Though this question feels a little more like history than biology, since I was able to easily & quickly find information that answers this question, I will provide a response anyway.

  What species of bird inspired Nebraska's nickname Bug-Eating State?

After a bit of research, it appears that no species of bird contributed to this nickname. Instead, Homo sapiens are the culprits! =P

According to the Official Nebraska Government Website:

  This bug-eater business is said to have originated during the potato-bug and grasshopper times. An eastern man came out here to visit his relatives. On his return they asked him, of course, how things were in Nebraska? It was our worst time, our one year of a double plague, so he answered, 'Oh, everything is gone up there. The grasshoppers have eaten the grain up, the potato-bugs ate the 'taters all up, and now the inhabitants are eating the bugs to keep alive.' Some newspaper man heard it and published it as a good joke, and it stuck to us for a good while.

..

  At the very first meeting of the [Territorial] Pioneers [Association] in May, 1892, a member protested against the nickname, or totem name as I call it, of Nebraskans, namely, 'bug-eaters.' The 'Sons and Daughters of Nebraska,' composed of those born in the state, was organized at the same time, and they were on the street with ribbons and badges of their order, which had printed on them a big bug and the legend, 'Bug-Eaters.' Of course they did not think how it looked or sounded, but did it merely as a joke. A committee was appointed at the time to suggest a more euphonious and appropriate name, but nothing was really done about the matter until our October meeting this year when the name of 'TREE PLANTERS' was suggested and adopted at once, as emblematic, a pleasant sounding name and most appropriate, for Nebraska has planted more trees since she was named and settled than any other state in the Union.

..

  By all means, then, give us the 'Tree Planters,' which is an honor, a glory, a fact and a pleasant reminiscence of the great change that has come to our prairie country in the short time since its first settlement. Help the Pioneers to fix this name in the public mind, and say good-bye to the Bug-eaters forever. -- Jno. A. MacMurphy, Secy. T.P.A., 1921 Farnam St., Omaha, Neb.

Nebraska now carries the official nickname "The Cornhusker State", and has done so since 1945. More information about the history of Nebraska's nicknames can be found here and here.


Are spinal nerves myelinated and unmyelinated at the same time?

Spinal nerves are mixed nerves containing afferent and efferent neurons of various types. Anatomically, they protrude from the spinal column bilaterally at each vertebral level. They contain both myelinated fibers (e.g., A fibers) and unmyelinated fibers (e.g., C fibers).

The answer is (c): both myelinated and unmyelinated.

Please note that spinal nerves are NOT located in the spinal cord, despite the fact that neurons in each spinal nerve will either originate or terminate there. A spinal nerve is a peripheral structure. It starts at the point where the dorsal and ventral root converge (See April's Clinical Anatomy, Ch. 1). If you have the opportunity to observe back surgery or dissect a human cadaver, you can see and touch a spinal nerve. They are cable like structures containing bundles of many many many axons, but no neuron in its entirety. A nerve is not a neuron. This is a common misconception.

Just to add, the details here may seem like trivia, but they are not. Similar questions (and questions that require you to understand the distinction between a nerve and a neuron) are often asked on US medical licensing exams. This is because they are relevant to understanding and interpreting neurological symptoms and physical exam findings.


Significance of prostaglandins in semen?

Nevermind. While writing out the question I found the answer on wikipedia.
Prostaglandin type PGF2α will act on the FP receptor to initiate uterus contraction which will help propel sperm further into the reproductive tract.


Why are there species instead of a continuum of various animals?

Mathematician/computer programmer's answer here:

There is a continuum of different animals — in fact it's pretty fair to say that every animal occupies a different place on this continuum. They're just not uniformly distributed over the continuum; they're clustered around forms that are most likely to survive and reproduce, and the lowest-energy paths between them.

This is because evolution is basically a stochastic optimization algorithm, one that finds the "best" set of parameters for maximizing some function by randomly perturbing an initial set of input values. In fact, some of the best optimization algorithms today are based on ideas drawn directly from evolution and called "evolutionary algorithms".

In mathematics, given enough time, these algorithms will all converge on one optimum solution and nothing else. Why isn't it like that in nature? Because in mathematics, the "fitness function" that we're optimizing for stays the same for a given problem for as long as the algorithm runs. It represents the specific problem we're trying to solve. In nature, there's no outside force imposing a fitness function; an organism's survival depends on millions of factors in its environment which change over time, many of which depend on the survival and properties of the other organisms in its environment (competition, symbiosis, predator/prey relationships, etc.) This is a chaotic system so complex that it could easily go for billions of years without reaching a steady state, and even if it did, external changes (like the odd asteroid impact, to use an extreme example) would still come around to shake things up.

Another reason for the clustering is because a lot of the "intermediate states" in the genetic space have a fitness of zero — these are the states between species that can't interbreed, or that have sterile offspring. The categorization of "species" is based on this, and although it's not exact, it's still generally true that the more different two creatures are, the less likely they can have viable offspring. This makes evolution more likely to explore the spaces near already-successful organisms, and less likely to produce radical new things by hybridization.


There are two main reasons for the pO2 in the alveolar air being lower than the atmospheric pO2. First, the diffusion of CO2 from the blood lowers the alveolar pO2. But the most important is the second one: there is a lot of water inside the lungs, and all this water lowers the alveolar pO2 as well.

This is the equation:

PaO2 = FiO2(Patm - PH2O) - PaCO2[FiO2 + (1-FiO2) / R]

Source: https://en.wikipedia.org/wiki/Alveolar_gas_equation


Physiological indicators of happiness and well being

There are beahvioral, physiological, and psychological indicators of happiness, and on the flipside of depression, all of which are quantitative.

Levels of the neurotransmitters serotonin and dopamine in the brain are a physiological indicator of depression. Higher levels of serotonin are correlated with increased happiness and decreased anxiety. Dopamine also contributes to good mood, and in addition causes an increase in activity and willpower. Both serotonin and dopamine show decreased levels in depression. However, it is important not just to look at general levels of the neurotransmitter, but to also consider which parts of the brain show decreased neurotransmitter levels. Depression correlates with decreased serotonin and dopamine levels in the amygdala, thalamus, and hyppocampus. (http://www.health.harvard.edu/newsweek/what-causes-depression.htm)

Behavioral tests of depression are used on laboratory animals. The most common tests are the forced swim test (in which scientists measure how long a mouse persists swimming in a water container before it gives up) and the tail suspension test (in which scientists measure how long a mouse struggles to free itself when suspended by its tail). (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3270071/)

In addition, self report questionnaires are designed to quantify depression in people. Some popular ones are the Beck Depression Inventory (BDI-II) (http://en.wikipedia.org/wiki/Beck_Depression_Inventory) and the Beck Hopelessness scale (BHS) (http://en.wikipedia.org/wiki/Beck_Hopelessness_Scale).


Energetics and Products of Pepsin/HCl Protein Digestion

This is well-explained on the Wikipedia page for pepsin. You are misinterpreting the use of the word activated. The protein is secreted by chief cells in the gastric glands in the form of pepsinogen, an inactive pro- form which has an extra ~40 amino acids at its N-terminus (the propeptide). The propeptide binds at the catalytic site of the enzyme and keeps it inactive. At low pH (this is where the HCl comes in - HCl secreted by parietal cells of the gastric glands acidifies the stomach) the protein is able to cleave off its own propeptide, making it fully active.


Why is the neuronal plasma membrane more permeable to potassium ions than sodium ions?

The cell membrane is inherently quite impermeable to any ion, because it is made of hydrophobic fatty acids. Ions are hydrophilic because of their charge and small size. Metal ions are relatively small and, indeed, have therefore a high charge density. They gather a lot of water around them and hence, they are hydrophilic.

