other words, do individuals within a generation tend to have a more similar fitness values than the individuals of another generation? When variation in fitness is spatial than one should not expect such correlation. When variation is temporal one should expect such correlation.
Hoping you can read a code in R, the easiest is probably to read some code that make a simulation and look at the output. So here is a code that performs simulations. The key difference between simulations with spatial and temporal variation is the line that gets fitness value (runif).
set.seed(43)

temporalVariation = function(N, lowestFitness, highestFitness, nbgenerations)
{
    Ns = numeric(nbgenerations)
    Ns[1] = N
    for (generation in 2:nbgenerations)
    {
        fitnessPerIndThisGeneration = runif(1,lowestFitness, highestFitness) # All individuals have the same fitness in a specific generation
        N = N * fitnessPerIndThisGeneration
        Ns[generation] = N
    }
    return (Ns)
}

spatialVariation  = function(N, lowestFitness, highestFitness, nbgenerations)
{
    Ns = numeric(nbgenerations)
    Ns[1] = N
    for (generation in 2:nbgenerations)
    {
        FitnessOfEachIndividual = runif(N, lowestFitness, highestFitness) # Individuals differ in fitness within a generation
        N = sum(FitnessOfEachIndividual)
        Ns[generation] = N
    }
    return (Ns)
}

N = 1000
lowestFitness = 0.95
highestFitness = 1.08
nbgenerations = 200

spatialNs = spatialVariation(N, lowestFitness, highestFitness, nbgenerations)
temporalNs = temporalVariation(N, lowestFitness, highestFitness, nbgenerations)

plot(y= spatialNs, x=1:nbgenerations, col='blue', xlab = 'generation', ylab = 'N')
points(y= temporalNs, x=1:nbgenerations, col='red')

In blue is the simulation with spatial variation. In red is the simulation with temporal variation. You will note that the geometric mean is always equal or lower than the arithmetic mean.
Whether the arithmetic or geometric mean fitness matters most will affect the reproductive system that will be most successful. In this regard, you should read Ripa et al. 2009 about bet-hedging

"Roughly speaking, if changes in fitness are over space, then you should use arithmetic mean fitness and if changes in fitness are over time, then you should use the geometric mean fitness but it is not quite that easy."  Remi, would you explain/elaborate on this?

@sterid See edit. I am not 100% sure how to explain it, so I decided to write and show results of a simulation. Hopefully that will make sense when reading the code.

I appreciate your writing the code, but I don't know the R language.  I have a couple questions if you feel like indulging:

Never mind.  I understand the program.  Will study it & probably have questions.  Thank you.

OK I see why that result was obtained.  Would you please explain the relevance of "You will note that the geometric mean is always equal or lower than the arithmetic mean." ?

It means that environmental variance on fitness causes a greater decrease in long term fitness if this variance is temporal rather than spatial. This whole subject is very interesting especially in the bet-hedging literature. The first one to point out to this effect was Richard Levin. His book evolution in changing environment is all focused on that (IMO it is old and not very pleasant to read though).

But isn't it true that if you consider the effects of selection, you must have spatial variance in order to have temporal variance and vice versa (as long as heritability is high)?


text:
How to write a stoichiometric matrix for a part of the Pentose phosphate pathway
maybe this is more bioengineering than biology but I didn't find any such group.
So I got the following photo:

And I was asked to do the following for the network inside the red area.
1) Write the stoichiometric matrix for the network
2) Draw a pathway map for the network
3) Draw primary metabolite connectivity maps
4) Write the mass balance equations for primary metabolites
I know that for the first one the columns are the reactions taking place and the lines are the "chemicals". Should the markings on the columns be the same as the numbers that are written on each reaction? (like "3.1.1.31")
Almost every reaction can go in both direction, is there anything that says which chemical should get minus and which one gets plus?
My attempt at the matrix was:

As for the pathway map, isn't that basically the photo is given?
And finally what would be a "primary metabolite" in this case?
All help and hints very well appreciated!

This is not a particularly well written homework question. I'll try to give some hints based on how I interpret it.
1) The stoichiometric matrix. You have exactly the right idea. I would write the reactions as enzyme names or gene names instead of the EC numbers (e.g. G6PD or G6P dehydrogenase instead of 1.1.1.49). For the reversible reactions, there's no a priori reason to write them in one direction or another, but convention would be to make glucose consumption the positive direction. I would not include "glycolysis" as a separate reaction. I would also consider including cofactors and byproducts in the molecules affected by the reaction (e.g. CO2, NADP+, NADPH, (maybe ADP, ATP, NAD+, NADH also if those come up)).
2) Yes, it's basically what you already have. It's not a particularly great diagram, so you could draw it in a clearer way.
3) I have no idea what this means, but perhaps the next point will help.
4) Primary metabolite is not a super well-defined term, but I think in this context, I would say that the way they're intending the question, they're looking for a "total pathway reaction" that describes the net inputs and outputs of the pathway.
Something like this:
$$
X_1 G6P + X_2 NADP+ \implies X_3 GAP + X_4 FBP + X_5 CO_2 + X_6 NADPH
$$
(G6P=Glucose-6-phosphate, GAP=Glyceraldehyde-3-phosphate, FBP=Fructose-bis-phosphate)
I'll leave it to you to figure out what the X's are or whether I left anything out (since it's a homework assignment after all.)

Thank you so much!
But okay since H6PD has the same EC numbers as the two reactions below (1.1.1.49 and 3.1.1.31) should that be considered as a separate reaction or is it enough to only have the other two?
Also if glycolysis shouldn't be included as a separate reaction how do I mark down the carbon going in and out of the network?

Yeah some enzymes will catalyze more than one reaction. You'll have the same problem with transketolase. Nothing wrong with suffixing them _A and _B or whatever. I didn't mean to say that using the EC numbers was wrong either -- I would just say that if you want human-readable names, biologists/biochemists are more likely to recognize gene names. Few people have the entire EC number hierarchy in their head.

Sorry, misunderstood your first question. Each reaction should only appear once, however you name it. The EC number (1.1.1.49) refers to the type of biochemical reaction going on. The gene name refers to the enzyme that catalyzes that reaction. They refer to the same reaction, just in different ways.

