How does cold water help to overcome high fever?

Fever is triggered when pyrogens cause release of prostaglandin that acts on hypothalamus (which is the center of thermoregulation).

Fever assists in the healing process by:

enhancing phagocytosis
decreasing negative effects of endotoxins
stimulates proliferation of lymphocytes

Although is a good reaction, when the temperature gets too high it could determine negative effects, like convulsions at children. Brain damage appears when the temperature rises as much as 42 degrees Celsius, and most febrile conditions go up to 40.6 degrees Celsius.

So fever must be kept under control, and cold water helps lowering body temperature. Lowering the temperature will prevent negative effects of fever. Cold water is a symptomatic treatment for fever. Most important is to determine cause of fever and do an ethiological treatment.

Source: Wikipedia contributors, "Fever," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Fever&oldid=614212619 (accessed June 27, 2014).


Enzyme kinetics: Effect of immobilization on kinetic parameters

The main factor influencing the kinetics of immobilized enzymes is thought to be the rate of diffusion of substrate and product towards and away from the enzyme, respectively.

This has been discussed on ResearchGate and an article in Process Biochemistry from one of those in the discussion quotes figures for effects on immobilized laccase: approx. 100x increase in Km and 2–5x reduction in Vmax (as noted in the poster’s comment).

There are several theoretical treatments of the question:

http://www1.lsbu.ac.uk/water/enztech/summary3.html
http://link.springer.com/article/10.1007%2FBF02460071#page-1
http://www.amazon.co.uk/gp/search?index=books&linkCode=qs&keywords=9780849369872


What happens to the absorbed blue and red light in the chlorophyll molecule?

It is glad to say that we can enter to this question due to having of valuable theorem of 1st law of thermodynamics. Energy cannot be destroy but it can convert in to another type of energy.The chlorophyll molecule decide it to, become photo energy to chemical energy.

while happening the electron transport chain electrons are going through the primary receptors. This is not happening as the electrons traveling on a trip, this is really a complicated procedure.While they are passing through the primary receptors some reactions are happening. So from which should be contribute to have energy for this reactions. By the energy of absorbed blue and red lights. So it turns it to chemical energy. It store as ATP, and NADPH. So there is no more way for emit that light away. This scenario  is firm by the following.

Reference
- The Light Reactions of Photosynthesis. In: Biochemistry. 5th ed.


What are the environmental conditions for SARS-CoV-2 to survive?

Because "any" Coronavirus is so dangerous, much research have been done on viruses with similar properties. They are called "surrogates". Because nCoV is new, we don't have any studies, so we need to estimate it's behavior from previously studied similar viruses.

Here:

RH   = Relative Humidity.
Tr   = Room Temperature
TGEV = Transmissible Gastroenteritis (surrogate)
MHV  = Mouse Hepatitis (surrogate)

Viral survival for the TGEV/MHV surrogate:

on stainless steel:      4°C @ 20% RH:  28 days
in water/sewage (TGEV):  25°C: 22 days
in water/sewage (MHV):   25°C: 17 days
contaminated water is a potential vehicle for exposure if aerosols are generated

For airborne Human Coronavirus 229E (HCV/229E):

Optimal survival:  6°C @ 50% RH:
Poor* survival:     20°C @ "High" relative humidity (RH)
(* "poor" in terms of 20°C but varying RH.)

For SARS CoV-P9:

Serum: 96 h = 4 days
Sputum & Feces: 96 h = 4 days
Urine: 72 h = 3 days

For SARS-CoV (GVU6109):

in diarrheal stool (at low pH): 4 days
in respiratory/air droplets:  >7  days @ 20°C (Tr)
in respiratory/air droplets:  >20 days @ 4°C

  "The main route of transmission of SARS CoV infection is presumed to be respiratory droplets. However the virus is also detectable in other body fluids and excreta. The stability of the virus at different temperatures and relative humidity on smooth surfaces were studied. The dried virus on smooth surfaces retained its viability for over 5 days at temperatures of 22–25°C and relative humidity of 40–50%, that is, typical air-conditioned environments. However, virus viability was rapidly lost (>3 log10) at higher temperatures and higher relative humidity (e.g., 38°C, and relative humidity of >95%)."

  "We and others have reported that infectivity of SARS CoV (SARS coronavirus) was lost after heating at 56°C for 15 minutes but that it was stable for at least 2 days following drying on plastic."

UPDATE: 2020-03-13

From [7]:

  "We found that viable virus could be detected in aerosols up to 3 hours
  post aerosolization, up to 4 hours on copper, up to 24 hours on
  cardboard and up to 2-3 days on plastic and stainless steel. HCoV-19 and
  SARS-CoV-1 exhibited similar half-lives in aerosols, with median
  estimates around 2.7 hours. Both viruses show relatively long viability
  on stainless steel and polypropylene compared to copper or cardboard:
  the median half-life estimate for HCoV-19 is around 13 hours on steel
  and around 16 hours on polypropylene. Our results indicate that aerosol
  and fomite transmission of HCoV-19 is plausible, as the virus can remain
  viable in aerosols for multiple hours and on surfaces up to days."

For SARS-CoV-2:
Experiments were performed @ 40% RH and 21-23°C.

Copper (Cu):      4 hours
Stainless (Fe):   48 hours (2 days)
Cardboard:        24 hours
Plastic:          72 hours (3 days)
SARS-CoV-2 is most stable on plastic and stainless steel.

References:

[1] 20xx https://aem.asm.org/content/76/9/2712.short
[2] 1985 https://www.microbiologyresearch.org/content/journal/jgv/10.1099/0022-1317-66-12-2743
[3] 2005 https://academic.oup.com/cid/article/41/7/e67/310340
[4] 2009 https://www.sciencedirect.com/science/article/abs/pii/S0043135409000785
[5] 2010 https://www.hindawi.com/journals/av/2011/734690/
[6] 2003 https://www.ncbi.nlm.nih.gov/pubmed/14631830
[7] 2020 Aerosol and surface stability of HCoV-19 (SARS-CoV-2) compared to SARS-CoV-1


Dorsal vs Posterior and Ventral vs Anterior

Short Answer
This page on wikipedia gives a good synopsis of these concepts.
The confusion lies in the fact that many websites on anatomy discuss/describe/define these terms in relation to humans. However, in quadrupeds and fish (and  birds), Anterior/Posterior lies orthogonal to Ventral/Dorsal and are instead synonymous with Cranial(Rostral)/Caudal. Examining the etymologies of the 4 terms in question will demonstrate why there seems to be an inconsistency in their usage:
Ventral -> "belly" side
Dorsal -> "back" side
Anterior -> "before" or "toward the front"
Posterior -> "after" or coming after (opposite to) the anterior

Based on the body orientation of the organism (often associated with forms of locomotion), these terms can sometimes overlap (as in bipedal humans) but often lie perpendicular to each other (as in quadrupeds, fish and most birds).

A note about quadrupedalism (as summarized on Wikipedia [my emphasis added]):

Although the words quadruped and tetrapod are both derived from terms meaning "four-footed", they have distinct meanings. A tetrapod is any member of the taxonomic unit Tetrapoda (which is defined by descent from a specific four-limbed ancestor) whereas a quadruped actually uses four limbs for locomotion.

 Long Answer
Think of ventral (Latin venter = "belly") as being associated with the belly side (with belly referring to "swelling" or "inflating") -- or typically the side of the organism containing the digestive and respiratory organs. Dorsal (from Latin dorsum meaning "back") refers to the body region/"side" opposite that of ventral (and typically called the "back").
Anterior (from Latin ante meaning "before" or "in front of") refers to the "front" of the organism (i.e., the part of the organism you'd encounter 1st or before other body regions). Posterior (from Latin, comparative of posterus ("following") from post- meaning "after") is the opposite and refers to the part of the organism encountered "after" (or opposite) the anterior side.
Depending on the orientation of the organism, these terms may be synonymous in some instances but be orthogonal in other instances).

Sometimes anterior/posterior would be synonymous with ventral/dorsal, as is the case in humans or other bipedal organisms.
In other instances (e.g., in quadrupeds, fish or birds), posterior/anterior lies relatively orthogonal to the dorsal/ventral orientation. In these cases, dorsal/ventral is instead synonymous with superior (from Latin superior, comparative of superus "that is above," from super "above") and inferior (from Latin inferus meaning "low" or "below").

Often in these cases, anterior/posterior are instead associated with caudal/cranial (common alternatives for cranial  include cephalic or rostral).  Caudal (from Latin cauda meaning "tail") refers to the tail side of the organism (i.e., the side associated with coccygeal vertebrae or sometimes simply the side of the organism where waste is excreted). Conversely, cranial (Greek kranion = "skull") or  cephalic (from Latin cephalicus, from Greek kephalikos, from kephalē meaning "head") refer to the side of the organism containing the head. Rostral (referring to rostrum from Latin meaning "beak") is another synonym for cranial and refers to being "situated or occurring near the front end of the body, especially in the region of the nose and mouth or (in an embryo) near the hypophyseal region."

Some notes:

This English.SE question addresses etymology of the suffix "-erior."

You can find a pretty good list of anatomical etymologies here, here, here, or by simply searching "[word of interest]  etymology" in Google.

Also, this Bio.SE post addresses anatomical terminology usage in plants and body organs.

More generally, a frontal plane always divides an organism into ventral/dorsal.

Although these terms differ between shapes/orientations of organisms, using such terms for more specific body parts (e.g., heads or feet) are not always as inconsistent.

For example, anatomical positional terminology for brains is consistent across organisms.

One final note:
This approach to anatomical positional terminology only works with bilaterally symmetrical organisms. See here for terminology usage for other organisms.


Some mollusks have lungs and can use breath for nest building, defense and diving. They have 100 times less neurons than arthropods.

semi-aquatic insects can control air for going under-water, and some spiders, beetles and spittle-bugs can control bubbles. There are even shrimps that snap at water to produce bubbles.

Fish can hoover and squirt out targets using gulps, without even having lungs, build bubble nests and they also have a swim bladder that they can use to control buoyancy. Human lungs and fish swim-bladders are thought to have evolved from primitive fish that gulp air: https://mainichi.jp/english/articles/20160819/p2a/00m/0na/004000c

It illustrates early vertebrate control of breath-like mechanisms. It's sometimes their main mode of interacting with objects and prey.