Therefore ions, including Na+ and K+ are transported via dedicated ion channels, which form specialized pores in the membrane. They consist of vast families with many members and a host of different characteristics. Hence, the size of the ion does not matter, because they are transported through channels.

There are indeed leaky K+ channels, but not leaky Na+ channels. And exactly this feature is the reason cells are negative on the inside, because positively charged K+ leaks from the cell.

There is just so much the Na+,K+-ATPase can do. In the end  it burns ATP to fuel each cycle to pump out Na+ and pump in K+. At a certain point it cannot transport anymore Na+ out (K+ diffuses relatively freely) because the concentration gradient of Na+ and the electrical gradient (inside negative) gets too steep.


What is meant by "Expression" of Non-Coding RNA?

With many non-coding RNAs, the RNA is the functional endpoint. Therefore, ncRNA "expression" simply refers to the production of that functional component. Similarly to with proteins, this involves looking at differential tissue production of that noncoding RNA (i.e. in which tissues the RNA is produced).

Gene expression is defined in the Oxford Dictionary of Biology as:

  The manifestation of the effects of a gene by the production of the
  particular protein, polypeptide, or type of RNA whose synthesis it
  controls.

In other words, gene expression means the same thing whether the functional product is a protein or a noncoding RNA. Of course, there is no translational component to expression of ncRNA.


I think you're asking why don't we take antibodies from previously-infected host animals and treat humans with them. In principle, that could work, but it's impractical as you describe it. You give the example of "rabies in bats". Imagine trying to get enough blood from a 25-gram bat to treat a single person. Farming bats is hardly practical, and if you're bleeding wild bats, you're probably collecting both known and unknown viruses that you're then injecting into your patient. So this is completely impractical with wild animals, which are the donors of most of the diseases in question.

However, there's nothing magical about the antibodies from the original wild animal. (This seems to be widely misunderstood, probably from movies that make medically idiotic and impossible claims.) Any antibody can be potentially valuable for treatment, whether it comes from the original host or not, and whether it comes from the live pathogen or from a vaccine made from the pathogen.

So a more practical approach is to infect a large, easily-handled domestic animal with the pathogen in question; or better yet, with a vaccine made from killed pathogens, so there's no risk of the animal getting sick or or infecting your patient. This used to be done with rabies, in fact, using equine hyper-immune serum to treat rabies patients (Production of hyperimmune antirabies serum in horses).

However, there are major problems even with this approach. It's difficult, it means keeping large numbers of large and potentially uncooperative animals around for long period, etc. Here is a WHO document reviewing some of the problems with this approach.

A third approach is to make monoclonal antibodies. This is the most popular approach now; it lets you make sterile, safe antibodies with completely defined characteristics, with minimal risk of contamination, under controlled conditions.

There are many monoclonal antibodies out there that are used in modern medicine, including some that are used to treat pathogens. However, it's worth pointing out that antibodies are not magical panaceas; they're often much less effective than conventional antibiotic or antivirals and are often more expensive and less practical to use.


How do you design a drug to be delivered to the CNS?

In a nutshell: in order to pass through the blood-brain barrier (BBB) the substance has to mimick soee properties of the substances that are allowed to pass through.

There are different types of "transporters" -- integral proteins going through the cell membranes and accounting for the active transport of the substances they can actively bind to. Smaller molecules of drugs can use solute carrier transporter (SLC), whereas bigger molecules (oligo- and polymeres) would use the receptor-mediated transporter (RMT).

There is a nice article on this topic published by ScienceDaily.

Here is the quote:

  One technology for enabling active transport of small molecule drugs
  across the BBB involves targeting endogenous nutrient transporters.
  These transporters are members of the solute carrier (SLC) transporter
  superfamily. Transport of small molecules across the BBB by these
  membrane proteins is known as carrier-mediated transport (CMT).

  In order to design drugs that utilize CMT to cross the BBB,
  researchers modify their chemical structures so that they resemble
  nutrients that are transported across the BBB by specific SLCs. The
  prototypical drug that uses this strategy (which was developed long
  before mechanisms of CMT were known) is L-DOPA, the major current drug
  for Parkinson's disease. L-DOPA is used to replace dopamine that is
  lost due to degeneration of dopaminergic neurons in the substantia
  nigra of the brain.

  Another major system that is used in normal mammalian physiology to
  enable needed molecules to cross the BBB is receptor-mediated
  transport (RMT). The brain uses RMT to transport proteins, peptides,
  and lipoproteins that are needed for brain function across the BBB.
  Examples of biomolecules that are transported into the brain via RMT
  include insulin, insulin-like growth factor (IGF), leptin,
  transferrin, and low-density lipoprotein (LDL).

  In RMT, molecules in the circulation may bind to specific receptors on
  the luminal surface of brain capillaries (i.e., the surface that
  interfaces with the bloodstream). Upon binding, the receptor-ligand
  complex is internalized into the endothelial cell by a process called
  receptor-mediated endocytosis. The ligand may then be transported
  across the abluminal membrane of the endothelial cell (i.e., the
  membrane that interfaces with brain tissue) into the brain. This whole
  process is called receptor-mediated transcytosis.


Short answer is yes, of course. Maintaining a healthy synapse is very energy-consuming process.

Let me first note that forgetting as we know it is more complicated than just pruning of synapses. It might involve rearrangement of proteins in pre/post-synaptic membrane and near it, local de-regulation of local protein synthesis, decrease in synaptic mRNA content and epigenetic change of transcription.

Secondly, average energy spending on a synapse, if it is not being used too often, includes mainly maintaining of membrane potential at resting -80mV level. Cellular membrane is a leaky barrier, so that without ion pumps, such as $K^+/Na^+$-ATPase, potential will quickly go to zero. Maintaining and recycling neurotransmitter pool also require energy.

Action potentials itself are passive processes, its generating does not require energy. ATPase will have to maintain potential at rest and keep it from fluctuating.

You can read this review for more: Synaptic Energy Use and Supply (Neuron, 2012). It generally describes where energy comes from and how it is being used.


Genetic engineering for experimenting at home?

Doing genetic engineering experiments at home is generally referred to as either "biohacking" or "DIY Bio". There's a number of forums out there filled with hobbyists who are doing that sort of work in their homes and garages, and discuss how to do such things in a hobbyist environment. With those terms (and the info in the Wikipedia article), you can probably find those forums on the internet. (Suggestion: look for ones where the regulars emphasize safety and appropriate conduct - not only is it better for you, it's a sign that the regulars know what they're talking about.)

However, 200 USD might be a little small to set up a decent (and safe) "biohacking" space in your own home. Possibly a better bet is to see if you can find a local "makerspace" which has a biology component. Makerspaces are places where, for a small fee, fellow enthusiasts pool together to purchase equipment (and space) to do various projects. Most makerspaces are geared toward the computational/mechanical (e.g. building robots), but there are some out there which have biotech equipment. Your mileage may vary, though, and you're likely to have more success in finding a decent makerspace in a large city than in a small town.

A final caveat is to make sure you research your local laws to figure out what is legal in the jurisdiction you're living. Especially with laws targeting illegal drug production, there are locations where possession of basic scientific equipment by normal homeowners is criminalized. There's also regulations about waste disposal and material storage that you'll need to follow. Also, in most jurisdictions accidents/damage from home labs are penalized much more harshly than, e.g., cooking accidents. Know what's legal/illegal in your jurisdiction (and by your homeowner's insurance) before attempting to set up a home lab.


Do sodium channels keep renewing themselves with new subunits made by genes?

You are asking about two different processes: turnover (degradation) of mRNA and turnover of proteins.  In a typical mammalian cell the mRNA half-lives of stable messages approach the length of the cell cycle (e.g. 24 hr). One mRNA could be translated around the clock if needed. The resulting proteins will also have a measurable half-life, and that will vary with the protein and the cellular conditions. If a cell ran out of protein and its mRNA there is often a feedback loop that activates transcription of the structural gene back in the nucleus.