As for carbon going in out, you sort of already have this (e.g. a -1 for G6P in the G6PD (1.1.1.49) reaction. At the end of the day, the point of this matrix is that if you multiply your matrix by a vector of how much flux is going through each reaction, you'll get a vector with an entry for each metabolite that tells you how much is being produced or consumed. For this to be sensible, every reaction should be mass-balanced (so nothing that produces something out of thin air).


text:
Is designing alien life still just science fiction?
As we continue to search for life in very different environments than the earth, it would make sense to me to think about and design lifeforms (theoretical) that could work in these environments. I know that we are searching for life in extreme environments, but are we thinking about lifeforms that could have evolved in such environments? (Even if we dont find any)
The idea of the atom comes from ancient greek philosophers long before one could find any evidence for it. Although their views on what atoms look like and how they behave were incorrect, one could later refine this model through evidence and experimentation.
I think some good thought could makes us learn what to look for in the first place.
Is this still just a field that science fiction thinks about, or are there any serious publications on this topic? If not, why not?
Clarification: I mean the theoretical design of lifeforms. Not just manipulating and editing existing lifeforms, I mean designing completely new theoreticaly plausible lifeforms, within the constraints of a given environment. On paper or simulation etc, not actually making them physically.
If you find any scientific papers on how and what kind of life could exist for example on Titan, Europa, below Earths crust etc... or any other environment, please link to them in your answer. Thanks!

What is your definition of "new lifeforms"? You said without the use of existing life forms so you mean to synthesize a new strand of DNA as a genome (by selecting some genes you want to be present in the "new" organism"  and then let this grow or what?

No, I don't mean anything physical. Just thinking about what kind of life could exist.

First, you can check out this Wikipedia entry: Hypothetical Types of Biochemistry. I caution you that the scientific utility of many of these hypotheses isn't great since they are, at least currently, untestable.
Second, your question brought to mind some current research by two groups of scientists in the field of synthetic biology which may, in some way, answer your question. I will briefly mention these below.

Scientists are attempting to create synthetic organisms with minimal genomes (those in which every gene is essential). In one of the more recent studies (Hutchison CA, et al. 2016. Design and synthesis of a minimal bacterial genome. Science.), they randomly knocked out genes of an organism and then, based on survival and growth, classified them as essential, non-essential and quasi-essential (deletion results in growth impairment). They were then able to pare down the genome to 473 genes, which they claim "has a genome smaller than that of any autonomously replicating cell found in nature".
Important points from this research with respect to your question:

Of the 473 genes in the organism described above, 149 have an unknown function. In other words, we still have a limited understanding of what exactly is required for the basic biochemistry of life on Earth. To quote the article:

...biological functions could not be assigned for the ~31% of the genes... Nevertheless, potential homologs for a number of these were found in diverse organisms. Many of these genes probably encode universal proteins whose functions are yet to be characterized.

Additionally, before their knockout approach described above, the researchers attempted creating minimal genomes by rational design. Note that this is not designing new organisms but rather deleting genes from an existing genome based on whether they are thought to be essential. They failed. Quoting a press release (emphasis added):

[The researchers] initially formed two teams, each with the same task: using all available genomic knowledge to design a bacterial chromosome with the hypothetical minimum genome. Both proposals were then synthesized and transplanted into M. capricolum to see whether either would produce a viable organism.
  “The big news is we failed,” Venter says. “I was surprised.” Neither chromosome produced a living microbe. It's clear, Venter says, that “our current knowledge of biology is not sufficient to sit down and design a living organism and build it.”

In another avenue of research, scientists are attempting to create synthetic cells based on self-replicating RNA and compartmentalization by spontaneously forming fatty acid vesicles, perhaps somewhat plausibly mimicking how life may have arisen on Earth. Of interest to you may be this review (Blain and Szostak. 2014. Progress Toward Synthetic Cells. Annu Rev Biochem.) which, in their words:

[focuses] on bottom-up approaches to the construction of artiﬁcial cells from molecular components or subsystems. We do not discuss the top-down approach of systematically removing genes from extant organisms to achieve a minimal genome, nor do we consider the creation of new types of cells by genome synthesis or extensive genome editing.

They say in the article (emphasis added):

In vitro translation systems have successfully been incorporated into vesicles, resulting in the efﬁcient synthesis of proteins... However, replicating the entire system, including DNA and RNA polymerases, transcription and translation factors, transfer RNAs, the ribosome, and other components, is still a distant goal, and proposals to do so involve more than 100 genes. Properly coordinating the replication of such a large synthetic system may require additional regulatory components.

Take away message: We are not yet able to design or create, de novo, living organisms based on known biology, let alone organisms based on some hypothetical biology of another planet.

Interesting answer +1! But I just want to draw your attention to this line I mean the theoretical design of lifeforms. Not just manipulating and editing existing lifeforms, I mean designing completely new theoreticaly plausible lifeforms, within the constraints of a given environment. On paper or simulation etc, not actually making them physically. to which only your last paragraph seems relevant.

@another'Homosapien' Thanks. The point I was trying to get across is that people are trying to design synthetic life within the framework of known biochemistry. However, they haven't succeeded. Given that, how could we possibly design organisms with an entirely new and made up biochemistry for life on planets that we know almost nothing about?

Also, I want to emphasize that it is leading researchers in the field that are saying we don't possess the knowledge to design and build a living organism, and the ability to do so is far away.