Some reptiles hold their breath under water and use bubbles, i.e. iguanas, water anoles and crocodiles. Some reptiles can vocalize, i.e. gecko's : https://www.youtube.com/watch?v=0Q_1KW0Q-10
Scientists don't think that they have much conscious thought.

Amphibians can hold their breath for long periods to swim and use the throat to hoover prey, and most frogs can vocalize: https://youtu.be/y7F0ObBiHio

orang-utans can blow bubble gum, swimming birds and mammals can often do a lot of bubble stuff.

Perhaps the truth pivots on knowing what animal consciousness is, which is amply debated on the web.

Manual involves hands. Consciously and voluntarily involve thought, and those are the words used in biology.

Animal will and conscious reasoning is one of the most controversial topics in science, and scientists still argue both ways, because they CAN argue, and there is no agreed measure of consciousness.


This is a Burrowing Mayfly nymph (order Ephemeroptera), more than likely of the family Ephemeridae.  The Bugguide site has very few photos of nymphs, but you'll find a near miss here (the species shown is not Californian, but the related Ephemera simulans Walker, 1853 is; see here for other possibilities [you'll want to look for nymph photos of the species listed from "USA: SW"]).


Interpretation of picture of human chromosomes

The picture can be a bit misleading because it represents 22 autosomes (autosome = non-sexual chromosome) while there are 22 pairs of autosomes (so the homologous chromosome is not represented). And it represents the whole pair of sexual chromosomes (the individual is a male).

homologous chromosome

For each autosome represented, there is another one which would be its homologous chromosome.

Sister chromatids

As you can see, each chromosome looks like an X. The right and left side of this X there are chromatids (two chromatids per chromosome here). The chromatids are attachedf by the centromere.

Note

Please note that 1) chromosomes looks like they are represented here only during the metaphase (when they are condensed). 2) A chromosome is not always made of two chromatids. Sometimes it is made of single chromatid only. It depends on the moment in the cell life cycle.


Slow-oxidative fibres vs fast-glycotic fibres

This is well-explained at the Wikipedia page on skeletal striated muscle.

  There are two principal ways to categorize muscle fibers: the type of
  myosin (fast or slow) present, and the degree of oxidative
  phosphorylation that the fiber undergoes. Skeletal muscle can thus be
  broken down into two broad categories: Type I and Type II. Type I
  fibers appear red due to the presence of the oxygen binding protein
  myoglobin. These fibers are suited for endurance and are slow to
  fatigue because they use oxidative metabolism to generate ATP. Type II
  fibers are white due to the absence of myoglobin and a reliance on
  glycolytic enzymes. These fibers are efficient for short bursts of
  speed and power and use both oxidative metabolism and anaerobic
  metabolism depending on the particular sub-type. These fibers are
  quicker to fatigue.

In the terms used in the article, the Type II fibers rely on anaerobic, glycolytic metabolism, whereas the Type I fibers use oxidative metabolism which, of course, requires mitochondria for the TCA cycle and oxidative phosphorylation.The Type I fibers also contain myoglobin which promotes rapid movement of O2 through the cytosol to the mitochondrial ATP synthase.


Why is arterial pO2 normal in carbon monoxide poisoning?

First, let's think about what pO2 means:

pO2 is not the same as "oxygen concentration." pO2 is the partial pressure of oxygen, you can think of it as proportional to the "number of oxygen molecules per unit area leaving the solution" (or colliding with the side of the container). There is also pO2 for the atmosphere, which is going to be approximately 21% * 760mmHg = about 160 mmHg. Partial pressures are often a convenient way to measure gas concentrations, but that only works when there aren't any other interactions happening, so it's not valid for blood.

When blood comes in contact with inspired air, there are >100 mmHg of oxygen molecules hitting the solution and <100 mmHg of oxygen leaving, so there is a net diffusion of oxygen from the inspired air to the blood. If the gas in the alveoli and the blood in the lung capillaries have the same partial pressure of oxygen, there is no more net transfer of oxygen, they are at equilibrium.

Hemoglobin can't do anything to cause the blood to carry more "partial pressure" of oxygen. What hemoglobin does is to "hold on" to oxygen molecules. These "held" molecules can't leave the solution, so they don't "count" as much towards the partial pressure. Hemoglobin instead allows for a higher concentration of oxygen at the same partial pressure of oxygen. Another special thing hemoglobin does is to change its affinity for oxygen in the acidic environment of metabolically active tissue, releasing O2 at a higher partial pressure than it was initially dissolved at.

If you pumped plain saline through the lungs, it would get to about the same partial pressure of oxygen, but it wouldn't have as many oxygen molecules.

If not enough fresh air is entering the lungs, or if the air entering the lungs is low in oxygen, you would expect the blood pO2 to drop, but this isn't what happens in CO poisoning.

There is also the issue that what actually happens in CO poisoning is that affinity of hemoglobin for oxygen increases, but this is actually irrelevant to the pO2 question. The oxygen tightly bound to carboxyhemoglobin (CO-poisoned hemoglobin) doesn't "count" towards the pO2.


How did the Chromosome #2 Fusion propagate?

Was it necessary for the common ancestor with fused chromosome 2 to
  mate with another creature whose 2 chromosomes fused in a similar
  manner?

Of course not.  People with balanced translocations have kids with people with the wild-type chromosome arrangement all the time.  Such people have some fertility problems, due to problematic meiosis leading to more inviable gametes, but they can still reproduce.

Someone already mentioned Robertsonian translocations to you in your previous question.  Didn't you look it up?

  would they also need to mate within themselves or could they mate with
  the chimp population?

What chimp population?  There were no modern chimps when the fusion happened.

Look, you could ask a million questions here, and still learn nothing.  This board is helpful for people who have a good, accurate framework of the facts of biology, but who want specific holes in their knowledge base filled.  I don't think that's you.  I think you think you know the right answers to your questions, based not on science, but on other things, have imbibed or made up a whole slew of very wrong stuff about biology, and are asking questions here expecting people to confirm your wrong beliefs, trying to trick people in to confessing that mainstream biology is wrong, and you are right.

Picking at one bit or another of evolutionary biology is not going to help you.  You need to start by assuming that a lot of what you think you know about the scientific facts is wrong, and learn the real stuff.  It is not at all easy to get wrong information out of our brains, but until you do, this exercise isn't going to educate you much at all.


Is it possible to Interpret Nerve Signals As to Where They Are Going In The Human Body And What Their Task Is?

I agree with previous comment from com.prehensible but I would like to change the emphasis ever so slightly.
Its great that you 1. get inspired by experiences you find in the world 2. you think about them and 3. you reach out to other people to check if your ideas are correct. This is basically how any scientific project starts.

I don't think that an informal tone is detrimental to serious and precise scientific discussions on any topic, quite the opposite, so I wouldn't worry about talking about animes or high school. Ask away and as you talk more and more with people with the same interests your language will automatically change to reflect more precise and specific objects/subjects.

Nonetheless, and to the point of the previous commenter, I'll try, instead of general statements of form, to point out some specific things you might want to look at in order help you think about your question:

A precise statement of your hypothesis is a must. You almost make a precise hypothesis about different charges and currents. A lot is known in terms of neuronal communication, both at the single cell level as at the group level. I would start from the wiki entry on action potentials it might help you understand exactly how neurons "talk" to each other. Also it might be useful to have a more specific insight on how these cells are physically organised. Again the wiki on the CNS is a good place to start.
You should have a specific idea of a particular experiment that would allow to you to test your hypothesis. Thinking about the experiment will require you to know what is possible and what is not. Usually animes, movies, and books are quite a bit more advanced in terms of what is nowadays possible, hence the word "fiction" in science fiction. Thinking of an experiment also allows you to operationalise your hypothesis, which is science speak for deciding exactly what you will measure and how. This will tell you if you can answer your question as you stated it and is super important to plan an experiment.

If you have these 2 things i.e., a good idea and a doable experiment that would answer your question the hard part is done!
Well... then you will probably need time and money, but that is a different problem altogether...

Answering your question though, yes, it is possible to interpret nerve signals, both in terms of their targets or downstream areas, as in terms of information content they might relay in order to accomplish a particular task. There is a whole field of Neuroscience that studies neural coding and its trying to solve how neurons transmit messages to each other or how they can encode information in general. However looking at the signals by themselves is usually not enough and people are very careful about the particular behavior that is going on while these signals are being recorded, basically it turns out that one needs context to properly interpret the messages that are intercepted.

Good luck :)


3 flaws of genes from the perspective of a programmer

Your individual questions here are reasonable enough - although you could do a bit better at knowing some more details of the systems you are dismissing as 'flawed'. However, I think the bigger problem is your overall approach, which seems to be to make analogies between human-made computers and biological systems and then critiquing the 'missing' parts from biological systems.

Analogies like this are necessarily limited. Take the idea of DNA as 'like' a hard-drive of a computer. The nucleotides = bits, genes = contiguous segments of memory, promoters = pointers, etc. Where does this model go wrong?

Well, hard-drives are not (currently!) self-assembling structures that read themselves by coding for more, smaller fragments of hardware that additionally compress or expand parts of the structure of the hard-drive according to which part needs to be read. Moreover they don't do this while floating in liquid and self-repairing from chemical and radiation damage.

There is an excellent book called "Cats' Paws and Catapults: Mechanical Worlds of Nature and People" by Steven Vogel that covers this kind of flawed analogical reasoning between biological and human-made systems. It's not that such analogies are useless, but it is very important to recognise the limitations and fully understand why certain design choices are made by biological systems due to the particular environmental and evolutionary constraints that they work under.


Statistics: How are protein species distributed over cell types?