Wheatgrass juice or extract has shown some promise for reducing the required frequency of blood transfusions in thalassemic patients, possibly due to iron chelating activity.  However, few high-quality controlled studies have been conducted so it may be too early to form a definite conclusion.

References:

Choudhary, Dharma R.; Naithani, Rahul; Panigrahi, Inusha; Kumar, Rajat; Mahapatra, Manoranjan; Pati, Hara Prasad; Saxena, Renu; Choudhry, Ved P. (April 2009). "Effect of wheat grass therapy on transfusion requirement in β-thalassemia major". The Indian Journal of Pediatrics 76 (4). pp. 375—376. doi:10.1007/s12098-009-0004-6.
Das, Priyabrata; Mukhopadhyay, Ashis; Mandal2, Suvra; Chandra Pal, Bikas; Mishra, Raghwendra; Mukherjee, Debarati; Mukhopadhyay, Soma; Basak, Jayasri; Kar, Manoj (2012). "In vitro studies of iron chelation activity of purified active ingredients extracted from Triticum aestivum Linn. (wheat grass)". European Journal of Medicinal Plants 2 (2). pp. 113—124. doi:10.9734/EJMP/2012/1059.
Marwaha, R.K.; Bansal, Deepak; Kaur, Siftinder; Trehan, Amita (July 2004). "Wheat grass juice reduces transfusion requirement in patients with thalassemia major: A pilot study". Indian Pediatrics 41. pp. 716—720.
Mukhopadhyay, S.; Basak, J.; Kar, M.; Mandal, S.; Mukhopadhyay, A. (2009). "The role of iron chelation activity of wheat grass juice in patients with myelodysplastic syndrome". Journal of Clinical Oncology (Meeting Abstracts) 27 (15S). p. 7012.
Singh, Karnail; Pannu, M. S.; Singh, Palwinder; Singh, Jaswinder (January 2010). "Effect of wheat grass tablets on the frequency of blood transfusions in thalassemia major". The Indian Journal of Pediatrics 77 (1): 90—91. doi:10.1007/s12098-010-0002-8.
Tirgar, P. R.; Desai, T. R. (September 2011). "Investigation into iron chelating activity of Triticum aestivum (wheat grass) in iron-dextran induce iron overload model of thalassemia". Journal of Pharmacy Research 4 (9). ISSN 0974-6943.


Forensic genetics- why is mtDNA comparison sometimes better than nDNA comparison?

mtDNA is present in a much higher copy number per cell than nuclear DNA.

According to this paper, there are approximately 4000 or so mitochondrial DNA copies per human muscle cell.

  copy number of mtDNA per diploid nuclear genome in myocardium was 6970 ± 920, significantly higher than that in skeletal muscle, 3650 ± 620 (P = 0.006).

This makes it far more likely that a non-degraded copy of mtDNA exists, considering that there are normally only 2 or 4 copies of nuclear DNA per cell per locus for almost all kinds of cells.


Okay, he's not wrong, technically speaking. Practically speaking never ever fertilize your plants with ammonia.

The ammonia you spilled will be converted into nitrates eventually, so it's not like you spilled lead into your garden. On the other hand the populations of nitrifying bacteria take a fairly long time to adapt to a bounty like "a bunch" of household ammonia (their idea of a banquet beyond their wildest dreams is 2-4 ppm ammonia) but they will eventually eat it all.

(Fishkeepers should know about the nitrogen cycle, because you have to set up a complete yet tiny version of the real thing, which takes at least a week to establish)

So your plants will be fine... next year. This year they might have a little bit of trouble considering ammonia is a base and can burn plants directly or indirectly. Don't fertilize your plants with ammonia. They will probably die.


How are epigenetic marks transmitted during cell division?

I can get the ball rolling..
Found a nice paper which looks at this phenomenon in yeast.
So as a primer, 8 histone proteins come together to make a spool of sorts which DNA wraps around:

Histone proteins have many sequence variants, and each one of them can be covalently modified with methyl, acyl, phospho, SUMO, adp and many other sorts of chemical groups via a chemical bond.  Although its not yet clear exactly how it works its clear that these modifications can change the behavior of the histones which prevent transcription of the gene when they have the chromosomal DNA all wrapped up.
So as to the question a pattern of inheritance of modified histone patterns is indeed seen and has epigenetic effects.  (that is, it modifies the genetic phenotype of daughter cells which retain the histone modifications of the parent cells).  In this paper, newly synthesized (and labelled) yeast histone can be found incorporated into certain segments of the genome, which demonstrates that large segments of the histones are carried forward from the parent cell.
They also found a particular case of histone epigenetic labeling carried forward through division:

Furthermore, if the heterochromatin-binding protein Sir3 is unavailable during DNA replication, histone H3-K4

So there's evidence that histone configurations are transmitted epigenetically, In this 2011 paper, the author support a 'conservative distribution model' and compare it to a 'semi-conservative' model:

The conservative distribution model proposes that newly synthesized histone molecules form nucleosomes that are randomly inserted among preexisting parental nucleosomes.
The semi-conservative distribution model proposes that a hybrid nucleosome that contains both newly synthesized and parental histone H3-H4 dimers is formed, which facilitates the transmission of epigenetic information within the basic nucleosome unit.

They go on to say that a conservative model of histone inheritance allows for strong epigenetic inheritance as the remaining parent histones will tend to attract similarly labelled histones as the new histones incorporate themselves among the parental histones on the daughter chromosome.
Its still being worked out though...


What would it take to recognize a deer by its photo?

There is a lot of variation in how and when deer shed their antlers. In most arctic and temperate-zone species, antler growth and shedding is annual, and is controlled by the length of daylight. In tropical species, antlers may be shed at any time of year, and in some species such as the sambar, antlers last several years. Some equatorial deer never shed their antlers.

The horns change every year and, especially, increase the number of branches (and consequently, change their shape). You can't recognize them by antlers, but by other features, such as color of the hair or the lineaments. Like us, animals have individual morphological differences that are recognizable and listable.

Biologists specializing in studies of particular animal species not only take photos, but also make drawings and write descriptions of behavior, to identify individuals within herds.

An optical examination, however, of the subject through drawings and photos (and if possible, direct observation), is more useful than a PC program. This involves identifying particular similarities and equalities that are not "identical". This is possible to do visually on a large (but limited) number of specimens. The human eye is the best computer.


Computers rely on cooling mechanisms like heat sinks( an aluminum alloy mounted over the micro integrated chip) and fan. So far none of these mechanisms are utilized by nature, but analogies like cooling mechanisms in elephants which are in turn considered to be a model quite like the fan.
As the largest land animal, elephant's ears have crucial role in regulating homeostasis. When we see an elephant, it always wave its ears in order to reduce the brain temperature. On the other hand humming birds which are very smaller in size reduces its temperature by flowing blood to its wings. Humming birds wings flutter 90 times a second and it allows them to exchange much of its heat to the environment and the cooled blood is driven back to the brain.
The  carotid rete or rete mirabile in birds have been developed for heat exchange. In mammals, a pool of the cool venous
blood  returns from the nose or
head skin, exchanges the heat with
warm arterial blood of the carotid artery.
These arteries are sub divided into hundreds of
small arteries forming a net like structure which significantly improve the
heat transfer in brain.