The answer to this question can go as far as anybody's imaginations. So I'll just tell why the answer is what it is, and try to include scientific facts (possibly with references) wherever possible.
Simple Answer: Designing alien life forms on the basis of current theoretical and practical knowledge of science (if this is what you mean) is still, and seems to remain, a field of science fiction only.
Why? Because, simply, the proposed organisms can be unlimited. Even if this field matures as a science, it will remain as large as the universe itself, because there are literally no boundaries and limitations to speculation and imagination. Only recently have researchers agreed that discovering organisms similar to humans is much much less likely than any layman thinks. Actually, there is even a formula for it, known as the Drake equation after Frank Drake who proposed it. The equation is:
$N = R^* \times f_p \times n_e \times f_l \times f_i \times f_c \times L$
where:

$R^* =$ the average rate of star formation in our galaxy
$f_p =$ the fraction of formed stars that have planets
$n_e =$ the average number of planets per star that can potentially support life
$f_l =$ the fraction of those planets, fl, that actually develop life
$f_i =$ the fraction of planets bearing life on which intelligent, civilized life has developed
$f_c =$ the fraction of these civilizations that have developed communications i.e. technologies that release detectable signs into space
$L =$ the length of time over which such civilizations release detectable signals

Obviously, this answer comes out to be very small, meaning that intelligent life is very difficult to find. But that doesn't mean finding life is difficult. And this claim gets even more support when scientists find water on mars and even mercury! Now, to give a bit of knowledge, this field is not really limitless; there are (at least) two limits (i.e. I'm not including more). The first limit is source of liquid water$^*$. Now, knowing that water is easy to be found almost anywhere, this does not seem quite a difficult one. Another one is source of energy. Now this is a difficult one. The problem with discovering life (in near future at least) is the area in which we are searching. Most of the searches (by telescopes of course) are being conducted near red dwarf stars. There are quite some reasons for it:

red dwarf stars are quite stable
they have very long life
they are pretty less shiny (making observations easier)
they may be home for many super-Earths

But being less shiny also poses a problem: too little energy for life. Red dwarf stars emit most of their radiation in the infrared portion of spectrum, which is pretty useless for plants (on Earth at least). Now, to survive in a red dwarf system, plants need to capture infrared light. Thus, the speculated plants in red dwarf systems will be pitch black just to absorb more energy. Also, red dwarf stars are pretty lightweight, as less as 7.5% of sun. This means they have less gravitational pull i.e. they will have much lighter planets in their Goldilocks zone. Now, much lighter planets means much less gravity on planet's surface. Thus, the speculated plants in red dwarf systems will be a lot higher than plants on Earth. But, less gravity also means much less density of air even on surface. Now, you can interpret it yourself. And, not just to surprise you, there would be absolutely no surprise if in future a satellite discovers silicon-based life, because it is really possible for life to emerge from silicon instead of carbon!
$^*$why I am continuously saying liquid water has a reason. Water is actually one of the very few candidates that can serve the purpose of maintaining life forms. Its one of a handful of liquids which are liquids at desired temperature. As one might think, life cannot survive below a certain temperature, simply because below that temperature, the liquid itself would absorb all the metabolic heat from organism and evaporate. So, it is quite relevant to say liquid water here.
What I meant to say is that there are technically no boundations to designing alien life forms, as long as you talk about the whole universe. So, this does not really count as science. After all, if you search science definition on Google, you get this:

the intellectual and practical activity encompassing the systematic study of the structure and behaviour of the physical and natural world through observation and experiment.

This does not include imagining alien life forms in any way. So, I do not think this subject would ever be considered as scientific by the scientific community. Mostly, scientists are not indulged in this kind of work because they like to observe and interpret natural phenomena rather than imagining them. Scientists make laws from nature rather than applying laws on nature. Still, there are some scientists who take this matter seriously and publish scientific papers about it. I could find only one (PDF) related to this point. You might get some more on the internet.
In the end, if you think about how plants would look on a planet in a red dwarf system, you might end up with this:

Bonus: Dawn space probe from NASA has detected organic materials on Ceres(!) Now, what kind of organisms would you expect to see there based on our current knowledge about Ceres?

"What I meant to say is that there are technically no boundations to designing alien life forms, as long as you talk about the whole universe". However if you consider only one environment (for example the moon Titan) you already get a lot of limitations. Do you know of any scientific papers that consider these limitations and try to come up with various possible lifeforms that could survive in such an environment? (Also note that you don't absolutely need water for life, you probably just need some kind of solvent that behaves in a similar fashion)

Why are scientists not interested in these things? This seems rather odd. If you find any good scientific papers please add them to your answer.

Thank you for a good answer. I will award the bounty to the best answer at the end of the period. I am very interested in this and the more diversity I can get with different answers the better.

Is there a biological field for designing life?

The field is called synthetic biology. It is a very new field. With not many player. Currently being constructed is a synthetic yeast Sc2.0. There is attempts to get interest and funding for a synthetic mammalian genome. The synthetic human genome HGP-Write.
More serious work is adapting life to do something. Stuff that we are more familiar with like GM crops. De horned cattle. Better race horses.  etc

There is also some cool research designing life forms that use synthetic de nova nucleotides (so non-A,C,G,T or U). http://www.pnas.org/content/114/6/1317.abstract


text:
Is it possible to color sperm cells so they look more clear under a microscope?
Im working on something that requires me to check the velocity of a sperm cell under a microscope but I imagine it would be very hard for a program to keep track of the sperm cells.

You can check this http://www.vivo.colostate.edu/hbooks/pathphys/reprod/semeneval/morph.html


text:
How many plants arise from a polyembryonic seed?
When I asked this question to my teacher she said that she doesn't know. So I wanted to know? Is there any use of polyembrony in plants?

In plants due to programmed cell death only one plant arises.
Here is a good article

The enigma of plant monozygotic polyembryony is that only one embryo in a polyembryonic seed usually survives while the others are eliminated at an early stage.

If that is so, what is the need of polyembrony (Sporophytic budding). It's there any use in the process?@JM97


text:
Are there any exceptional cases in which a person with O negative blood group cannot donate?
Are there any exceptional cases in which a person with O negative blood group cannot donate or any case in which compatibility might not be established between O negative an any other blood group?

There are some situations, where, depending on the interpretation of Rh status, an exception could become possible. Rh +/- commonly refers to the D antigen. However, the Rh group has many antigens in it, including C and E. One can become sensitized to these other antigens and develop a hemolytic response to incompatible C or E type.
Dean L. Blood Groups and Red Cell Antigens [Internet]. Bethesda (MD): National Center for Biotechnology Information (US); 2005. Chapter 7, The Rh blood group.