From my searches, there is no single resource that includes an atlas of all human proteins produced across all human cell types.  However, there are several recent mass spectrometry studies that look at cell-type-resolved proteomes for specific human and mouse tissues that provide some insight into the distribution of proteins across different cells.
A Cell-type-resolved Liver Proteome
This study identified between 6200 and 8500 mouse gene products in each of four cell types -- hepatocytes, hepatic stellate cells, Kupffer cells, and liver sinusoidal endothelial cells -- and a total of 10,075 gene products across all four cell types.  Figure 1D shows that there is significant overlap between the proteomes; 5,246 proteins (52.1%) are shared by all four cell types, and only 1,451 proteins (14.4%) are cell-type exclusive in this set.  Besides cell-resident proteins, the authors also report secreted proteins unique to hepatocytes and Kupffer cells.  These results by-and-large corroborate an earlier publication, Cell-Type-Resolved Quantitative Proteomics of Murine Liver, where the authors reported 8,338 of 11,520 (72.4%) proteins were common to the five hepatic cell types tested.
Cell type- and brain region-resolved mouse brain proteome
This study looked at four types of isolated neurons from specific regions of the mouse brain as well as five types of primary cultured neurons.  Of 13,061 total proteins, 10,529 (80.6%) are common to the five cultured cell types tested, and only 194 (1.4%) are unique to a single cell type.  Figure 2D makes clear that protein abundance across cell types - not just binary presence/absence - is important to cell identity.  (More on that below...)
Region and cell-type resolved quantitative proteomic map of the human heart
Getting to the human proteins mentioned in your question, this publication analyzed three cardiac cell types and adipose fibroblasts across 16 anatomical regions, giving both spatial and functional perspectives on protein type distribution in the human heart.  Figure 5A, like Figure 1D for the mouse liver proteome paper, shows a great amount of overlap of proteins between cell types:  of 11,163 total proteins, 7,965 (71.4%) are common to all cell types (including adipose fibroblasts), and 617 (5.5%) are unique to one type of cell.  Interestingly, and perhaps not surprisingly, the subsets of proteins unique to specific cells are enriched for cell surface markers. (Related:The in silico human surfaceome)
Social network architecture of human immune cells unveiled by quantitative proteomics
These authors identified more than 10,000 different proteins across 28 primary human hematopoietic cell populations, with three or four biological replicates per cell type, including 17 distinct types of immune cells.  They identified an average of 9,500 proteins per cell type, and, for the immune cells, generated both "steady state" and "activated" proteomes, giving insight into how the proteome changes both across cell types and within each type between states.
To directly answer your question,

How are the protein species distributed over the cell types?

I took the data from Supplementary Table 6, averaged the replicates, converted protein copy-number values to a binary presence/absence matrix, and computed the number of immune cell types (1 - 17) represented by each unique protein ID.  The inset graph combines cell type and activation state labels to ask whether the effect of activation dominates over cell-type differences in proteome divergence.

Presence/Absence, no threshold -- Unique protein distribution across 17 primary immune cells types.  A protein is considered "present" in a cell type if average copy-number value is greater than zero.  Data from Rieckmann et al. Nat Immunol. 2017.

Because the inferred protein copy-numbers from the mass spectrometry data cover a high dynamic range, I also looked at the distribution of proteins that had average copy-number values at least double the zero-depleted cell-type-specific median copy-number value.

Highly abundant proteins -- Unique protein distribution across 17 primary immune cells types.  Protein-cell pairs are only counted if the average protein copy-number is at least double the median protein copy-number for each cell type.  Data from Rieckmann et al. Nat Immunol. 2017.

Taken together, these distributions suggest a few things:

for this diverse set of immune cells, a majority of proteins are present in all cell types when looking at strict presence/absence data
after subsetting for highly abundant proteins, a bimodal distribution appears, suggesting that protein abundance is a better metric for functional comparison of proteomes than a simple binary metric
the proteomes of one cell type between different activation states are more similar than the proteomes of different cell types in the same state

For anyone interested, I've made the cleaned-up data available on Dropbox.
A more complete answer might combine the data from the immune cell and heart cell publications to get a sense of proteome concordance across tissues, but, just from a cursory analysis, differences in protein labels between the datasets would make comparison tedious, so I'll leave that to someone else!


Short answer: probably not.

Long answer: for your body to build immunity against something, it needs to identify it as something harmful to you. Otherwise, how would it know if this is just some random particle in your environment that it should ignore? There are molecular clues that your body uses to recognize better whether something is likely a pathogen (that means it should try to build immunity against) and those are some of the additives (known as adjuvants) present in man-made vaccines.

Also, the route of administration is also important. Things that you eat or breath in are triaged by the waldeyer ring because maybe you just ate something that is alive, but not exactly a pathogen. Dysfunctions in this process (thinking a normal protein is part of a dangerous pathogen) is believed to be one of the possible causes of allergies. Injecting it into your blood-stream often makes it more effective (but there are exceptions: polio vaccine however can be orally administered).

A nice read about this topic is this: The dichotomy of pathogens and allergens in vaccination approaches.

This is perhaps a must read on this topic: What to expect of a good vaccine and how to achieve it.

I'm not really sure what else to tell you. The process you described is a part of the manufacturing of some vaccines, so you are on the right track. But vaccines are hard to make, you can't do it for every disease and involves a lot of experimenting.


Which function do nicotinic receptors have in the periphery?

Short answer
1

Background
Nicotinic recepeptors (nAchRs) are widely distributed in the central and peripheral nervous system. Your question seems to focus on the peripheral nervous system. Taken from (Taylor, 2012):

In the periphery, nAchRs are found in:

Innervated skeletal muscle, especially postsynaptically in the motor end plate;
The presynaptic nerve ending in some motor neurons to control Ach release;
Ganglia at the postsynaptic dendrite and nerve cell bodies, and presynaptically to control Ach release.

Now in your answer the options 2 and 3 are incorrect, as muscarinic Ach receptors regulate gastric fluid secretion (Aihara, 2005) and contraction (Kitazawa et al., 2006). Given that nAchRs are excitatory receptors. In muscle cells, the binding of Ach leads to an opening of the associated ion channel, in turn producing a rapid increase in the cellular permeability of sodium and calcium ions, resulting in the depolarization and excitation of the muscle cell, thereby producing a muscular contraction (source: EMBL-EBI). This leaves only one opion left, namely 1). Since this was basically answering the question by exclusion, below Fig. 1 shows that answer 1) is indeed the correct one through a more positive approach - the top panel clrearly confirms that the sympathetic pathway deploys Acetylcholinergic neurons to stimulate its postganglionic adrenergic neurons.

Fig. 1. Ach in the peripehral nervous system. source: Austin Community College

References
- Ayhara, Gastroint, Liver Physiol (2005); 2886): G1199-207
- Kitazawa et al., Eur J Pharmacol (2007); 554(2-3): 212-22
- Taylor, Primer on the Autonomic Nervous System (3rd Ed. ( 2012}


Can I use TBE to elute a plasmid shipped on filter paper?

In my experience it does not matter if you use water, TBE or TE buffer. Even with a little EDTA in it, it will not mess up enzymatic reactions as the concentration is way too low. TBE/TE buffer usually contains 1mM of EDTA which can chelate 1mM of bivalent cations.
Since you not use the DNA undiluted (which also binds a lot of magnesium needed for most enzymes btw.) this really doesn't affect you in reality (been there, done that multiple times).
Additionally, I would recommend not using this DNA directly but transform it into bacteria first and then do a proper miniprep so you have enough material to work with (maybe even do a few restriction cuts and run it on a gel, to ensure the right identity) and a stock you can go back to if something goes wrong.


Why is ATP produced in photosynthesis used to synthesize glucose?

As far as I can understand your question, you wish to know why a plant cell consumes ATP to produce glucose when it can directly use the ATP as an energy molecule.

ATP is an energy currency and is required in different biochemical pathways. However, it is not a good energy storage molecule. Following are the reasons why production of an energy molecule such as glucose is essential:

Not all parts of the plant are photosynthetic. These non-photosynthetic pzrts need an alternate source of energy. Since ATP is unstable, it cannot be transported to different parts of the plant without degradation.
Since photosynthesis cannot happen in the dark, the plants would require some energy molecule that can be utilized later on, in the dark conditions.
Chloroplasts themselves require ATP in the dark conditions. They express an ATP-ADP translocase that actually imports ATP from the cytosol while pumping out ADP+Pi (See this review).
Plants also need energy storage for seeds. This storage is usually in the form of starch (a polymer of glucose).
Glucose is required for synthesis of cellulose which makes the cell wall of plants.
The glycolytic pathway (including pentose phosphate pathway) produces important metabolites such as ribose (in the form of PRPP, which is important for nucleotide synthesis), pyruvate (which is used to synthesize alanine) etc.
Glucose and some glycolytic metabolites (such as glycerol) also serve as osmolytes i.e. they maintain osmotic pressure in the cell.

Basically, points 4-7 convey that Calvin-Benson cycle not only produces sugar but what it actually does is fix inorganic carbon (as CO2) to organic form (in the form of sugar). So, most (practically all) of the carbon that a photosynthetic plant has, comes from this carbon fixation process and that's how plants are photoautotrophic.


What is the physiological difference between snorting/swallowing cocaine

You can easily google for this question and find plenty of disreputable sources, but this is another case where Wikipedia does an okay job.  There are some misleading and erroneous sentences, but this one basically sums it up:

  Compared to ingestion, the faster absorption of insufflated cocaine results in quicker attainment of maximum drug effects.

Mainly, take a look at this 1981 article.  The researchers gave participants cocaine, measured drug activity, and did then did a great review of the literature.  They found that, like plenty of other drugs, ingesting cocaine results in a slower but longer-lasting effect.

Your stomach is not an efficient route of absorption for things besides water, alcohol, and aspirin; besides, it's highly acidic.


Using evolution of bacteria against themselves

Mutating Bacteria is a very plausible idea. If you mutate a particular strain of 'helpful' bacteria to become extremely positively selected for in the current environment then it is possible that the rest of the bacteria interacting with your new mutated will face heavy competition and eventually die out.

The major hole in the idea however, is that bacteria regularly undergo horizontal gene transfer which makes this idea extremely, extremely dangerous for humans. (If your mutated bacteria accidentally passes on the mutated gene to, say, a bacteria that causes Tuberculosis, it would initiate a pandemic. It is also equally possible that a dangerous bacteria might transfer its genes to your mutated bacteria.) It is generally accepted that mutating bacteria or other pathogens(most of which mutate at high rates) is generally a bad idea, because once released into the environment, the possibilities of the mutation going haywire are high(other mutations might make them dangerous).