Vascular retia mirabilia are also found in the limbs of a range of
mammals. These reduce the temperature in the extremities. Some of
these probably function to prevent heat loss in cold conditions by
reducing the temperature gradient between the limb and the
environment. Others reduce the temperature of the testes increasing
their productivity. In the neck of the dog, a rete mirabile protects
the brain when the body overheats during hunting; the venous blood is
cooled down by panting before entering the net.Reference

In Humans,

The net effect of heat production in the brain and brain cooling
keeps the brain cooler than the rest of the body and is achieved by
surrounding and bathing the brain with venous blood that has been
cooled outside the cranial vault, by bone and fat acting as
insulation, by the veins of the face and scalp through conduction,
convection, sweat and evaporation and by cooled venous blood flowing
through the cavernous and suboccipital cavernous sinuses cooling
incoming blood in the internal carotid and vertebral arteries before
it enters the brain. The combined effect of the brain cooling system
keeps the temperature inside the vault and brain about two to three
degrees cooler than the rest of the body. The effect is important
enough that some physical anthropologists attribute the extra-large
size of the human brain more to its exceptional cooling capacity than
to the increase in arterial blood flow that comes with upright
posture. Anthropologists refer to human encephalization due to
enhanced brain cooling capacity as the "radiator theory".
Reference

Also yawning and panting are considered to be mechanisms to reduce brain temperature.


Why is the Red Fox colored bright orange?

Their fur colour is actually a pretty good camouflage


This is a interesting question and for a long time it was thought that they do not age. In the meantime there are some new papers which say that bacteria do indeed age.

Aging can be defined as the accumulation of non-genetic damages (for example oxidative damage to proteins) over time. If too much of these damages are accumulated, the cell will eventually die.

For bacteria there seems to be an interesting way around this. The second paper cited below found that bacteria do not divide symmetrically into two daughter cells, but seem to split into one cell which receives more damage and one which receives less. The latter one can be called rejuvenated and seems to make sure that the bacteria can seemingly divide forever. Using this strategy limits the non-genetic damage to relatively few cells (if you consider the doubling mechanism) which could eventually die to save the others.

Have a look at the following publications which go into detail (the first is a summary of the second but worth reading):

Do bacteria age? Biologists discover the answer follows simple
economics
Temporal Dynamics of Bacterial Aging and Rejuvenation
Aging and death in an organism that reproduces by morphologically
symmetric division.


It is known that Ebola uses at least one cholesterol transporter called "Niemann-Pick C1" (NPC1) to enter its host cells. Cells with a mutated form of this transporter were not infected by the virus (this extends to other viruses from the Filovirus group as well), which seems like a proof that this can make people "immune" to the virus. However, these are only experiments in cell culture. Other experiments show that a small molecule inhibitor that mimics the transporter can inhibit Ebola from entering cells and infecting them.

There are two papers on this topic:

Ebola virus entry requires the cholesterol transporter Niemann-Pick
C1
Small molecule inhibitors reveal Niemann-Pick C1 is essential for
Ebola virus infection

If a person manages to survive an Ebola infection the immune system fights the virus by making highly specific antibodies against it. These antibodies bind to the viruses and mark them for the immune system (mainly through mast cells) for take-up and degradation while inhibiting them from infecting other cells. Serum from Ebola survivors has been used as experimental treatment for infected people (here mainly the antibodies can be helpful). People who survive the infection are immune against another infection of the same virus strain.


Hutchinson–Gilford progeria syndrome is almost always due to to a de novo mutation (i.e. not an inherited mutation) in the lamin A gene (LMNA). The mutation responsible is a C-to-T substitution at position 1824. Remarkably this doesn't change the encoded amino acid but rather creates a new splice donor site in the RNA transcript. When this splice site is used it results in the deletion of information corresponding to about 50 amino acids internal to the protein and near to the C terminus.

During biogenesis of normal lamin A a C-terminal -CAAX motif is recognised as a signal for isoprenylation, in this case farnesylation. The added lipid group acts as a C-terminal membrane anchor. However this anchor is subsequently removed when the protein is proteolytically cleaved near the C-terminus, removing 15 amino acids including the C-terminal cysteine (by this point the three C-terminal residues have been trimmed away). The cleavage site for this final modification is missing in HGPS lamin A so the farnesyl group cannot be removed. The accumulation of unprocessed lamin A causes the observed defects in the nuclear membrane.

Eriksson et al. (2003) Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome. Nature 423: 293-298

Capell et al. (2005) Inhibiting farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome. Proc. Natl. Acad. Sci. USA 102: 12879-12884


Theoretically, is domestication of (virtually) any animal possible?

As the previous answers clarify, all organisms have heritable traits that may be manipulated through selective breeding. It is the pragmatics that can be prohibitively challenging. From an (zoo)archaeological point of view, few animals have actually been domesticated, and only recently in our species' history. The dog is an unusual case, perhaps domesticated 14,000 years ago; most domesticated animals only show skeletal changes within the last 10,000 years. Cats, compared to livestock's total dependence on humans, are 'barely' domesticated--they got used to humans while camping out in Egyptian storehouses where all the mice were, perhaps around 4,000 years ago, but even today a fluffy house cat will revert to a feral state if abandoned.

Many animals are behaviourally unsuitable for domestication. If an animal is dangerously aggressive, for example, they cannot be penned and isolated--so the many controlled generations it takes to reduce their baseline aggression cannot occur. Humans also tend to co-opt pre-existing social structures in a species, such as becoming the 'alpha' in a dog pack or the head 'ram' of a sheep herd. Species without a hierarchy or herd mentality are difficult to control and keep track of, and so do not lend themselves to human care.

You mentioned tigers in your question. Tigers have little to offer people (other than pelts), they're massive/aggressive, and they're jungle loners. You can't raise a herd of tigers; they'll kill each other and the survivor will kill you. That they're carnivores is also challenging, since a carnivore is much more expensive to feed than a bunch of grass-munching sheep. Altogether, there was never a situation in prehistory that would have turned tigers into giant house cats. House cats eat unwanted mice; tigers eat your cattle (and children). The occasional tiger 'pet' won't change that.

Domestication, outside of recent experiments (like the Russian foxes mentioned above), has always been a protracted, indirect process. People started interfering with animals that were already useful in some way(s). Dogs offer warmth, hunting aid, defence, transport, and (in a pinch) food. Alligators, tigers, and sharks are not useful enough to make the danger and cost of raising them worthwhile. Even if you did eventually produce a 'human-friendly' shark, there would still be a 'wild' population ready to eat you--and your complacent pet sharks, too!

For a very readable explanation, try the chapter on domestication in Jared Diamond's (1997) Guns, Germs, and Steel.


Have you used hhpred to search for homologues? What was your criteria for defining there was no homologues? You could potentially go down to around 30% sequence identity to model.

I would submit the the query sequence to both I-Tasser and Rosetta and see if both of the servers agree on the topology. I-Tasser will always provide 5 models of your query sequence (even if they are rubbish) ranked by a confidence score.

While you wait for the above servers to finish, I would submit the sequence to a number of secondary structure prediction servers to come to a general consensus for the secondary structure of your protein. Some servers you could use are:

Predict Protein
Phyre2
Raptor X
Jpred
Psi-Pred

If the servers come to a consensus, compare the secondary structure prediction with that of the secondary strucutre of the models, to see if the ab initio modelling concurs with that of the secondary strucutre prediction. This will give you more reason to be confident in your model.

I would then validate your models using:

Prosa - This calculates a Z-score, and plots where it fits with structures with a similar amino acid length, from the PDB.
DOPE Score - This is employed in Modeller and measures the "nativeness" of your model, the lower the score the better. But you will need to install Python and have some knowledge of how to use the command line. I can provide the code to Run Dope with modeller.

Finally, are there any constraints you could introduce such a oligomerisation site or a protein-protein interaction site, to help with the modelling?


Consider the phenomenon of zygotic induction, as originally observed by Art Pardee, Francois Jacob, and Jacques Monod (sometimes called the "PaJaMo", or "PaJaMa" experiment): regulation of a repressed promoter can be affected by the copy number of the promoter in the cell. Put another way, if the copy number of the lac operator in the cell is high enough to bind or titrate all of the available lac repressor protein in the cell, then some of the lac promoters in the cell will be expressed.