When the donor has some infections in the blood (HBsAg, HIV, HCV, VDRL etc positive)the blood cannot be donated. For otherwise normal donor, there is no such theoretical contraindication. However, it is always good to do a cross match test before blood transfusion, as there is always some possibility of cross reaction.


text:
Why is glucose used in oral rehydration therapy?
What is mechanism of action of glucose in the intestine to reduce the watery and electrolyte secretion?

Oral Rehydration Therapy uses electrolyte solution containing some glucose. It is because, the absorption of electrolytes is more efficient when glucose is added. Sodium uptake from intestine is carried out by sodium glucose co-transporters.


text:
Cholesterol and fatty acids role in bile?
The composition of gallbladder bile is 97% water, 0.7% bile salts, 0.2% bilirubin, 0.51% fats (cholesterol, fatty acids and lecithin)1. Bile's role is mainly help for digestion of lipids via bile salts and acids (emulsification) but i dont understand what is cholesterol and fatty acid role in bile. What is cholesterol and fatty acid's function in bile?

What research have you done before asking it here?

First i was studying to biochemistry of lipids generally at Lehninger and i read an information about bile. It says that bile has cholesterol and fatty acids. After i thought there is a mistake and looked to wikipedia (i editted the link) and the same information is writing at wikipedia and i asked here.

extra cholesterol is excreted by the body through bibles and fatty acids are needed to maintain this cholesterol in soluble form otherwise it leads to gall stones.

@JM97 your thought makes sense thank you. Can you find a resource including this information ?

@AhmetÖz see this https://goo.gl/tnE9go.  typo * bile

The main function of bile is to emulsify large fat molecules into small fat droplets. You must have heard about micelle formation by soaps. Well, bile acids perform quite similar function. Bile acids, having both hydrophobic and hydrophilic parts, form micelles and trap fat molecules and form emulsion, hence naming the process emulsification. Similar function might be performed by fatty acids. See this article:

Bile acts to some extent as a surfactant, helping to emulsify the lipids in food. Bile salt anions are hydrophilic on one side and hydrophobic on the other side; consequently, they tend to aggregate around droplets of lipids (triglycerides and phospholipids) to form micelles, with the hydrophobic sides towards the fat and hydrophilic sides facing outwards. The hydrophilic sides are negatively charged, and this charge prevents fat droplets coated with bile from re-aggregating into larger fat particles.

Now lets have a look on bile acids. The principal bile acids are cholic acid, chenodeoxycholic acid, glycocholic acid, taurocholic acid, deoxycholic acid and lithocholic acid, all of which are synthesized from cholesterol (see this). Now this partly explains why a small amount of cholesterol is released along with its derivatives; it might be the 'unprocessed' cholesterol which 'leaked out' from liver. But, in fact, it seems to do a bit more. Actually, cholesterol secretion into bile needs to be carefully controlled; too less secretion may lead to accumulation of cholesterol in blood vessels, leading to cardiovascular diseases (this is why cholesterol secretion is the final stage of elimination of cholesterol from reverse cholesterol transport), while too much secretion into bile may cause gallstones (see this). Hence, cholesterol secretion into bile also serves as a way to maintain cholesterol homeostasis (see this). In fact, bile acids serve as hormones in cholesterol homeostasis in the body. Similar reason may cause fatty acid elimination through bile.
Cholesterol and fats are hydrophobic, so they cannot be released as it is into GI tract. This is why they are released with bile. Bile acids are amphiphatic i.e. have both hydrophilic and hydrophobic parts. Hydrophilic part helps it in dissolving in chyme (containing HCl) while hyrdrophobic part helps it in dissolving fats and cholesterol (and lipids of course) into itself.
source


text:
Identification of colorful jelly-like marine creature
I'm on my trip to Gulangyu Island, Xiamen, Fujian Province, China. Today(4th February 2017), at 12:13 A.M., I saw a beach filled with huge rocks on which various dry shells reside. Among the shells, I spotted a colorful eye-like marine creature.

To figure out what it is, I torn it off from the rock. (don't worry, I've put it back after taking this photo)

Also, it feels soft when I poked it, and its size is approximately 1cm to 1cm. Could anybody please tell me what I've found?

You've found a sea anemone, a cnidarian of the Order Actiniaria. In this case, the anemone is closed and thus hiding its characteristic tentacles (likely as a form of protection while "out to dry").
I'm by no means an expert, but my guess is that you have a vertically striped species of the genus Diadumene  -- likely one of many morphotypes of the species Diadumene lineata. I've seen common names vary between "Striped Sea Anemone", "Lined Bead Anemone" and "Orange-Striped Green Anemone."
Here is a double stripe specimen from San Francisco, and below are two pictures from Ria Tan's Wild Singapore image collection:
Closed:

Open:

Without further information regarding size, color/length of tentacles etc., it will be hard for a non-expert like me to find a better answer.
According to the Wikipedia page, this species originated along the Pacific coast of Asia, but has spread more globally from attachment to ship bottoms, oyster shipments, and seaweed farming.
It appears from your picture, that you found your specimen out of water along the shoreline. Again according to the Wikipedia  article:

Diadumene anemones display high tolerance to inter-tidal exposure and drying out in extreme summer heat


text:
Possible complications due to gene-therapy?
Edward Lanphier, CEO of Sangamo BioSciences mentions here(https://youtu.be/dJ1B8XnyEnM?t=1215) that scientists can now specifically target cells, change the genome within a cell. Say you want to cure a type of disease, which can be linked to your genome. You have successfully removed the faulty gene in your genome (GenomeA), replaced it with a correct gene resulting in a improved genome (GenomeB) in a single cell. The next step will probably be to put it back into the human body. However, as I understand it every human cell contains your faulty human genome (GenomeA).
Question:

Even if you put a few cells with the correct genome sequence (GenomeB) into your human body, it is probably going to be overwhelmed by the other cells that contain your faulty genome (GenomeA). Cells containing the correct genome (GenomeB) will divide and multiply but so will cells containing the faulty genome (GenomeA). In this “genomic war” will the fewer cells containing the correct Genome (genomeB) ever win? Or will you need period infusions of cells with the correct genome "forever"?