Horizontal Gene Transfer: Transfer of genes due to recombination processes like Transduction, Transformation and Conjugation which can occur between bacteria of same or different strains, species, domains. etc


What is mean by the term "an organism's genotype is its specific combination of alleles for a given gene"?

From wikipedia

  An Allele is a variant form of a given gene.

Let's consider a simplified example. There is a gene for eye color and there are different alleles at this gene. The allele for blue eye, the allele for brown eye etc...

In a diploid (see ploidy) individual (humans are diploid), we have two copies of each gene (exception of sex chromosomes). Let's imagine, at a givne gene, there are 3 possible alleles called A, B and C. The possible combinations are

AA
AB
AC
BB
BC
CC

The genotype of an individual for a given gene (I should say locus for the sake of generality) is called the genotype of an individual.

  Is it talking about heterozygous and homozygous[?]

The terms "homozygous" or "heterozygous" are adjectives to define whether, in a diploid genotype, the same allele is found on both haplotypes or not. In the above examples, 3 genotypes are homozygous (AA, BB and CC) and 3 genotypes are heterozygous (AB,AC and BC).

  [I]s it talking about the nuclear bases?

For two alleles to be different, they must differ in their sequence of nuclear bases of course.


Do ants know the direct (approximately shortest) path to their nest from the food morsel?

Terms that may help you research are dead reckoning or path integration. From Wikipedia:

In navigation, dead reckoning is the process of calculating one's current position by using a previously determined position, or fix, by using estimations of speed and course over elapsed time. The corresponding term in biology, used to describe the processes by which animals update their estimates of position or heading, is path integration.

There are many animals and certainly some species of ants that use dead reckoning/path integration for navigation. Here are some papers about the Cataglyphis genus by one scientist and some colleagues:
Wehner, R., & Räber, F. (1979). Visual spatial memory in desert ants, Cataglyphis bicolor (Hymenoptera: Formicidae). Experientia, 35(12), 1569-1571.
Wehner, R., & Wehner, S. (1986). Path integration in desert ants. Approaching a long-standing puzzle in insect navigation. Monitore Zoologico Italiano-Italian Journal of Zoology, 20(3), 309-331.
Müller, M., & Wehner, R. (1994). The hidden spiral: systematic search and path integration in desert ants, Cataglyphis fortis. Journal of Comparative Physiology A, 175(5), 525-530.
Collett, M., Collett, T. S., Chameron, S., & Wehner, R. (2003). Do familiar landmarks reset the global path integration system of desert ants?. Journal of experimental biology, 206(5), 877-882.
The last one on the list is particularly relevant because it seems to show that the ants are not using landmarks as markers of position, because moving landmarks doesn't alter their paths.
My intuition is that the extent of path integration will depend on the environment. Species living in a fairly "flat" terrain can gain a lot from knowing the direction towards their home. In a tree canopy, however, the direction "home" doesn't matter a whole lot if your path is constrained by paths down foliage, etc.
Therefore it's unlikely to be able to make any general statement about ants as a whole group, and better to investigate individual genera/species.
However, the Cataglyphis genus from the papers above live in a desert, and their dead reckoning abilities seem to be the ones most studied (there are many many more papers than the ones I pasted here, try searching Google Scholar for "path integration" ant or "path integration" Cataglyphis).


What is the non-local impact of a large-scale destruction of coral reefs?

Disclaimer: the question is too broad and speculative to some extent, and thus less likely to get complete answer (at least in a single post).

As is already known, thousands (or millions) of species are dependent on coral reefs for their survival and are likely to get extinct (unless they adapt) because of destruction of coral reefs. A short list includes fishes, turtles, sharks, eels, crabs, shrimps, urchins, sponges, algae, and so on1. Now, telling which of them will be immediately affected will be largely speculation, yet the first 5 species to lose the race, as per a speculation, are2:

Butterfly Fish: Species of fish that are obligate corallivores, such as many butterfly fishes (Chaetodontidae), feed exclusively on coral polyps. Obviously, survival would not look good for these fish if their food source disappeared.  Like parrotfish, butterflyfish assist in keeping algae from smothering corals.

Spiny Lobsters: Spiny lobsters rely on coral reefs for protection, especially during their vulnerable molting episodes. These lobsters have a significant role in maintaining a balanced ecosystem. Like sea otters, spiny lobsters are predators of sea urchins, which feed on kelp forests and can destroy them if populations are not predator-controlled. Kelp is important for many reasons, including those listed on OGP’s kelp recipes.

Whales (and dolphins): Many scientific studies have substantiated that dolphins and whales have extreme emotional intelligence. Sadly, their intellect won’t be enough to help these animals if coral reefs are destroyed. Dolphins and most whales (cetaceans) are predatory animals and they are all carnivorous. It’s a fish eat fish world and many fish survive by consuming fish that rely on coral reef habitats. Every species lost will affect another…and another…and many others. So, these come under the indirect adverse effects of coral depletion, since they themselves don't rely on corals.

Whale Sharks: Whale sharks are an important indicator of marine productivity and have a role in the conservation of other marine organisms. Although there has not been adequate research to understand why whale sharks are dependent on coral reefs, it has been shown that decreases in whale shark populations in the late 1980’s and early 1990’s may have been linked to increased rates of coral destruction.

Hawksbill Sea Turtles: Although all sea turtles would be affected by the loss of corals, Hawksbill sea turtles have become critically endangered species and are highly dependent on coral reefs for their food sources, mainly consisting of sponges. Sea turtles play significant roles in their ecosystems in that they help with nutrient cycling from ocean to land, maintaining healthy sea grass beds, and balancing food webs.

Coral reef fishes are in general rather sedentary and territoriality and home range behavior patterns are highly developed. However, many species migrate, often relatively long distances compared to body size and often with spectacular precision. Migrations in reef fishes may be associated with3:

Life history: movements of
planktonic larval stages to reefs or movements of juveniles from nursery areas to reefs
Seasons: precisely timed spawning aggregations drawing fishes to particular locations from wide areas of the reef
Diel patterns: movements to and from feeding or resting areas associated with dawn and dusk.

Another species, which is to be affected, though not immediately, by destruction of corals, is humans(!). As per experts4, coral depletion will bring threat to not only income and economic stability, but also to survival by causing depletion of food and increased risk of coastal disasters, which are likely to kill millions.

Coral reefs also serve many purposes, a few of which are5:

protect coastlines from the damaging effects of wave action and tropical storms
provide habitats and shelter for many marine organisms
are the source of nitrogen and other essential nutrients for marine food chains
assist in carbon and nitrogen fixing
help with nutrient recycling.

Finally, I suppose most of the species will be affected because of depletion of source of food rather than more-than-sufficient amount of something. Also, I was unable to find any simulations of the global consequences of destruction of coral reefs. I hope this much would help!

EDIT: I did some online research, and found lack of research about this topic. But I found a paper regarding relationship between seagrass, mangroves and coral reefs6 regarding life cycle of migratory fishes. From the same:

  Coral reefs showed the highest mean fish species richness and were dominated by adult fish, while juvenile fish characterized seagrass beds and mangrove sites...Our results suggest that connectivity of seagrass, mangrove, and coral reef sites at a species and site levels, should be taken into consideration when implementing policy and conservation practices.

It becomes evident from this research that depletion of coral reefs would certainly affect life cycles of these fishes, which include Scarus iseri (Striped Parrotfish) and Lutjanus apodus (Schoolmaster Snapper), which will, in turn, affect biodiversity in seagrass beds and mangroves, leading to further break in food chain in more diverse areas.

Some researches have also suggested that seabirds might also be on a high rank in this list. Seabirds survive by eating fishes, and studies have shown that increasing water temperatures halt their growth while higher sea levels cause them problems in nesting. Now, it has also been suggested that due to coral bleaching, many fish species which live on corals might either die or move to other places, because of which seabirds could also face survival crisis7.

Another point regarding your demand I'm interested in effects which are not obvious and/or have not been broadly publicized, specifically not been broadly publicized, is that it has now become difficult to find such papers. This topic (climate change) has become so much publicized now that all related papers get attention immediately. So, it is quite difficult to find environmental research papers about climate change which hasn't gained much attention. Yet, I'll keeping on adding more research papers as I find some more.


Do transcripts always start and end with exons?

Most (almost all, AFAIK) mRNAs and lncRNAs start with exons for the reasons already mentioned by David. In a typical splicing event, the nucleotide that is 5' to the splice donor site (lets call it pre-donor) and the one that is 3' to the acceptor site (lets call it post acceptor) are joined together and the intronic sequence between them is removed.

If you look carefully at the mechanism, you'll notice that the pre-donor (i.e. the 3' end of the first exon) renders a nucleophilic attack on the phosphorous of the post acceptor (i.e. the 5' end of the second exon) which leads to the release of the intron.

   Image courtesy: http://mips.helmholtz-muenchen.de/proj/yeast/reviews/intron/spliceo_splicing.html

Therefore there is always an exon preceding an intron, in the transcript.

However, RNA processing can occur via a different mechanism in which the ends are just chopped off. This happens in tRNA processing, where RNAseP chops off a portion 5' to the mature tRNA region, called the leader sequence (see the figure below). I am not aware of such a mechanism happening in the case of mRNAs but a possibility certainly exists. One possible reason for mRNAs not having this kind of mechanism is because their 5' end is capped (co-transcriptionally) and cleavage of the 5' would lead to loss of cap and destabilization of the mRNA (all guesses, though). Similarly, the 3' of mRNAs is polyadenylated which also renders stability to them. Many lncRNAs are also capped and polyadenylated but there are exceptions (mRNAs too).

Since this mechanism is not very common, there is no systematic name for the excised ends. For the case of tRNA, it is simply called the "leader" sequence.

   Image courtesy: Leigh & Lang, 2004


What is the definition of "dry weight" and "dry cell weight"?

According to my Henderson's Dictionary of Biological Terms, dry weight is

  The weight or mass of organic matter or soil after removal of water by heating to constant weight.

So yes, your definition is correct and it is also applicable to cells. The dry weight of cells is the weight left when their water content has been removed by heating.