Will a garter snake eat unusual prey if made to smell like something normal?

Yes, changing the scent has been accepted by most snake breeders as a method to feed stubborn snakes (reference). For example, if your snake prefers chicken, and wont accept mice, rub a chick on a pre-killed mouse and this may trick it into eating the mouse (reference).  With regard to garter snakes, the diet may change based on its habitat, its age and even being kept in captivity can change its diet. This article should provide you information with feeding your garter snake if it is stubborn (reference).


The overall energy expenditure of a myelinated axon is lower compared to a non-myelinated axon, because myelination causes the action potential to be conducted in a saltatory fashion, i.e. the action potential jumps from one node of Ranvier to the next (Fig. 1). Saltatory conduction depolarizes only a small fraction of the membrane (i.e., the cumulative exposed membrane surface in the nodes of Ranvier) when an action potential travels through the axon, as opposed to the whole membrane in an unmyelinated axon. Hence, less ions are transported across the membrane for any given action potential. Therefore less work is required from the sodium-potassium pump (a.k.a. the Na+,K+-ATPase) to restore the electrochemical gradient across the cell membrane after the action potential. Because the sodium potassium pump  uses ATP to pump Na+ out and K+ into the cell (Lodish, 2000), myelinated axons require less energy than unmyelinated axons for an action potential to be conducted.

Fig. 1. Saltatory nerve conduction. Source: Antranik.

Note that this is different from the activation energy of a neuron. For physiological action potential generation in neurons with chemical synapses, the activation threshold is generally expressed in terms of activation voltage change, i.e. the depolarization amplitude necessary to generate an action potential. This is likely very similar between myelinated and non-myelinated neurons.

In terms of temperature; the action potential is mediated by the opening and closure (i.e. the gating) of ion channels. When an action potential travels through an axon, the depolarizing potential opens sodium channels which result in further depolaization, opening up new channels etc (Fig. 2).

Fig. 2. Action potentials travel through axons by voltage gated opening of sodium and potassium channels. Source: Rice.

The voltage differences that are sensed by the ion channels are generated by current flow. Increasing the temperature will enhance diffusion of ions through the channels and it will enhance the response kinetics of the ion channels. However, most proteins are highly temperature sensitive and too much of a temperature increase will impair ion channel functioning and eventually even denature the protein.

Reference
- Lodish, Molecular Cell Biology. 4th ed. New York: W. H. Freeman; 2000


Are there any predators without camouflage?

Poison dart frogs have aposematic colouration, making them the exact opposite of camoflaged.

They are also predators, since they feed on ants, termites and beetles.


Do we actually know the molecular dynamics of any enzyme?

MD simulations.
Molecular Dynamics algorithms like Gromacs and AMBER aim to simulate atomistic mechanisms of biological macromolecules.
This video shows a good example of a resulting video from such a simulation for the CmAAT1 Enzyme, CmAAT1-Hex-aCoA complex. Much more data such as energy values and electrostatic interactions is available from the simulation, but that's not as pretty as the video!

Implicative mechanisms.
There are also telltale signs of active regions of crystal structures. Software like Consurf can show conserved residues. This implies possible biochemically important features like key structural or enzymatic residues, areas of a protein. The image below is from the consurf gallery and is based on the crystal structure 3COQ. Pink is areas of conservation. It therefor appears that those residues are involved in binding DNA.

Consurf is only one of many tools for identifying key residues. After these residues are identified, mutant knockouts of the protein can be made to see exactly how the function of the protein is altered. From that, a fairly good mechanistic model can emerge.
Uncertainty

"Can we know..."

The word "know" is a philosophically ambiguous word and I've gathered that scientists generally tend to avoid it. This is particularly true when it comes to the simulation side of things. It is generally best to regard MD simulations as an approximation of what happens.


Try YEASTRACT http://www.yeastract.com/

  YEASTRACT (Yeast Search for Transcriptional Regulators And Consensus
  Tracking) is a curated repository of more than 48333 regulatory
  associations between transcription factors (TF) and target genes in
  Saccharomyces cerevisiae, based on more than 1200 bibliographic
  references. It also includes the description of 298 specific DNA
  binding sites for more than a hundred characterized TFs.


What cell types comprise the median eminence and the tuber cinereum?

The tuber cinereum is the "swelling" at the ventral surface of the hypothalamus (Subarachnoid space surface) at the base of the infundibular stalk. The median eminence (a circumventricular organ) is an elevation on the ventricular surface of the infundibular recess of the 3rd ventricle.


Equilibrium and Metabolism: Can cells exist at STATIC equilibrium? What about dynamic equilibrium?

There are some things that should be addressed first.

Chemical-Equilibrium
This is a condition at which the forward reaction rate is equal to the backward reaction rate for a reversible reaction.
$$\ce{A<=>[k_f][k_r]B}$$
In this case, $k_f.A=k_r.B$, at the equilibrium, if the reactions are first-order. If $k_f>k_r$, then the concentration of B would be higher than the concentration of A, at equilibrium point.

Steady-State
It is a state of the system at which the overall concentration of all the components (reactants and products) remain constant with time, or oscillate at a constant amplitude and frequency. Mathematically, the differential equations that denote the system (as mentioned by Dexter) would equate to zero.
If this condition applies only for one or more but not all the components of the system, then it is said to be in a Quasi-Steady-State.
If there are only two species which inter-convert but do not get formed or degraded, then steady state would be same as the chemical equilibrium. However, it is to be noted that chemical-equilibrium is a property of a reversible reaction whereas steady state is the property of the system.

Coming to your main question, I do not know what your teacher really had in mind, but this is my explanation.
According to the above definitions, you cannot say that the cell is in equilibrium because the cell is a system and not a reaction. The usage of the term "equilibrium" varies between different fields of study and physicists do use steady-state and equilibrium interchangeably. However, this is not the practice among chemists and biochemists.
Having said that, I would say that a cell does attain a steady state. I think what your teacher wanted to imply was that a cell constantly responds to the external stimuli (which is randomly changing) and therefore never remains at any given steady state for a long time.

Can the cells not exist at static equilibrium?

No, they don't. In fact the term "static equilibrium" in never used in chemistry because it never really happens. At a static equilibrium all the rates have to be zero, whereas in a dynamic equilibrium the rates have to balance each other out. Static equilibrium usually applies only for macroscopic objects (which do not include molecules).
A note on stochasticity: Chemical reactions follow probabilistic kinetics i.e. the reactions occur with some probabilities, instead of fixed rates (these probabilities can be unequal for different reactions). Chemical systems can be approximated by deterministic models at the thermodynamic-limit which reflects the "average" behaviour of the system.

when something is at dynamic equilibrium, why does this mean that the
concentrations of reactants and products are not necessarily equal?

See the first section. Similar logic applies for steady-state. The steady state concentrations depend on the kinetic parameters.


What is it the most common reason for community acquired pneumonia?

You are right in that there are several ways to split down CAP, and plenty of different pathogens to look at.  But then we are looking for the most common.  Pnumonia is most common in children and adults over the age of 75 (or 65 depending on who's counting).  Luckily there are plenty of good reviews for both populations.
From the pediatric side we have Iroh Tam PY(1):

Pneumonia occurs more often in early childhood than at any other age,
with the exception of adults older than 75 years, and kills more
children than any other disease worldwide

As far as pathogens:

Streptococcus pneumoniae and Haemophilus influenzae type b (Hib) have
been characterized as 2 bacteria predominately responsible for cases
of fatal pneumonia in children.  However, widespread introduction
of Hib and pneumococcal conjugate vaccines has led to significant
declines, especially of Hib, although Streptococcus pneumoniae is
still the predominant bacteria isolated from bacterial CAP in
children.  There is increasing recognition of the prevalence of mixed
bacterial and viral infections, which have been documented in 23% to
33% of cases of pneumonia.