How would you guys think about this?
Optional questions:

Even if it wins, it will probably take a very long time to completely replace all the cells with the faulty genomes. How much time is required before you can completely replace all the cells with the incorrect genomeA, with cells containing the correct genomeB?
Say you realize that you have a faulty genome (GenomeA), and you attempt to replace your genome with a correct genome (GenomeB). After 2 years, you have another disease and realize that you have to again correct your genome with GenomeC. However, 2 years is not enough to replace all your cells with the incorrect GenomeA, with the correct GenomeB. If you attempt to undergo genetherapy, now you will have to introduce another group of cells with GenomeC. Now you have cells with multiple different types of genomes floating around: genomeA, genomeB and genomeC. Are there any complications that happen due to the presence of multiple types of cells with different genomes in your body?

good questions... but way too many posed in a single entry... can you try and focus your question? it's very unlikely that anyone will answer all of them in one post.

I feel the question is useful and raises good points and those points shouldn't be removed.  Even if a person may not answer all of them in one post, he or she may answer some of them, with other answers to be obtained in other posts.  In terms of the question, I don't see why only a few cells can be put into the human body.  What technology can do to one cell at a time now, it should be able to do to thousands or millions at a time in the future.

Hi Vance, you are right, my question is a bit broad, since my specialization is not biology/gene-therapy. Since 2 people pointed out that the question is a bit broad, I only highlighted the first question and left the 2nd and 3rd questions as optional. It kind of a compromise, so as to address Sterid's request as well.

Your question is too broad. It is better to take some specific example.
Not all cell's in the body divide. If you take cell out of the body and want to return it back, it must divide. So we probably could talk about stem cells for example. The stem cells don not really sit in one place. And it almost impossible now to get such cells from the place that they sit in it, and then return in back. It is possible with bone marrow for example.
If we take some example, like ALS - some percent of the disease is thought to be genetic. But the mutation is in all the body cells. Mostly it's affects astrocytes, microglia and motor neurons. You cant take them out of the body, fix and return back. The only chance to fix is to work inside the body. For example by using some sort of virus (AAV for ex.) And CRISPR.
However, if we follow your story and we insert cells with genomB, they will live together with cells with genomA, if there is not some bigger mortality of the original cells.

Thanks for pointing out some use cases. My specialization is not biology, and I am coming in from a 30000 feet so you are right that the question is perhaps a bit broad.  I guess my intuition was kindof right. It seems you do need some kind of periodic infusions of modified cells or viruses carrying the modified genes, as pointed out by this article. http://www.nytimes.com/2005/07/03/books/chapters/more-than-human.html?_r=0


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Indirect pathway of movement and Parkinson's?
So Parkinson's disease leads to the loss of dopaminergic neurons. I understand how the direct pathway (an excitatory pathway) is inhibited, leading to a loss of movement. However, how can the loss of dopamine neurons cause enhancement of the indirect pathway (which enhances its inhibitory effect, leading to a loss of movement)?
I assumed that loss of neurons would decrease stimulation of both pathways.

It's not that simple. There are still several theories out there...each of them fairly complex.

The dopaminergic neurons of the substantia nigra pars compacta are a part of neither the direct nor the indirect pathway. The dopaminergic system rather acts as a modulator between those two pathways. More dopamine steers the system towards the direct pathway, less dopamine towards the indirect pathway.
One of the best explanations of the basal ganglia that I've ever seen were video lectures by Dr. Najeeb on youtube.
explanation of the basal ganglia pathways
pathologies involving the basal ganglia
At the beginning of the second video there is a short review of the pathways he explains in the first one. At 5:06 he starts talking about Parkinson's disease.
A paper about the topic:
Functional organization of the basal ganglia: Therapeutic implications for Parkinson's disease (Obeso et al. (2008)


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Accurate surveys of urban pigeon and bird populations
I've been working on an assignment to develop mathematical models of urban pigeon populations. (As a disclaimer, this is part of a math course, not a biology course). I already understand the mathematics behind this and have developed several plausible models, but I'm at the stage where I need more detailed data in order to validate my models.
It's surprisingly difficult to find accurate population dynamics data for urban pigeons (especially given my inexperience with this kind of a literature search and general "unsophisticated" understanding of biology).
I do have access to some journals (e.g., via my university library, Google Scholar and Amazon.com), but the best resource I've been able to come up with so far is Illinois Birds: A Century of Change (published by the University of Illinois). The books on urban bird populations I've found so far all seem to be targeted to bird watchers (which I'm not).
Is anyone aware of a detailed/accurate data set on population dynamics (either of urban pigeon populations in particular or of urban bird populations in general)?

What kind of data are you looking for exactly? Spatial distributions, temporal patterns, population demographics, life histories, community data, behavior, etc. ??

@theforestecologist Primarily population demographics and trends.

@theforestecologist thanks for editing BTW, it's definitely an improvement (I'm still new to the field)

Everything I've ever read about pigeons complains about how poorly studied they are, so you may be out of luck

@iayork I was afraid of that. The best I've been able to find so far is general bird surveys that include attempts to survey the pigeon population (e.g. the study I found of birds in Illinois; that data seems pretty good but it's unfortunately really geographically narrow); is that the best I'm likely to do?

You can find population data for lots of species at The Global Population Dynamics Database, which can be used to test and fit population models. When searching for Columbidae (the dove family) I find 16 datasets of different lengths, but none for Columba livia though.
To search and download data you first need to register for a user account.

Thanks; out of curiosity, do you know why pigeons tend to be so poorly studied? It seems like the fact that they live mostly in urban environments (at least in areas like Illinois that mostly lack cliffs) would make them easier to study if anything.

I don't know, but I assume it's because familiarity breeds contempt. No one cares about pigeons, any more than you'll find people doing detailed surveys of Norwegian Rats.  It's unfair because (I've only recently learned) they are fascinating birds in many ways, but there just doesn't seem to be any interest in describing them.


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How to automatically obtain the "kingdom" of a species from its name?
I'm looking for a simple way (such as a database) so that a program can get the kingdom of a species, knowing its name (such as "Prunus persica"). As a matter of fact the species I'm concerned with are the ones in the miRBase database.

Bear in mind that since plants and animals use different nomenclatural codes, it is possible (but extremely rare!) for the same species name to be present in both Plantae and Animalia. Here's an example: https://species.wikimedia.org/wiki/Centropogon_australis

@Gaurav huh, really?? I always wondered  if this ever happened.  cool fact!