How can I obtain a uniform bacterial sample?

You could inoculate your sample in a selective medium or an enrichment medium to kill off the unwanted species. Of course, you will need to do a literature search to find the optimum medium for the species of your interest.
Another option is to streak plates like so. With successive 'generations' of streaks, the inoculum gets diluted, so that you ultimately get separate colonies. Each colony is founded by a single bacterial cell: by picking up one such colony, you get a pure sample.
For even better results, combine both the methods described above by first growing in a selective medium and then streaking on a solid medium to get individual colonies.


A very clear description is given in Wikipedia.

The starting point is an alignment for the region under investigation.

A. Basically, to get the height of the stack of letters for every position one has to calculate the degree of certainty about the residue (= degree of conservation) at this position in the sequences belonging to this class. I'll explain what it means:

The key parameter in this context is information. 1 bit of information can be understood as the amount "knowledge" you get when receiving an answer to one yes/no question.

Let's say we have equal proportions of all four bases at a certain position in a set of DNA sequences. To "guess" a base at this position in some sequence we have to ask two binary questions. For example: "is it Pyrimidine?" If 'yes' we'd ask "is it 'T'?" Otherwise: "is it G?". So, when the frequencies are equal we can get 2 bits of information from one observation of a base at this position in a sequence.

If the frequencies are distorted, we already have some ideas about the bases when coming to an individual observation. If we already know, say, that we have just G and A at this position with ratio of 1:1, we can just ask "is it G?", so we get clearly 1 bit. When the ratios are not even (or when the number of alternative states is not 2n), the analogy with the questions becomes much less clear and we have to resort to the very simple formula for Shannon entropy. Intuition and brief inspection of this formula would bring you the idea, that when the ratios of the residues are biased, we always have less information than for the case of equal frequencies (2 in the case of DNA).

Now to estimate the "the degree of certainty" we simply calculate the information based on the observed frequencies of different residues at this position and subtract it from the theoretical maximum (again: 2 in the case of DNA):

certainty = maximal information possible - actual information

This value defines the height of a stack of letters at each position.

The maximum value (2 bits) would be observed when we always have the same base, because "actual information" would be zero (there is no need to ask questions - we "know" the answer anycase). The minimum (0 bits) is when we have no idea about the base. One bit would be obtained if we had, say, just two equally frequent bases. And, for example, the value of 0.6 would be observed if you had, e.g. 68.5% of the time the same base A and in all other case C, G or T with equal frequencies of 10.5%.

B. As you probably already know: the proportions of all alternative bases are shown as relative heights of individual letters.


Why is graft-vs-host so selective against phylogenetically close cells?

Since this has gone unanswered, I'll give my best guess. My guess is that closely related MHC* can still be recognized by CD4/CD8 (while not in distant relatives phylogenetically), but, the MHC + eventual bound peptide will not be recognized as self (with or without bound peptide), since its structure may differ even when binding self-antigen peptides that were exposed to T-cells during central tolerance "traning".
I am very intersted in what the established explanation is including references, and invite better answers if there is competence to produce that.
*in the context of the question, i.e., at species level, within species sufficiently close MHC genes are not attacked at all and compatible.
I'll attach potential reference to my guess that ability to recognize MHC as... MHC, decreases with phylogenetic distance,
Vignali, D. A., Moreno, J., Schiller, D., & Hämmerling, G. J. (1992). Species-specific binding of CD4 to the beta 2 domain of major histocompatibility complex class II molecules. Journal of Experimental Medicine, 175(4), 925–932. https://doi.org/10.1084/jem.175.4.925
that references this,
Lamarre, D., Ashkenazi, A., Fleury, S., Smith, D., Sekaly, R., & Capon, D. (1989). The MHC-binding and gp120-binding functions of CD4 are separable. Science, 245(4919), 743–746. https://doi.org/10.1126/science.2549633
that says this,

"although human and mouse CD4 share a high degree of amino acid sequence identity (19), the murine homolog does not bind gpl20 (11) and does not interact with the human class II MHC molecule HLA-DP as assessed by functional and adhesion assays (20). "


Synthetic life creation - status of attempts

There have been lot's of attempts, no success so far, a few groups are still working on. However, many steps forward have been done in the last decades.

Starting from the Miller experiment which demonstrated that the building blocks of life chemistry can be obtained starting from fairly simple chemical compounds. Following, Luisi and Szostak showed that 1) nucleic acids can polymerize without the help of enzymes and 2) autocatalytic micelles form spontaneously in many different conditions. It is also important to remember the work of Otto that showed how different molecules can self-replicates.

There are many more examples reported in the literature, still, the complete "creation" of life from matter has not been yet accomplished. However, the results from the experimental work done so far suggest that it is only matter of time and lots of combinatorial work. Unfortunately, there are little to no investments in this field. It's very hard to get the funds needed to start an international cooperation (like the one made to sequence the human genome or to build the CERN's Large Hadron Collider) with the goal of actually making life in the lab. I think that the work of a few (uncoordinated) groups will not get to the goal in the next few years.


Cellulose is one of the most common sources of fiber in the nutritional sense. Because oranges are plants, their cells have cell walls, made out of cellulose, so some of the fiber in an orange is surrounding each individual cell. Both vascular cells and pith cells tend to have particularly thick cell walls, so they are probably higher in fiber (this article also suggests that the pith is particularly high in fiber - vascular tissue is probably not mentioned because it is less prominent).


As Mowgli pointed out, a bone marrow transplant involves destroying the patient's own immune system with radiation and, essentially, replacing it with a new one from the bone marrow donor. If you did a double kidney/bone marrow transplant from Alice into Bob, then Bob's new immune system (which is the same as Alice's) would recognize the new kidney from Alice as self (because it is) and not attack it. Yay!

The problem is that, to the new immune system, all the rest of Bob appears to be non-self and will get attacked. This is called Graft-versus-host disease and is at least as serious a problem as organ rejection.


What is the total number of rounds of cleavage during mammalian embryonic development?

It's not a totally answerable question, since some types of cells are going to divide more times than others.  But for an estimate, take as a starting proposition that there are 1 trillion cells in the adult human body. [1]  The average weight for a human is 62kg. [2] Average birth weight is about 3.4 kg.  [3]

So that implies roughtly (3.4/62)* 1 trillion = 55 billion cells in a newborn.

You then take the log base 2 of 55 billion, which gives you the exponent you have to hang on 2 in order to get 55 billion, which is about 35.  Then add one for that additional cell division to get from one to two cells == 36 divisions.

Of course I'm just using math, not biology, so your actual reality may vary.  Certainly some cells will reproduce more often than others, maybe cells actually grow in mass instead of dividing (i.e., baby cells might have less mass than adult cells) so the baby-cell-count could be off, lots of possible sources of error.

[1] http://www.nichd.nih.gov/publications/pubs/fragileX/sub3.cfm

[2] http://en.wikipedia.org/wiki/Body_weight#Average_weight_around_the_world

[3] http://en.wikipedia.org/wiki/Infant#Weight


How much of the Neanderthal genome is living on in humans?

Even though individual humans only have around 2-5% Neanderthal genome, it's not the same 2-5% across people. In total, at least 20%, and perhaps as much as 40% of the Neanderthal genome could be recovered from modern human populations:

  We identified Neandertal lineages that persist in the DNA of modern humans, in whole-genome sequences from 379 European and 286 East Asian individuals, recovering more than 15 gigabases of introgressed sequence that spans ~20% of the Neandertal genome

--Resurrecting Surviving Neandertal Lineages from Modern Human Genomes

However, there are stretches of the human genome that are almost completely devoid of Neanderthal genes. These include male-fertility associated regions (leading to the suggestion that male sapiens/neandertalis hybrids may be been subfertile or sterile):

  Genes that are more highly expressed in testes than in any other tissue are especially reduced in Neanderthal ancestry, and there is an approximately fivefold reduction of Neanderthal ancestry on the X chromosome, which is known from studies of diverse species to be especially dense in male hybrid sterility genes. These results suggest that part of the explanation for genomic regions of reduced Neanderthal ancestry is Neanderthal alleles that caused decreased fertility in males when moved to a modern human genetic background.

--The genomic landscape of Neanderthal ancestry in present-day humans

And some brain-specific regions (suggesting that those are uniquely human):

  Regions depleted of archaic lineages are significantly enriched for genes expressed in specific brain regions ... A large region depleted of archaic sequence spans 11 Mb on chromosome 7 and contains the FOXP2 gene (Fig. 4B), which has been associated with speech and language

--Excavating Neandertal and Denisovan DNA from the genomes of Melanesian individuals


There are two possibilities: First, that an individual develops a mutation de novo and is the first to carry it.
When we talk about recessive expressed allels, than both parents need to have a copy of the allel, otherwise it will not show up in the kids. In this case a mixed population of siblings is to be expected (some carrying both recessive allels, some only one).
However, its most likely, that the eye color at this time was brown. As far as I know, there has been no evidence so far from ancient DNA that this has been different.

The oldest DNAfrom Europe, which has been analyzed and which showed a difference for the eye color comes from Spain (La Brana-Arintero site in Valdelugueros) and is about 7.000 years old. See this report about it. This individual is thought to have an "african" type of pigmentation but blue eyes. The original publication is called "Derived immune and ancestral pigmentation alleles in a 7,000-year-old Mesolithic European."

Another paper claims that the blue eye color comes from a mutation which occured in a gene called "OCA2" in the black sea region some 6-10.000 years ago. See here: "Blue eye color in humans may be caused by a perfectly associated founder mutation in a regulatory element located within the HERC2 gene inhibiting OCA2 expression"
.


What is effectiveness of methyl-alcohol as sporicide?

Methanol (methyl alcohol) tends to lack sporicidal activity on its own. However, fresh mixtures of methanol and hypochlorite, with at least 15% methanol, are known to have low sporicidal activity.

With an increasing methanol concentration, right up to about 50% methanol, the sporicidal activity can be increased. The preparation, however, isn't overly stable and the sporicidal activity will start to decrease after 8 hours. It is thus recommended, should a methanol + hypchlorite mix be used to counteract spores, to only use a freshly prepared solution of 50% methanol and a sufficient amount of (sodium) hypochlorite that provides 2000 parts per million available chlorine in distilled water and allow for a contact time of at least 15 minutes.