Then we move to the geriatric side of things with Falcone et al (2):

Common pathogens include H. influenzae, enteric gram-negative bacilli,
the atypical organisms, S. aureus, Pseudomonas aeruginosa, and M.
catarrhalis, although the relative prevalence of each tends to vary
among studies. Among elderly individuals with aspiration pneumonia,
gram-negative bacilli are the predominate organisms (49 %), followed
by anaerobic bacteria (16 %) and S. aureus (12 %).

Though I should note, having done them myself, getting accurate cultures is difficult, and viral levels a very likely to be under reported because of handling and skill.

For example, in different prospective studies in which the
microbiologic etiology of CAP was systematically sought in the
elderly, a definite or presumptive pathogen was often reported in <60
% of the patients. (2)

And again in children:

There are 2 main challenges in the diagnosis of CAP: the first is the
definition of CAP, particularly in young children, in whom bacterial
and viral infections can occur with similar frequencies, and in whom
overdiagnosis of mild symptoms and signs may lead to unnecessary
antibiotic use; the second is the identification of a causative pathogen, which is frequently impractical and inadequate in children, and
in whom the failure to isolate an organism can result in unnecessary
antibiotic use. (1)

Taking into account more global sources, I'm actually thinking Hib infection has dropped more due to vaccination than I gave it credit for, putting my bet on S. pneumoniae, and showing my regional experience may not be representative (3, 4, 5, 6).
(1) Iroh Tam PY. Approach to common bacterial infections: community-acquired pneumonia. Pediatr Clin North Am. 2013 Apr;60(2):437-53. doi: 10.1016/j.pcl.2012.12.009. Epub 2013 Jan 12
(2) Falcone M. et al. Pneumonia in frail older patients: an up to date. Intern Emerg Med. 2012 Oct;7(5):415-24. Epub 2012 Jun 12.
(3) Brown JS. Community-acquired pneumonia. Clin Med. 2012 Dec;12(6):538-43.
(4) Kurutepe S, Ecemiş T, Ozgen A, Biçmen C, Celik P, Aktoğu Özkan S, Sürücüoğlu S. [Investigation of bacterial etiology with conventional and multiplex PCR methods in adult patients with community-acquired pneumonia]. Mikrobiyol Bul. 2012 Oct;46(4):523-31.
(5) Tao LL, Hu BJ, He LX, Wei L, Xie HM, Wang BQ, Li HY, Chen XH, Zhou CM, Deng WW. Etiology and antimicrobial resistance of community-acquired pneumonia in adult patients in China. Chin Med J (Engl). 2012 Sep;125(17):2967-72.
(6) Capelastegui A, España PP, Bilbao A, Gamazo J, Medel F, Salgado J, Gorostiaga I, Lopez de Goicoechea MJ, Gorordo I, Esteban C, Altube L, Quintana JM; Poblational Study of Pneumonia (PSoP) Group. Etiology of community-acquired pneumonia in a population-based study: link between etiology and patients characteristics, process-of-care, clinical evolution and outcomes.  BMC Infect Dis. 2012 Jun 12;12:134. doi: 10.1186/1471-2334-12-134.


The answer can be found in PubChem, which is linked in the comment by anongoodnurse.

I would not say that

Norepinephrine is beta2 adrenomimetic

because norepinephrine has many roles such as neurotransmitter.
I would just say that

Norepinephrine is alpha, beta adrenoagonist.

More pieces of information about it from PubChem:


Obtaining a mapping of RefSeq ACs to Uniprot ACs

You have a bunch of options:

You can use Biomart.
Biomart is a standalone tool, but also have a pyton and R libraries. So it gives you more options depending on your preferred programming language. This is a widely used tool and in general works well.

biomart http://www.biomart.org/
biomart python library
biomart R library (from bioconductor)
Biomart is widely used and have extensive documentation.

Use a python library called pyEntrezID
https://pypi.python.org/pypi/pyEntrezId/1.4.7
You can do all sort of conversions of ids, however I've never tried it.
You can try NCBI eutils or one of the Ensembl REST API endpoints


This is the shell of a marine mollusk called a chiton.

They are also sometimes known as sea cradles or "coat-of-mail shells", or more formally as loricates, polyplacophorans, and occasionally as polyplacophores.

In Puerto Rico, they call these animals "Quitones."

All chitons bear a protective dorsal shell that is divided into eight articulating aragonite valves embedded in the tough muscular girdle that surrounds the chiton's body.

My initial guess as to the species is: Chiton tuberculatus.
 (Disclaimer: I know almost nothing about these animals, so this is at best a guess).

 Source: NATURAL HISTORY MUSEUM ROTTERDAM

 Source: NATURAL HISTORY MUSEUM ROTTERDAM
You can find additional images that look even more like your specimen here and here
According to Wikipedia:

This species can be found under rocks and in spray zones of rocky shores, in the intertidal, shallow subtidal zone of Western Central Atlantic (USA, Colombia, Bermuda, Mexico, Venezuela and the West Indies)

This includes Puerto Rico

Based on Fig 1 of Crozier (1918) showing typical sizes of various ages of C. tuberculatus, you have a fairly young specimen (likely only a few years old).
The Quitones of Puerto Rico by Cedar García Ríos (ISBN: 1-932271-16-3) is probably a good tool for definitively IDing your specimen to species.


How do you differenciate between the eukaryotes and prokaryotes?

There are lots of ways to distinguish between eukaryotes and prokaryotes, as listed by microbiologynotes.com:

Difference:             Eukaryotes:                Prokaryotes:
-------------------------------------------------------------------------------
Size                    > 5µm                      1-2µm by 1-4µm
Nucleus                 Nucleus with nuclear       No true nucleus; nucleoid
                         membrane
Complexity              Usually multicellular      Unicellular
Chromosome              Multiple linear; histones  Usually single circular;
                                                    no histones
Cell Division           Mitosis, meiosis           Binary fission
Reproduction            Involves meiosis           No meiosis
Zygote                  Diploid                    Merozygotic
Genes                   Expressed individually     Operons
Gas vacuoles            No                         Possible
Mesosome                Yes                        No
Ribosome                Found on membranes         Distributed in cytoplasm
Mitochondria            Usually present            No
Chloroplast             Possible                   No
Cell wall               Simple if present          Freq. present, complex
Endoplasmic Reticulum   Possible                   No
Golgi apparatus         Possible                   No
DNA usage               Transcription in nucleus,  Transcription at the same
                         translation in cytoplasm   time as translation
Duration of cell cycle  Usually long (hours)       Usually short (<1 hour)

N.B.: I have used the list on microbiolgynotes only as an outline, editing as needed.  For instance, Mitochondria is not necessarily present in eukaryotes, neither are chloroplasts.  Also, I have not included everything, since I do not presently have the time to verify everything.


How do rare mosquito borne diseases get transmitted if they are so rare?

Via Wikipedia:

The virus is transmitted in saliva to a vertebrate host when an infected mosquito takes a blood meal. It thus cycles between mosquito and vertebrate amplifier hosts, mainly white-tailed deer. In a study from Newfoundland, JCV was significantly associated with large mammals such as sheep, cattle and horses. In Michigan and Ontario moose and bison are believed to be the primary reservoir.[3]
The virus winters in mosquito eggs, which it reaches by transovarial transmission. The female mosquito lays eggs that carry the virus, and the offspring can transmit the virus to deer or ruminants and humans. Infected mosquitoes were found equally distributed throughout the state of Connecticut, irrespective of land use.[4]

So, the virus has a reservoir in (primarily) deer, an infected deer gets bitten by a female mosquito, the mosquito lays eggs with the virus, the resulting mosquitoes can spread the disease by biting another large animal or human.
The reservoir needs to be large enough to ensure the virus survives year over year, but there doesn't need to be any special mechanism for it to travel outside the predominant range; there have been cases in several states in the northeast, though rare.