I've seen several such examples earlier, one can I remember is Acetabularia, an algae; and a fungus (later the name for fungus hasbeen rejected, new name Cyphellopus). IMO there should be some universal rules, too.

Here's a paper about cross-kingdom homonyms: http://www.mapress.com/bionomina/content/2011/f/bn00004p072.pdf

You could try the Catalogue of Life

The Catalogue of Life is the most comprehensive and authoritative global index of species currently available. It consists of a single integrated species checklist and taxonomic hierarchy. The Catalogue holds essential information on the names, relationships and distributions of over 1.6 million species. This figure continues to rise as information is compiled from diverse sources around the world.

You can export the search results (in the above example indicating Kingdom Plantae for search term "Prunus persica") and analyze the exported table in your program of choice.


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Bird species ID in the Northern Territory, Australia
I was visiting Darwin, NT, Australia a few years back and I encountered this bird. I must say it was in Darwin's Botanical Gardens, so I can't be absolutely positive the Northern Territory is its original habitat. However, I'm pretty sure it's a NT native, as the whole Gardens were packed with, and dedicated to NT's wildlife.

The photo is kind of dark and a bit fuzzy due to poor lighting conditions. I already tried to digitally enhance it by removing shadows and so forth.
I tried Google Images reverse search to ID this bird, but I'm not a hero with that tool. Although it looks a bit like it - it's definitely not a Jabiru.

That's an Australian White Ibis (Threskiornis moluccus).

It's widespread across much of Australia:

You can find more info on Wikipedia.

Can't accept it yet due to system limitations -- but wow that is quick - thanks!

I was just in Australia this year, so I recognized the species fairly quickly. "A Pocket Naturalist Guide: Australia Birds" was a useful tool while I was there.

Oh thanks for that pic of Oz - I was already wondering whether it truly was native in SE and NT - it's a big country!


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Jamaican/Caribbean insect, plant identification keys/field guides
Where can I find plant and insect identification keys and Field guides for Jamaica specifically, or for the Caribbean as a whole?
I've searched Amazon and google for Jamaican and Caribbean identification keys/field guides, to no avail. I'm taking pictures of organisms in my backyard, and I want to identify them and post them to iNaturalist. For my own sake I want to be able to identify them myself, prior to and independent of the (long) wait for a community ID to be given and confirmed.

I've never been to nor botanized Jamaica or the Caribbean, but a quick Google search turned up the following references for Jamaican plants:

Iremonger, S., 2002. Guide to the Plants in the Blue Mountains of Jamaica. University of West Indies Press, 280p. ISBN: 9789766400316
Fawcett, W. and A. B. Rendle. 1910. Flora of Jamaica, containing Descriptions of the Flowering Plants known from the island. Longmans & Company. Found here.

You can also find a list of Jamaican species on Wikipedia and a list of medicinal plants in Jamaica here.

I've never seen "botany" in verb form as botanize/botanized; I like it.

@Bryan apparently you didn't like it enough to upvote :p. But yeah, "botanize" is quite commonly used among plant folks. I never really thought it strange, but I guess if you consider ornithize (we usually say "birding") or herpatize ("herp hunting"?) which aren't commonly used, it does seem kind of odd 0.o

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


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What type of animation software is used to create these molecular motor motions?
Recently, I came across this video on molecular motor motion. Can someone suggest software that can do similar animations? I am not sure what they (at Harvard Medical School) used but the animations are really cool.

I'm voting to close this question as off-topic because it is not about biology.

Most any reasonable animation/modeling software can handle this sort of animation. I have developed an educational iOS app with interactive biological macromolecules, including several animations. Here is how I would approach this, I suspect something similar was done here.
The models are likely built up from PDB files, or equivalent. These files allow viewing and manipulating large molecules in 3D with special viewers.  Many 3D modeling/animation apps can also view and convert these molecules into polygonal models that can be used as components and then animated within the app. I use Cinema 4D, not cheap. There is a free, downloadable program called Blender. I'm sure Blender can handle the animation but not certain whether it can read and convert the PDB file. If not, there may be other options for this.
This is not a challenge to be taken lightly. The person doing the animation you reference also knew how to assemble the parts as well as how the movement is effected. There is also a steep learning curve to using this type of software.

Thank you for the suggestion about Blender. I did a search on importing PDB files into Blender. It seems like there is an extension called atomic blender that does just this.


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Why do eyes close when we sneeze?
It is a behaviour that is very difficult to control. We can't sneeze with eyes open. Is it a reflex of brain to protect the eye from possible injury in sneezing motion or the neural pathway for sneezing is programmed to do so?

You might be interested in this.

So there is no explanation?

There are lots of things, most of which are indeed quite common like this one, about which we don't know yet. But there are proposed reasons and mechanisms for them. I am busy right now, so somebody will definitely give you a nice answer for this.


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Taxonomy and 'breeds' of animal species
How do taxonomists classify breeds of organisms in a species? When talking in such depths about organisms (using RNA and DNA), don't they have to unavoidably do it?
I read in another question that all the breeds of dog we domesticate belong to the same species. But they (the dogs) certainly have very apparent differences. Don't they?
So how do taxonomists handle/consider these 'breeds'?

Take at look at this.


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Identification of an Australian pigeon in the NT
This pigeon was spotted in Darwin, NT, Australia. I am not able to solidly identify it using my books or google searches. My best bet is a Torresian Imperial Pigeon (Birds of the NT website).

Do you have any other pictures?  Torresian Imperial Pigeon seems like a fair guess, but a better shot of the beak,  feet, or -- more importantly -- its tail feathers or covert feathers could help confirm that.

@theforestecologist - I know! But unfortunately this is the only pic I have from the bird. A pity for sure. The tail of the imperial pigeon is black and that seems a strong marker imho, but I don't have it on camera.

I'm just not sure too many other species are all white with black under the wing like that. The next best guess is the closely related Pied imperial pigeon. That species  is more concentrated in SE Asia,  but seems to show up in zoos worldwide, so could be an option in Northern OZ

@theforestecologist - Thanks for all your feedback. I'm not an ecologist - I'm a fake Biologist as I always say (i.e., a medical one) - so please feel free to vote to close if it is too unclear.