Sources:

Russell 1990 - Bacterial Spores and Chemical Sporicidal Agents
Kelsey JC, Mackinnon IH, Maurer IM Sporicidal activity of hospital
    disinfectants Journal of Clinical Pathology 1974;27:632-638.


How does zoo and laboratory animal feeding work?

I volunteered for 3 years at a large mammal laboratory where we diligently tracked the weight and caloric intake of each of our animals. Diets were weighed out each morning and total calories could be calculated based on the known caloric value of the particular food item.

We fed our animals during training sessions and would adjust the individual's food intake based on their appetite/motivation (i.e. if an animal was full, they'd drop the piece of food they earned or leave the session). This would indicate that we could decrease the individual's diet in small increments.

The animals were also weighed each week. Weight and caloric intake were recorded in daily logs using FileMaker Pro. This allowed us to view fluctuations of each throughout the year and compare to previous years. If an animal's weight was a bit lower at a certain time of year than it typically was in past years, we could increase their diet.

Diet items were selected based off of the animals' natural diet.


Which type of test tube should not be used for blood collection?

Your reasoning is sound and correct. The answer key is wrong.

An unclotted blood sample needs something to prevent clotting. Extracellular calcium is required for both the coagulation cascade and platelet activation. It even has its own name in this context, Factor IV. This why EDTA, a calcium chelator, is used in some blood collection tubes to delay clotting.

So, as you say, the most correct answer would be (1): Test tube containing calcium bicarbonate. That is the opposite of the kind of tube you should use for this type of sample.

The answer given by the key, (3): Test tube containing heparin, is incorrect. Heparin tubes are a good choice for plasma and whole blood analysis, as you indicated. Heparin is a good anticoagulant, both in vitro and in vivo.

See this nicely laid out list from UCI medical school for an example of specimen requirements for specific tubes.


Drinking soda triggers tingling on a tiny spot on my upper back... but how?

The skin is a very richly innervated organ, and minor strange sensory phenomena are not exceedingly uncommon.

The thing about sensory nerves is that they can misfire and you seem to feel something when there's nothing there. This actually happens all over our bodies all the time (mostly our brain blocks them out, like it blocks out background noises after a while): an itch for no reason whatsoever (no bug, no bite, no reason) is the most common manifestation of this phenomenon.

Sensory nerves start their journey out of the central nervous system as relatively large bundles coming off the spinal cord, and keep on branching becoming finer and finer as they reach the periphery.

since there's a lot of muscle under the skin, most of these sensory nerves have to come up through muscle.

Sometimes an inflamed bundle of muscle fibers (aka a "knot") will entrap a small branch of a sensory nerve, and the pressure on the nerve will cause it to "misfire", causing a sensory illusion, if you will. If this is the case (if it's in the exact same spot every time) and a slender nerve branch is being squeezed by a muscle knot in your back, you can do a little test on yourself: have someone run a fine sharp object (say the end of a toothpick) softly over an area starting away from the spot going through it. If the sensation changes right on that spot - going from sharp to dull, for example - and does so consistently, that's what's going on. If you have the person map the change of sensation with a pen, the spot will be about the size of a quarter or smaller.

If, however, the sensation is only associated with swallowing, and there's no change to light touch, I have no idea what's going on.

Anyone reading this should know, though, that strange neurological symptoms can be an early sign of MS.


Alpha wave frequency variance in EEG of single subject over period of a few hours?

I noticed that a strong background signal in the alpha-wave range was existent at ~10 Hz, but then after a while of doing other things and coming back to it the strong background signal at 10 Hz disappeared but a strong background signal at a smidgen over 8 Hz was present instead.

Alpha-waves (7-13 Hz) are related to a dozen of things. Here is an easy first experiment for you:

Sit still, stare at a wall, eyes open. Remove sources of noise such as TV, radio, etc.
Repeat the same, but now hold your eyes closed.
Record the signals in both conditions for about one minute.
Compare the power spectrums between the two conditions: you will see a big difference in the alpha power, especially at the occipital electrodes.
This is actually a standard test for resting-state analysis.

Back to the actual question: What you noticed is probably about drowsiness. When one gets sleepy, the alpha power starts to increase. You can try this by watching a boring movie.

  Can alpha wave frequencies vary within a single subject over the course of a single day? If they can, by how much, and under what conditions?

Yes, because of the varying cognitive load, thoughts, sleepiness, emotions, etc. The brain signals vary a lot.

Also notice that all sorts of artefacts (e.g. movement, cardiac, eye-blinks, biting of teeth) have a dramatic effect on the measured signal. If you blink your eyes it produces a signal that has 100x higher amplitude compared to the signal that comes from your brain. You cannot really say much what causes any differences in the EEG unless you would do research-level recordings with research-level equipment.


Its definitely a bovid, most likely an african antelope specifically a Hartebeest or Alcelaphus buselaphus . There are several sub-species but those horns are a dead giveaway. The the horn do vary a bit by sub-species. The Neumann's or Tora hartebeest might be your best bet but I can't be 100% sure. They are all popular hunting trophies since forever and are even kept in some european game reserves so it is not that hard to find there skulls in private hands. Search "hartebeest skull" and you'll find a million of them so you can try for a more exact match.


Ripening bananas artificially: What is the biological theory behind?

Ripening of bananas (and other fruits) is induced by acetylene and ethylene (Ethyne and Ethene) (see reference 1), which acts as a hormone and induces the ripening process. The incomplete combustion of the leaves produces ethylene, additionally the warmth of the process will help the enzymes as well. There is even a paper about this technique (although it is unfortunately not accessible), see reference 2 for more information. Smoking Chambers are routinely used in this process, see reference 3 and 4.

References:

Role of Ethylene in Fruit Ripening
Effects of smoking on some physiological changes in bananas.
Fruit Ripening
Technology for ripening fruits as important as marketing them


Can human brain memory be removed by EMP?

http://en.wikipedia.org/wiki/Electromagnetic_pulse mentions the following natural sources of EMP, which I have ordered by frequency / period, from the shortest to the longest:

Electrostatic discharge from objects coming into contact (normally too small to be of any concern)
Lightning (milliseconds)
Solar flares (hours.) Such flares cause geomagnetic storms (more on this later.)

Several artificial sources of EMP are mentioned, of which the only ones of interest are military:

Non-nuclear weapons. The page links to a general article on directed-energy weapons, which mentions microwave devices for causing pain and for targeted damaging of electronic equipment.
Nuclear weapons. http://fas.org/nuke/intro/nuke/emp.htm gives more information on this, listing three phases.

  The EMP produced by the Compton electrons typically lasts for about 1 microsecond, and this signal is called HEMP. In addition to the prompt EMP, scattered gammas and inelastic gammas produced by weapon neutrons produce an “intermediate time” signal from about 1 microsecond to 1 second. The energetic debris entering the ionosphere produces ionization and heating of the E-region. In turn, this causes the geomagnetic field to “heave,” producing a “late-time” magnetohydrodynamic (MHD) EMP generally called a heave signal.

The same reference also indicates:

  ...the region where the greatest damage can be produced is from about 3 to 8 km from ground zero. In this same region structures housing electrical equipment are also likely to be severely damaged by blast and shock.

As far as I am aware, memory loss was not a major recorded symptom among the survivors of Hiroshima and Nagasaki. The only recent data for sufferers of EMP would be from victims of lightning stikes. While the frequency spectrum is admittedly different from nuclear weapons, victims of lightning strikes are surely subjected to greater magnitudes of EMP than those who managed to survive nuclear bombings (who suffered many other traumas, such as blast waves and radiation.) Those who survive the immediate physical (burns) and neurological (cardiac arrest) effects of lightning strikes must surely be knocked unconscious and be disorientated when they regain consciousness. But again, I am not aware of medium or long term memory loss being a particular symptom.

It is worth comparing the structure of the brain (a fairly homogenous mass of tissue of high water content, relatively conductive) with the structure of electronic equipment (components of ever smaller size and greater resistance in order to save power, surrounded by a nonconductive medium such as air, and interconnected by wires, which serve to channel voltage.) It is unsurprising that the brain is less subsceptible to electrostatic damage than electronic components (electronics workers have to take precautions in order to avoid damaging sensitive components with static discharges from their bodies and clothing.)

The most widespread damage to equipment caused by EMP is from the long-period pulses, which are channeled by electric cables. These act over distances much larger than the size of the human body.

From the last reference:

  ...distortion of the geomagnetic field was observed worldwide in the case of the STARFISH test. ... the signal from this process is not large, but systems connected to long lines (e.g., power lines, telephone wires, and tracking wire antennas) are at risk

and

  The first recorded EMP incident ... nuclear test over the South Pacific ... resulted in power system failures as far away as Hawaii.

http://en.wikipedia.org/wiki/Geomagnetic_storm mentions cases of damage caused by long period EMP, including electric shocks suffered by telegraph operators during solar flare events.

So in conclusion, any amnesia caused by EMP is likely to be caused by normal biological shock mechanisms to individuals unfortunate enough to be electrocuted, and not by any direct electrical effect on the brain itself.


Optimizing Gel Electrophoresis: Ampere, Volts and Buffer concentrations

As far as I know you can either adjust the ampere or the voltage as
both is dependent of the resistance from the buffer. Which means that
I would suggest you to let the voltage as it is.
As the ampere = voltage / resistance and voltage = resistance *
ampere and as you can see that the voltage has to get higher if the
ampere is increased and the ampere has to get higher if the voltage
is increased (at least if I understand it correctly) the travel speed
should be increased the higher the ampere is set.
I would neither decrease nor increase the concentration of the buffer. Maybe easily using another kind of buffer would help you. But this depends on the different samples you are running. Maybe that could help you:
Brody, J.R., and Kern, S.E. (2004). History and principles of conductive media for standard DNA electrophoresis. Analytical Biochemistry 333, 1–13.
The resistance is more or less given. Therefore as far as I know: No.


Has Colony Collapse Disorder (or its equivalent) been noted in other species?