References [3] and [4] are:
[3] Goff G, Whitney H, Drebot MA (2012). "Roles of host species, geographic separation, and isolation in the seroprevalence of Jamestown Canyon and snowshoe hare viruses in Newfoundland". Appl. Environ. Microbiol. 78 (18): 6734–40. doi:10.1128/AEM.01351-12. PMC 3426688. PMID 22798366.
[4] Andreadis TG, Anderson JF, Armstrong PM, Main AJ (2008). "Isolations of Jamestown Canyon virus (Bunyaviridae: Orthobunyavirus) from field-collected mosquitoes (Diptera: Culicidae) in Connecticut, USA: a ten-year analysis, 1997–2006". Vector Borne Zoonotic Dis. 8 (2): 175–88. doi:10.1089/vbz.2007.0169. PMID 18386967.


The reference range for hemoglobin Hb content in whole blood is 13 - 17 g/100ml for adult men, and 12 - 16 g/100ml for adult women.

There are other related metrics : the mean corpuscular hemoglobin concentration MCHC, that is the concentration in a red blood cell (reference range : 31 - 36 g/100mL), and mean corpuscular hemoglobin MCH, which is mass in one cell (reference range : 29 - 35 pg)

So I think that book is refering to different values :  the concentration in the red blood cell itself (MCHC = 34g/100ml), and the resulting concentration in the whole blood (Hb = 15g/100ml).

By the way, there is a value relating Hb and MCHC, the hematocrit Ht, the proportion of volume of whole blood occupied by red blood cells. Reference range 40% - 50% for adult men, 35% - 47% for adult women.


This is determined by the promoter -- the DNA sequence to which RNA polymerase binds. It's assymetric, and the polymerase binds in a specific orientation, that determines the strand and the direction it will go once elongation begins.


what kind of bonds join the okazaki fragments

I'm pretty sure the "phosphodiester bond" part is correct.

The only thing I can think of that might be questionable is the word "directly". If directly = immediately, then the sentence could be termed false, because they aren't joined immediately.

Even then, it seems like that's just grasping at straws, so I wouldn't worry too much about it. It sounds like you understand the concept, which is what matters.


Short answer
People competent in mathematics have been shown to have higher activation of the left angular gyrus according to fMRI. EEG recordings have shown larger activity in the posterior parietal cortex.

Background
I think you are interested in what makes a good mathematician. A brain imaging study by Grabner et al. (2011). showed that the left anterior gyrus was more activated in individuals more competent in math. Specifically, the authors argue that the stronger left AG activity in the more competent subjects reflects a higher proficiency in processing mathematical symbols. The anterior gyrus is involved in mathematical symbol processing.

Left angular gyrus, lateral view. Source: Kenhub Neuroanatomy Atlas

ERP studies (event-related potentials deduced from the EEG) have shown higher activity in posterior parietal cortex in subjects excelling in math (Waisman et al., 2014). This region is associated with algebra and handling mathematical functions.

Posterior parietal cortex among other regions not relevant to the question answer. Source: Live Science

References
Grabner et al. Front Hum Neurosci 2011; 5: 130
Waisman et al., Int J Sci Math Edu 2014; 12(3): 669-96


Visualising a subset of the tree of life

http://phylot.biobyte.de/ performs the requisite task (generating a phylogenetic tree based on the specific organisms provided, using the NCBI taxonomy tables).

For example, the input of tree elements

  Trichomonas vaginalis,Trypanosoma brucei,Homo sapiens,Fibroporia
  radiculosa,Paramecium tetraurelia,Tetrahymena
  thermophila,Cryptosporidium muris,Cryptosporidium hominis,Blastocystis
  hominis

generates the tree


Relationship between immunologic response to specific gluten epitopes and clinical antibody testing

1) Can a person be sensitive to barley hordeins, while being unaffected by wheat gluten or rye secalins?

Possibly, but I haven't found a documented case.

According to What is gluten? (Journal of Gastroenterology and Hepatology, 2017):

  A variety of sequences from α, γ, and ω gliadins, as well as from the
  glutenins, have been identified to activate coeliac disease. However,
  several hundred gluten peptides are predicted to be immunogenic and
  trigger the T-cell mediated response.6 The most immunodominant T-cell
  epitope is from α gliadin, although T-cell cross-reactivity against
  gluten-derived, secalin-derived, and hordein-derived peptides have
  been confirmed. Additionally, within each grain, there exists a
  distinct hierarchy of immunostimulatory gluten peptides.6 Of all the
  peptides known to stimulate the T-cell response in coeliac disease, a
  given patient may react to only a few.

However, according to Coeliac disease: immunogenicity studies of barley hordein and rye secalin‐derived peptides (International Journal of Experiemntal Pathology, 2016):

  In conclusion, barley hordein and rye secalin appear to contain CD
  toxic epitopes that are found in wheat gluten, as demonstrated by the
  observed cross‐reactivity of CD‐derived gluten‐sensitive small
  intestinal T‐cell lines to wheat gliadin, barley hordein and rye
  secalin‐derived peptides.

2) Are the blood tests specific to wheat gluten antibodies?

I can't say for deamidated gliadin peptide Ab IgG test, but tissue transglutaminase antibodies IgA test (anti-tTG IgA) is not specific for wheat gluten; antibodies can be triggered by wheat gliadins, barley hordeins and rye secalins.

Gluten peptides (gliadins, hordeins, secalins) bind to tissue transglutaminase which deamidates them. Individuals with celiac disease have HLA DQ2/DQ8 dendritic cells, which present deamidated peptides to T cells, which stimulate B cells to produce antibodies against tissue transglutaminase:

  In CD, deamidation of gluten by tissue transglutaminase (tTG) in the
  small-bowel lamina propria promotes presentation of gluten peptides
  (gliadin in wheat, secalin in rye and hordein in barley) by
  HLA-DQ2 or HLA-DQ8 dendritic cells to pathogenic local CD4+ T
  cells...The most widely used serological test is anti-tTG IgA
  (Medscape)

3) Can barley affect the gut differently than wheat?

Possibly.

Nutrition and Celiac Disease (Nutrients, 2014):

  There is very limited data looking at the effect of barley hordein or
  rye secalin on CD outcomes in the published literature (e.g.,
  [66,67]), but evidence exists that these prolamins induce effects
  different to wheat gluten, at least at an immunologic level.

4) Do positive DGP and TTG test confirm celiac disease?

The specificity of IgG deaminated gliadin peptide (DGP) is 98% and of IgA tissue transglutaminase (TTG) 95% (American Family Physician, 2014), so when both tests are positive, celiac disease is very likely. The final diagnosis is by histological examination of a tissue sample obtained by duodenal biopsy.

5) Is it possible that, in celiac disease, symptoms disappear after removing only beer, but not wheat and rye from the diet?

It could be possible to have celiac disease confirmed by blood tests without any symptoms despite consuming wheat, barley and rye. Beer could trigger symptoms by irritating the bowel, not by gluten, but by alcohol or other substances, like in people with irritable bowel syndrome (American Journal of Gastroenterology, 2013).


Cough-variant asthma is a common cause for a non-productive dry cough.  Asthma is not a single condition involving bronchospasm and with associated wheezing - there is a variant that is primarily or only coughing.

There are different inciting factors that bring on symptoms cough-variant asthma.  Most commonly they are exercise-induced, cold-induced, allergy-induced, or quite commonly it happens following a viral respiratory infection (post-viral-URI).  Symptoms can be acute (exercise or cold) lasting minutes, or chronic lasting days-weeks or even indefinitely.

The pathophysiology for each is different.  The latter 2 are inflammatory processes, as you mentioned, each a little different (hypersensitivity versus residual infectious inflammation).  I am a little uncertain about the mechanisms you described, and I am not sure the correct thing to focus on is scarring.  I would focus primarily on the inflammation.  Inflamed mucous membranes are extremely sensitive, reacting to even dry or cold air.