I've expanded upon my comments to make a full answer. Hopefully it provides some closure :p.

@theforestecologist - He&& yeah mate, cheers.

Your bird appears to be an Imperial Pigeon of the Ducula genus. Based on the limited angle of the lone picture of your specimen, my best guess as to the species is the Torresian Imperial Pigeon (Ducula spilorrhoa).

The species is a relatively large, pied species of pigeon found in various habitats (forest, woodland, savanna, mangrove and scrub) in Australia (including in the Northern Territory where you saw your specimen), New Guinea and nearby islands.
You can see more pictures, videos, and calls here, as well as additional info here.
Your specimen is unlikely the closely related  Pied Imperial Pigeon (Ducula bicolor) because:

D. bicolor is a  Southeast Asian species

D. bicolor has a bluish grey beak, whereas your specimen and D. spilorrhoa both have a yellow beak.
Note: Your specimen is also unlikely Ducula subflavescens because the feathers are white and not yellow, and it is unlikely Ducula luctuosa because that species is endemic to only a few islands.


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Do sulfate reducing bacteria ingest their sulfate as solid, or as dissolved in water?
Do sulfate reducing bacteria ingest their sulfate as solid, or liquid or gas?
I understand that almost all forms of sulfate are solid.. and sulfate can be dissolved in water(thus no longer solid, but liquid).
So, do sulfate reducing bacteria ingest sulfate in its solid form, or do they require it to be dissolved in water?
A similar question in fact, for nitrifying bacteria, though if that's complex I might make it a separate question.
Also, even though it's respiration(which tends to be associated either with the breathing process - in the case of physiological respiration, or with having breathed prior - in the case of cellular respiration), here it's not using a gas. So i'm curious if biologists ever use the word "breathing" for such a process.  wikipedia for example, says https://en.wikipedia.org/wiki/Sulfate-reducing_bacteria  " In a sense, these organisms "breathe" sulfate.." I wonder if biologists use the term 'breath' in such a general sense(to include consuming a substance dissolved in water), or only in a specific sense of gas or air, or if they don't use the term 'breath' at all. So, how strictly is the term breath defined in biology.

Sulfates in water would not be liquid. Their melting points are far to high. When a sulfate dissolves into sulfate ions and some cation such as potassium, we say it is solvated, not liquid. Sulfates would also not be present as gasses due to their ionic nature as well as high molecular weights. So that leaves solvated sulfate ions and solid sulfates that have not completely dissolved.
To be ingested in bulk as a solid would require endocytosis which is not performed by prokaryotes: http://faculty.ccbcmd.edu/courses/bio141/lecguide/unit1/proeu/proeu.html
Further research indicates sulfate, as ions, enters the cell through permeases: http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.532.943&rep=rep1&type=pdf
Edit: Here's some files to help with the idea of how ions and other molecules enter cells. Again, bacteria do not engulf substances whole, in the process of endocytosis, such as eukaryotes are capable of. Here is an image of a nitrate ion within a transport protein. Only a few amino acids of the protein are shown here, the actual protein is much larger and spans across the entire membrane creating a channel for the ion to enter. http://www.rcsb.org/pdb/ngl/ngl.do?pdbid=4U4W&preset=ligandInteraction&sele=[NO3]
Here's another channel, aquaporin, which allows transport of water across the membrane. http://pdb101.rcsb.org/motm/173 The top left image shows the channel in the protein leading to the interior. The third image down shows the interaction between the water and the amino acids (backbones only are shown) which facilitate the water's passage.

what about salt.. when it breaks into Na and Cl, ions, are they also still solid? also I heard that most sulfate is solid but "dihydrogen sulfate" is a liquid, is that wrong?

@barlop. No. Solids are formed when the particles have close neighbors that have fixed positions relative to one another. When in water, most ionic substances, such as table salt, have their ions pulled apart from one another by attractions to the water molecules. Sulfate ions, being negative, will be surrounded by the partial positive charges on surrounding water molecules. This allows them to be delivered one at a time to the proteins, permeases in the case, that transport them into the cell

is it the same situation with nitrifying bacteria - the bacteria can consume small amounts of solid nitrate, and larger amounts of solvated nitrate? Also in the case of a tiny bit of solid nitrate(not dissolved), does it need to be in water for the bacteria to accept it, or can it accept it dry?

@barlop. I suspect the presence of a certain amount of water is essential. Even if most of the neighboring nitrate is in solid form, the nitrate ions would have to be peeled away as solvated ions before interacting with the prpteins that transport them into the bacteria. https://www.ncbi.nlm.nih.gov/pubmed/11289303

can you comment on the use of the term breathing (see last paragraph of my question)

@barlop. The process of bringing these substances into the cell is called transport. Breathing would not seem appropriate. Cellular respiration and breathing respiration are two entirely separate processes even though the breathing variety provides oxygen and eliminates the CO2 associated with cellular respiration. The Wiki reference is a useful simile but I've never heard nor read of the term breathing actually being seriously used in this manner.

Let us continue this discussion in chat.


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Why does Thiamine pyrophosphate have phosphates?
The reactions that Thiamine Pyrophosphate(TPP) catalyses are associated with the thiazolium ring. Why is pyrophosphate a part of the structure of TPP then? What benefit do the additional phosphates give TPP? Is there some reaction with TPP that does not center on the thiazolium ring?

The diphosphate* part of TPP does not serve any catalytic function but, rather, helps bind the coenzyme to the enzyme. In this respect it is similar to the non-nicotinamide portions of NAD/NADP (think, why the P?), and represents a general theme, rather than a unique instance.
A pertinent paper that I found from an internet search unfortunately requires access to an academic library. This is P. Arjunan et al. J. Mol. Biol. (1996) 256, 590–600, and describes the crystal structure of yeast pyruvate dehydrogenase. I quote the following from it:

The roles of Asp444 and Asn471 in binding the cofactor to the enzyme, observed in PDC and in their counterparts in transketolase (Lindqvist et al., 1992) and pyruvate oxidase (Muller & Schulz, 1993), conclusively establish the importance of a conserved sequence roughly 30 residues long (Hawkins et al., 1989) starting with GDG and terminating with NN (Figure 8). These residues are among the few highly conserved in all ThDP-dependent enzymes and form the Mg2+ binding site which assists in anchoring the diphosphate to the protein matrix.