In some ways tangent to what you are asking, but many cases of classical Allée effects (i.e. a positive relationship between population growth rate and population size, see Allée & Bowen, 1932, Drake & Kramer, 2011) should be relevant, especially after your clarification in the comments.

One famous, early example of species collapse and extinction in a colony living species is the Passenger pigeon. This was an extremely common North American bird, estimated to 3-5 billion individuals, and maybe the most numerous bird species on the planet. It was heavily hunted during the 19th century (mainly by netting), which coupled to deforestation of nesting grounds led to a population crash. One of the main reasons for the rapid collapse was probably that the species was a colony nester and depended on large flocks for courtship/reproductive behaviour. This also meant that conservation measures failed when the critical situation was noticed (although hunting bans/restrictions was also weakly enforced). The few remaining wild individuals failed to breed and artificial breeding attempts also failed. The last individual died in 1914 at Cincinnati Zoological Garden (extinct in the wild from ~1900). For more information on the Passenger pigeon extinction see the wikpedia page and Encyclopedia Smithsonian.

I hope you find this example useful, even though the collapse was initiated from hunting. There are many more examples of Allée effects in colony living species that describe similar effects, but maybe not as strikingly as the Passeger pigeon case. There is a fairly recent book "Allee Effects in Ecology and Conservation" (Courchamp et al, 2008), which might be of interest to you.


Could a biological process organically build solid metal "organs"?

That is an excellent question. I was a little confused at first because, without realizing it, you actually cited a perfect example of a biological process that manipulates metal: bone formation.

Bone is made of hydroxyapatite crystal, which is a mineral whose main ingredient is, of course, calcium (metal).

Now, to answer the how of your question; bone is formed, as you eluded, through protein to protein interaction mediated by cells called osteoblasts (osteo- = bone, -blast = immature cell). The osteoblast first locates a site on the bone that is to be expanded, then encases itself in a framework of collagen fibers. When this is done, calcium phosphate and hydroxide bind to the collagen and "harden" as hydroxyapatite (Ca10(PO4)6(OH)2). The osteoblast, now encased in a shell of hydroxyapatite (called the lacuna), transforms into an osteocyte (-cyte = mature cell) and projects long arm-like structures called filopodia which it uses as sensors and to communicate with surrounding osteocytes. All that adds up to look an awful lot like this (with respect to the fact that they are usually fully enclosed, but that would make for quite an insipid picture):

Finally, to put Filipe Rocha's concerns to rest, how is this fully organic and (almost) solid metal structure adapted and "unmade," should the need arise? Well, there is a third type of bone cell called an osteoclast (-clast = to break). Osteoclasts break down bone by secreting hydrogen ions to dissolve the calcium in hydroxyapatite, then cathepsin and other protease to digest the collagen network.

So there you go; a fully biological system with the capability to not only create a non-toxic, solid metal structure, but also maintain it and even manipulate and "unmake" it. Even though bone is not an organ, I'm sure this system could be modified for such an implement if we put our minds to it... :)

Edit:
If calcium isn't "metally" enough for you, you might want to check out limpet teeth, which are comprised of goethite, iron oxide-hydroxide (FeO(OH)). I can go further in depth with the biological processes necessary to produce this mineral if you want; just ask. :)


How many smaller muscles compose the interosseus muscle in the human hand?

The number of interosseous muscles is not constant, because of the evolutional process continuing in modern generations.

Some individuals have 4 interosseous muscles, other have three, however there are still debates about the subject:

+


Is it possible for any impurities to get through the apple peel?

The answer I got from Jan Kolář of Charles University:

The spores of fungi or bacteria in apples don't just emerge from nothing, they have to get into it from the surroundings. I often see apples, which rot while still hanging on the tree, the hole needed for the infection of the apple is usually made by a worm. The problem of the apples near roads isn't that they would rot. Indeed, plants can absorb all kinds of harmful substances from soil, water or air, including heavy metals, chlorinated organic compounds or organic compounds from the exhaust gases of cars. How much and which substances, that usually depends on the type of plant (specifically on where it stores most of the substances).

It's not enough to wash an apple because the impurities are absorbed in the fruit itself as well. And on the surface of the peel, there are waxes and other unsolutabe substances which can absorb toxic aromatic carbohydrates from the exhaust gases, and can't be simply washed off.

The greatest risc near the roads used to be contamination with lead because petrol used to contain it. Many of the plants can recieve the lead and hoard it up in some organs. Now, when the lead petrols are forbidden, the biggest risc pose the fumes from the diesel engines. So I'd rather not eat fruit near the roads (especially near the busy ones).


There are plenty of papers with models for this. For instance, check a few hundred here.

Edit: I'm not an expert in modeling these particular processes. However, I do know about mathematical models in biology more generally. The OP asked if there is "a model" of how the B-cell antibody pool matures ('evolves'). The short answer is 'no'. There is not 'a model', because anyone can make their own model, with their own assumptions, parameters, methods, etc. The 'algorithmic point of view' is not something that is valid on itself, it is only useful (sometimes). It is the job of the modeler to navigate the nuances of her/his own model so that it ends up being useful for some particular purpose or question at hand. Thus, there is no simple answer to this question, or any other modeling question (take, for instance, all the talk about epidemic models in the COVID-19 case: even experts differ about the relevance of some particular details/assumptions). This is my long answer.


Sometimes men wake up with an erection in the morning. Why does this happen?

Shortly speaking: REM (Rapid Eye Movement) is one phase of sleep. During this phase, we dream and some of our neurotransmitters are shut off. This include norepinephrine, which is involved in controlling erections. Norepinephrine prevents blood from entering the penis (preventing the erection). In absence of norepinephrine—during REM phase norepinephrine is absent—blood enters the penis, leading to an erection. This phenomenon is called nocturnal penile tumescence. Such erections typically occur 3 to 5 times a night. A related question concerning similar erections in women can be found here.

High pressure in the bladder may also lead to a "reflex erection". This erection allows for preventing uncontrolled urination. The drawback is that when in the morning one has an erection and can't wait to pee it might get hard to accurately target the toilets!

This video is also a nice and easy source of information on the subject.

Is it bad?

(Reading my "note" below, you have edited your post to get rid of this question, thank you)

It is perfectly healthy you don't have to worry about that. These erections are even thought of as contributing to penile health. At the opposite end of the spectrum, the absence of erections during the nights are an index of Erectile Dysfunction (E.D.).

Note

Be aware that medical questions are often considered off-topic on this site. Asking "is it bad?" turns your question into a medical one. Health-related questions (but not personal health) should be asked on health.SE


Is there a rule for the annotation of the basepair or gene locus origin in bacterial genomes?

[I'm sure we have a skilled microbiologist somewhere here, so he would correct my answer.]

The necessity to designate gene locations in classical bacterial model species predated the genomic era, so traditional maps were normally neither bound to origin of replication, nor were they necessarily expressed in base-pairs. In E. coli, for example the traditional map was created based on the F-pili-mediated DNA transfer experiments.

When whole genome sequences became available it was only natural to continue the traditionally defined numeration in terms of placing the "base-pair one". Thus, in E. coli "the traditional and physical maps ... linkage map are closely correlated".

My understanding of the current situation with bacteria without genetic prehistory is that their genomes are numerated either respective to classic closely-related species (if any) or according to the presumed location of ori. Just to give an example of how the dilemma was solved for the Buchnera genome: it was "assumed the DnaA box upstream of the gidA gene is the replication origin" and the authors decided to designate "the start of the DnaA box as base pair one".

As you see, still, even if the authors try to define "base-pair one" based on the position of ori, the problem is that this point depends on the ori-searching tool one uses and on the contemporary understanding of how ori-sites look like (direct determination of origins of replications are in many cases not easy). See e.g. this table with a revision of ori locations in a set of genomes: while most of the genomes received their numeration irrespective of ori, some of them were indeed bound to it, but the new analysis showed that these locations were inaccurate.


Can we change one's genome into the genome of somebody else

There are 3.72x1013 (37 trillion) cells in the average adult human body. It would be essentially impossible to target every single cell just to change a single base pair, let alone the massive genetic and epigenetic changes that would be necessary to change someone into a clone of another.


Are there any examples where 'magic bullet' drugs have worked in cancer treatment?

There are, indeed, several such mAb based treatments. From the Mayo Clinic:

  The monoclonal antibody drug rituximab (Rituxan) attaches to a specific protein (CD20) found only on B cells, one type of white blood cell. Certain types of lymphomas arise from these same B cells. When rituximab attaches to this protein on the B cells, it makes the cells more visible to the immune system, which can then attack.

(...)

  Cetuximab (Erbitux), a monoclonal antibody approved to treat colon cancer and head and neck cancers, attaches to receptors on cancer cells that accept a certain growth signal (epidermal growth factor). Blocking this signal from reaching its target on the cancer cells may slow or stop the cancer from growing.

(...)

  The monoclonal antibody bevacizumab (Avastin) targets a growth signal called vascular endothelial growth factor (VEGF) that cancer cells send out to attract new blood vessels. Bevacizumab intercepts a tumor's VEGF signals and stops them from connecting with their targets.

(...)

  Ibritumomab (Zevalin), approved for non-Hodgkin's lymphoma, combines a monoclonal antibody with radioactive particles. The ibritumomab monoclonal antibody attaches to receptors on cancerous blood cells and delivers the radiation.

(...)

  Ado-trastuzumab emtansine (Kadcyla) is one such drug approved to treat HER2-positive breast cancer. Ado-trastuzumab emtansine contains an antibody that attaches to the HER2 receptors on the breast cancer cells. The cancer cells then ingest the antibody, which releases a few molecules of chemotherapy.

It does eliminate side effects, although the treatment is not side effect-free.

Personally, my suspicion with this approach is this: At its heart, cancer is a problem of uncontrolled cell division. Most cells in the body do not divide rapidly, and this slowing down of proliferation is integrated into differentiation into whatever tissue the cells are in. The most obvious cells that divide rapidly are stem cells (themselves carcinogenic!). Furthermore, it seems to be a common theme in cancer that the less differentiated (or more de-differentiated) you are, the more easily you divide, and hence the nastier the cancer you generate.

As such, the worst cancers out there are going to be very undifferentiated, and express few eligible surface markers. What's more, tumors evolve. If you start selecting against cells which express your marker, you will encourage the tumor to simply evolve and stop expressing that marker. Back to the benchside to look for a new marker - meanwhile your patient gets worse and worse.

This is why generalized chemotherapies (or radiotherapy) are so attractive. They attack the rapid division of cancer cells, and the cancer cells cannot evolve to lose this property, because if they did, they would not be cancer cells.


Is it possible for virus infected cells to continue to present a self-antigen on the MHC1?

Self antigen is presented throughout viral infections.  You seem to think that cytotoxic T lymphocytes respond to absence of self. That’s backward. CTL respond to their specific peptide target no matter how much self antigen there is. In a typical response, there may be 100,000 self peptide/MHC complexes and 100 viral peptide/MHC complexes, and that’s enough for a CTL response.

One trigger for NK cells is absence of self, so perhaps that’s the source of your confusion.


traditional method to remove a plasmid from E. Coli is to grow the cells with Etidium bromide.

http://vlab.amrita.edu/?sub=3&brch=186&sim=1097&cnt=1


Is spliceosomal RNA called snRNP or snRNA?

snRNA: small nuclear ribonucleic acid

snRNP: small nuclear ribonucleoprotein

snRNA refers to the RNA itself. snRNP refers to snRNA complexed with some protein(s). You could call spliceosomal RNA either depending on the context.


What directs macromolecules to their cellular locations

This is fairly often question for molecular biology

  how does the mRNA know exactly how to get to those organelles

The secret to understand it, is that nothing knows where to go. Different molecules have different affinity to each other. Molecule A likes molecule B, but not molecule Y. Inside the cell, thermal fluctuations causes disorder that drives molecule A to bump into all kinds of molecules, including Bs, Zs, Ys, and others. However, when stumble upon molecule B, molecule A will very likely form some sort of stable complex with it. One example, is ribosome and mRNA.

When mRNA and ribosome join into complex, their inner parts can be considered in the same fashion: they will jiggle a lot around, but most likely jiggle will produce polypeptide, not, let's say DNA, or not cause mRNA to fall away from the ribosome.

So, you can say that mRNA tries to go everywhere it can, without any clear direction, apart from the fact that it will most likely form something stable (i.e. useful) with ribosome. Or maybe it will be mRNA degradation protein, such as ribonuclease.

PS: "will very likely form some sort of stable complex" means that in some reasonable time mRNA will find and bind to ribosome. However, it might take billions of years for ribosome to bind DNA and produce some sort of polypeptide.


How do scientists kill the bacteria they themselves made resistant?

You are absolutely right, flushing down the toilet (or the sink) or simply throwing them into the normal waste doesn't work for biosafety reasons. And it is also not allowed, depending on the country you would do this in, this can lead to hefty fines.

Biologically contaminated lab waste can be inactivated (=all potential dangerous organisms are destroyed) by two ways: Either by heat or chemically. Which ways is used, depends on the kind of waste.

The most commonly used way is autoclaving, meaning treating the waste with steam at high temperatures at higher pressure. The temperature used here is usually 121°C, the exposure time depends on the volume of the waste, since the temperature needs to be reached and kept for at least 20 minutes. See the references for more details.

Liquid wastes (like culture media) can also be inactivated chemically by adding chlorine bleach to decompose the cells. Bleach can also be used to decontaminate surfaces, although here more often alcoholic solutions (70% Ethanol or Isopropanol) are used. After chemical inactivation, the remaining solutions should not be autoclaved as the emerging fumes are either unhealthy (bleach) or explosive (alcoholic solutions) and this is unnecessary, too.
Liquid wastes can also be autoclaved to inactivate them.

Autoclaving has the main advantage that it is rather simple (put the waste into the autoclave, close it and run a appropriate program), the waste can afterwards simply be discarded as normal waste, which may not be the case for chemically inactivated waste, which may need special precaution for disposal.

References:

Decontamination and Sterilization
Decontamination of laboratory microbiological waste by steam
sterilization.
TECHNIQUES FOR STEAM STERILIZING LABORATORY WASTE
Decontamination of Laboratory Microbiological Wasteby Steam Sterilization


Do different chiral centers on ligands cause different confirmational changes and effects in their target proteins?

There a few things you have to take care of with chirality in biological systems:

First note, that for amino acids we usually use L and D instead of r and s nomencalture.

In chemistry the difference between chiral enantionemeres is usually really just a difference in light polarisation like you described, otherwise they can be thought of as identical, since they have identical chemical properties. This way of thinking does not apply to biochemistry - the moment enzymes (large molecules with very defined 3D structures) are involved the structural difference between the two forms becomes very important for each and every biological reaction.

In the case of single amino acids this means that D amino acids are toxic to eukaryotic cells, because their similarity to the D form allows them to interact with some of the enzymes that usually bind it, but the binding is not a perfect match so the enzymes get inhibited, which makes the D form toxic. (This is already described in the second paper you linked:)

  In animal studies, administration of D-amino acids to rats and chicks resulted in growth inhibition [18]. In addition, serious damages such as suppression of the synthesis of glutamate oxaloacetate transaminase, glutamic pyruvic transaminase, and lactate dehydrogenase resulted from D-amino acids accumulation in animal tissues [18].

Now in your question you are asking about the difference between a toxin made from the 'wrong' amino acid. The thing is, this change of the protein will most likely mean, that its not a toxin anymore. A protein toxin is toxic because it can interact with other proteins, based on its 3D structure. This structure is based on the chemical and structural properties of the amino acids building it. If you change the underlying structure of every amino acid it will fold differently and you will get completely different protein - and not a mirrored version of the original protein/toxin.


Is differential equation modelling in molecular genetics useful?

Are differential equation models useful to geneticists and biologists?

Well yeah, of course they are. Look up Alan Turing and "The chemical basis of morphogenesis", or look up "differential equations and gene regulatory networks" But folks have to specialize, and not every department studies every aspect of a field. You may just have ended up in a department where nobody is studying an aspect of genetics that can be well modeled by differential equations. At lot of molecular genetics is still figuring out the coarse grained phenomenology of the genome, like "How does a cell figure out which copy of the X chromosome gets condensed into a Barr body?" A lot of these problems involve picking out subtle signals from noisy data, thus the interest in statistics and machine learning.

If diff. eqns. are the passion of your life, you might have to look 'next door', to departments studying biochemistry and population genetics, both of which do huge amounts of modeling using differential equations. There are also applications of differential equations to molecular genetic methods like QPCR and next generation sequencing, but you'll either have to sell your mentor on the topic, or move to a different department.

On the other hand, if it's just a matter of diff. eq. being your undergrad emphasis, you may want to find a biological problem that interests you, branch out beyond diff. eq., and use your general mathematical maturity to pick up the relevant mathematical tools: say statistics, optimization, or dynamic programming.


Are there yearly variations in HIOMT (HydroxyIndole-O-MethylTransferase) availability?

This isn't really a complete answer but I can't fit it into a comment.
I've found that there is a large body of literature on seasonality of melatonin levels in various vertebrates, particularly livestock, because of its interaction with breeding patterns. Similar studies in humans are however, difficult to find, but the review paper cited below looks at a link between seasonal variations in melatonin levels and seasonal variations in immune system functions. It cites a few references that might be worth following up.

Srinivasan, V. et al. (2008) Immunomodulation by melatonin: Its significance for seasonally occurring diseases. Neuroimmunomodulation 15: 93-101 DOI: 10.1159/000148191
Abstract
Melatonin is not only synthesized by the pineal gland but also in many other organs and tissues of the body, particularly by lymphoid organs such as the bone marrow, thymus and lymphocytes. Melatonin participates in various functions of the body, among which its immunomodulatory role has assumed considerable significance in recent years. Melatonin has been shown to be involved in the regulation of both cellular and humoral immunity. Melatonin not only stimulates the production of natural killer cells, monocytes and leukocytes, but also alters the balance of T helper (Th)-1 and Th-2 cells mainly towards Th-1 responses and increas- es the production of relevant cytokines such as interleukin (IL)-2, IL-6, IL-12 and interferon-γ. The regulatory function of melatonin on immune mechanisms is seasonally dependent. This fact may in part account for the cyclic pattern of symptom expression shown by certain infectious diseases, which become more pronounced at particular times of the year. Moreover, melatonin-induced seasonal changes in immune function have also been implicated in the pathogenesis of seasonal affective disorder and rheumatoid arthritis. The clinical significance of the seasonally changing immunomodulatory role of melatonin is discussed in this review.


fibrinogens and fibrins - are they the same molecule?

You could say they are the same molecule, but a molecule whose function is to change its state and properties very quickly when activated by thrombin.

Fibrinogen is a soluble protein - a complex of six protein chains.
Thrombin is an enzyme called a protease which very specifically cuts the ends off of two of those protein chains.
Once those bits are removed from Fibrinogen, the resulting molecule creates fibers very quickly to form clots.

You could also say that fibrin is a different molecule than fibrin because it really consists of many fibrinogen fragments.


Is there any evidence that a virus can modify human evolution

The simplest example, that I can recall are the flu pandemics. The 1918 pandemic is the first to be described because of its severity, but quite possibly not the first in human history (see for example the Black Death - Yersinia pestis is a bacterium, but in the 15th century in just a few years it covered almost all of Europe, sometimes killing up to 40% of population in a given area).

Influenza pandemics appeared quite regularly during the 20th century, usually every 20 years and killed suspiciously many people compared to yearly influenza strains. Additionally, a person who survived one pandemic, was unaffected or only mildly affected by the next pandemic.

All this suggests, that the pandemics "clear" the population from susceptible individuals, and regularity of pandemics (notice, that 20 years is more or less the time of one human generation!) assures that the new generations also go through this kind of selection. The surviving individuals are more resistant to all strains of influenza then those, who never suffered from a pandemic. Maybe the influenza didn't mutate our DNA, but it could be a major force of natural selection.

And one more note: did you notice the great noise in media every time a new potentially pandemic strain is discovered? Actually, it's not just hyperboly of the danger. Last pandemic was in the '70s, so it's high time for a new one. And, since the last one was  almost 40 years ago, the new one (when it happens) will probably be very severe.