And the Figure 8 referred to is a stereo-pair diagram (squint at the centre — with your specs off if you wear them — to see it in 3D):

￼
This also has a Pfam designation. The structure was deposited in the Protein Data Bank as 1PVD, where there is a useful diagram showing the interaction of the protein and magnesium ion with the phosphates:

*The paper quoted refers to the pyrophosphate part as “diphosphate”, which I assume is the standard chemical nomenclature.


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Flow cytometry analysis

I've performed an experiment wherein I have stimulated cells (cell line) with a drug across different time-points - in its unmodified (Drug) or modified form (H-Drug or M-Drug).
All cells are seeded at the same concentration and all are harvested for analysis on the same day.
Method:

Cells were seeded on the same day. Cells were stimulated at 3:00 on a Wednesday (24 hour timepoint). Cells were then stimulated at 09:00 am on Thursday (6 hour timepoint) followed by 12:00 pm Thursday (3 hour timepoint) and so on until 3:00 pm on Thursday - at this time ALL cells were harvested and put into separate tubes according to what they were stimulated with and when e.g. 3 hour M-drug.
All tubes were analysed in sequence to measure the percentage of cells in that test tube that stained positive for that drug (i.e. as a means of measuring drug uptake)
Question:
I have measured the percentage uptake of a drug at different time-points (0.5 - 24 hours) for the three drug variants. % uptake is taken as the % of cells that stain positive for that drug
What would the correct stat test be? Would a 3-way ANOVA make sense?

Correct me if I'm wrong but I'd just do one-way ANOVA for 3 treatments. In a 3-way anova you'd get stats for the effect of [a and b over c], [a and c over b], and [b and c over a]. I don't think your experiment is designed to test these parameters in relation to one another, but whether the modification differ from the unmodified drug.


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Where do B cells produce antibodies?
I was recently at a Leukemia and Lymphoma Society conference where a particular oncologist lecturer claimed that all antibodies are created in the bone marrow (I won't mention his name, as he was a great lecturer, and I don't wish to sully his name if he happened to be wrong on this particular point).
Wikipedia seems to indicate that antigens are produced in "Secondary Lymphatic Organs" or occasionally in the bone marrow, but I've been misled by Wikipedia before.  It seems to me that evolution would favor creating antibodies close to the infection, and not far away in the bone marrow or lymphatic organs (how would the antibodies "know" how to get back to the original infection?  It would be very inefficient to send antibodies all over the body if the infection is localized.)
My questions is: Could someone "map out" the travel of a typical B-cell throughout the body from the time the B-cell detects an antigen up to the time it produces antibodies (and if it later stops producing anti-bodies, please include that)?

Related question:  http://biology.stackexchange.com/questions/15390/what-cell-types-produce-immunoglobins-and-where-are-those-cells-found

You are asking multiple questions here. The answer to the first two questions can be found in the post mentioned by @Roland. Please [edit] your post so that it does not contain multiple questions.

I'd be careful drawing conclusions about the location of events in the life of a B-cell from the answer to the question linked above. It's generally good, but has an important error if it is being used to answer this particular question.

The oncologist seems to be incorrect.
Antibodies are created all over the body inside secondary lymphatic organs (lymphatic nodes) or any other mucosal associated lymphatic tissue (MALT).
B cells mature in the bone marrow and finish their maturity in the periphery, then they can live in lymph nodes, MALT, spleen, omentum or other structures and they can create antibodies in all of those structures.
In regard of your localized infection question, you are right. When a pathogen enters the body the B cells closer to it are in the lymph node that is closer to that site and thus there is where the antibody response will take place. That is why when you have a sore throat (throat infection) your tonsils are swollen (they are lymphatic organs too).

While your answer is good, it would be great if you could add some sources to it.


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Determine percentage of crow hybrids
We had in class following question which I had no idea how to get to the correct answer:

The carrion crow and the hooded crow are fertile together,  but their
  reproductive success is reduced by 50%. In a certain region exist
  two populations of both species of roughly the same size. Thus,
  mixed couples occur in about 10% of all cases. What is the percentage of
  hybrids in the F1-generation?

(Translated from German.)
I thought it would be something like 5/95 = 5,3% but apparently the answer is 1%. Why?

why do you think it would be 5/95? and how, according to you, can the answer be 1%? please show some research effort before asking question here.

1% is the answer according to the solution. 5/95 because 90% of the couples have 100% success, and 10% have 50% sucess.  @another'Homosapien'

Homework questions are off-topic here unless you show some research effort. Tell us what research effort you have put on the question, lest this question is likely to be closed.

Well I told you what I thought was the correct approach. I did not find any hints in our material. I did further research before posting here. I didnt find any source dealing with mathematical discussions of this topic. Further, to me my solution seems correct. @another'Homosapien'

In order to make your reasoning clearer, you should use more formal notations and explain your thinking step by step. Here's a proposition.
Let's use the following notations :

$C$: the total number of couples (mixed and not mixed)
$r$: the reproductive success
$F1_h$: the number of hybrids in the F1 generation
$F1_{nh}$: the number of non hybrids in the F1 generation

You are looking for the percentage of hydrids in the F1 generation, which is:
$x = \frac{F1_h}{F1_h + F1_{nh}}$
You know that $10~\%$ of the couples are mixed couples and that their reproductive success is reduced by $50~\%$. This can be written:
$\begin{cases} 0.9\cdot C \cdot r = F1_{nh} \\ 0.1\cdot C\cdot \frac{r}{2} = F1_h \end{cases}$
Thus: $\displaystyle x = \frac{F1_h}{F1_h + F1_{nh}} = \frac{0.05\cdot C\cdot r}{C\cdot r\cdot 0.95} = \frac{0.05}{0.95}$
This is indeed the result you suggested. So the correction you were given might not be correct. Or maybe there was some more information in your homework that you ignored...