Using a long-term steroid inhaler is a preferred method of handling chronic cough-variant asthma, as it reduces airway inflammation.

There can be other causes of cough such as postnasal drip, chronic rhinitis, sinusitis, or gastroesophageal reflux disease (GERD or heartburn).


Does a software exist to automatically design antibodies that target a given protein or antigen?

Much easier said than done!

If I had sufficient funds and time to pursue your goal what I would do is comb the Protein Data Bank for all the PDB files of interest. Surely you have some protein that interest you. Might consider doing the following:

Figure out what family your protein belongs in, considering it's number and presence of motifs: coils, helices, beta sheets, etc...
Do a literature review of any protein that has already been studied belonging to this family. So when a protein in this family catalyzes a reaction what are its flexible and restrained regions?
Use a program like Autodock to dock your protein to a protein that its protein family might interact with.
Calculate the interaction energies using Gromacs, NAMD, or Gaussian. You can do a zero time calculation of initial states or pursue a molecular dynamics approach as the proteins move randomly to their most stable configurations, or even a molecular mechanics approach. Which systems are most favorable?
You got this far. Now what? But then none of these steps creates your candidates. It just gives you an idea of the physics involved in already structurally identified compounds. Yes, you can make point mutations in VMD and Pymol. But, if you want to add a new motif to an existing protein structure it will not work because more than 20 amino acids in a peptide do not fold properly.

To do some of the biological statistics, the research collaboratory of structural bioinformatics is right here: http://www.rcsb.org/pdb/home/home.do

You can parse through their folders with wget or curl in bash scripting
at http://files.rcsb.org/

But then assuming you do figure out a candidate protein that doesn't exist yet. How are you going to make it in the lab? It appears that it would be better to do microbial studies. Maybe you can screen for a match with micro-array plates.


How is honey not toxic to our epithelial cells?

I'll change my initial comment into a real answer.

The human digestive tract has evolved to allow us to be broadly omnivorous, safely consuming a wide range of vegetable, animal, and mineral-based foods. While honey can be damaging to exposed cells, the epithelial cells lining the digestive tract are not exposed like the endothelial cells that line the circulatory system. Eating honey is not the same as injecting it into your veins.

A layer of mucous covers the cells of the digestive tract from mouth to colon and provides both lubrication as well as protection to the cells underneath it. It is protective to varying degrees against such challenges as acid, osmotic stress, mechanical damage, and foreign microorganisms. Additionally, the cells themselves are layered and are continually being sloughed off and regenerated, so even if the mucosal lining isn't 100% effective, damaged cells will be replaced fairly quickly.

Food quickly travels from the mouth through the esophagus to the stomach, not allowing enough time for osmotic stress or enzymes to damage anything to any significant degree. (Obviously, if you swallow something extremely harsh like bleach, lye, or concentrated acid, that's a different story.)

Once in the stomach, a food like honey is diluted by the digestive juices and any other food or drink already present -- it's not like the stomach is totally empty and globs of honey can just sit in direct contact with cells for an extended period of time, allowing for osmotic or enzymatic damage. Digestive enzymes and the acidic environment quickly attack proteins and other substrates, so even if the glucose oxidase can become activated, it will be cleaved by proteases into inactive fragments long before damaging levels of H2O2 can build up.

Low-density lipoprotein (LDL) is found in the bloodstream, not in the digestive tract, so any methylglyoxal present in food would need to be actively transported into the blood to do any damage. The work in the paper you cited was done completely in vitro, with no evidence that MG-mediated glycation as a result of eating honey actually occurs in people.

Many foods we commonly eat would appear to be dangerous to our bodies in one way or another, yet we have evolved strong mechanisms to minimize harm. However, it's pretty clear that some foods are damaging in various ways over time, so we still need to moderate what we eat. I don't know if honey (or certain kinds of it) is one of those foods, so more research is needed.


Since no one else has done so, just gonna expand on what occurred here in the comments (mostly from @Alex Reynolds):

tl;dr: natural selection exists.

Longer version:

Mutations/replication errors/whatever will happen in the creation of new virus particles within a host cell. There is some distribution of number of mutational events that will occur as a function of the number of new RNA molecules created per cell and the replication error rate. Some subset of these RNA molecules will be packaged into new particles, yielding a new generation of viruses that get a chance to infect. Yes, this is potentially a large number of new mutations per infection event.
Some large proportion of these new particles will contain non-functional RNAs, due to inactivating mutations of one kind or another. Most of the new mutations will be worse at being a virus than the originally infecting virus (their immediate parent). So therefore, they will be outcompeted by non-mutated forms.
Among all those viruses which continue successfully infecting throughout the course of a year, on average we observe 24 substitution mutations in the genome over the course of that year. Every transmission chain included in the group of viruses at the end of the year must have remained viable for infection of hosts. In other words, it has survived natural selection.

In population genetics, this phenomenon is known as "mutation-selection balance"- e.g. new mutations arise in the population at a rate that is limited by the action of natural selection (at equilibrium).

Genotype-phenotype maps

What of course I am leaving unstated is exactly why "...new mutations will be worse at being a virus than the originally infecting virus..."

This is very hard to predict in many cases. In some cases it is very obvious why a mutant is bad at being a virus, if e.g. an essential gene is deleted from the RNA genome. But for many single mutations we don't really understand what their effect will be on virus function, we just observe that they drop out of the population due to negative selection.

If you are interested in this question, I recommend looking into genotype-phenotype maps. I know Jesse Bloom has done some work on influenza in this field, here is one example of such a paper. It is generally extremely laborious to do this kind of work, so relatively little is known about the functional effect of any specific mutation in any specific genome.

Hope it is helpful to have all that written out.


In reconstructions, how are various shapes of facial features determined from skull only?

Disclaimer: I am an evolutionary geneticist. I know nothing about anatomy and forensic methods....

You should just have a look at wikipedia > forensic facial recognition. There are a number of different facial reconstruction methods, one of which is the so-called Manchester method (see a review of the Machester method in Wilkinson 2010).

In any method of facial reconstruction, there is some part of artistic representation to fill the gap of what we fail to infer from the tissues available. It is typically not so uncommon esp. for recent(-ish) fossils to have remains of soft tissues as well. In absence of such soft tissue, the morphology of the mouth and ears are typically left to artistic interpretation.


Where does the proton come in the reduction of NAD?

In a very simple way the equation describes the reaction. NAD is reduced using 2 hydrogen atoms. The two hydrogen atoms can come from one reactant (lactic acid fermentation) or from two (in a reaction of glyceraldehyde-3-phosphate to 1,3-bisphosphoglycerate; as shown in the figure below).

First of all, I will pick a particular example from glycolysis, catalyzed by glyceraldehyde-3-phosphate dehydrogenase.

Phosphate by its own has one hydrogen at cytosolic pH (because of the pKA). Thus in this reaction, there are two hydrogen atoms. One hydrogen atom is in the form of a hydride (a proton and two electrons) from the aldehyde group. This hydrogen atom is used to reduce NAD+ to NADH. A second hydrogen atom (in the form of a proton) comes from the phosphate. In the bisphosphoglycerate form, the proton dissociates from the phosphate group and is in solution.

The eventual fate of the electrons that were used to reduce NAD+ to NADH is the electron transport chain (in the mitochondria). In some cases, though, for example muscle cells in an anaerobic environment, or other species that don't have an electron transport chain, the electrons are used in fermentation of pyruvate to alcohol or lactic acid. When NADH donates its electrons in either case, it is then oxidized back to NAD+.

References:

Glycolysis
NAD
Lactic acid
fermentation
HPO4


Is Bramble (blackberry bush) carnivorous?

Even if the adaptations to tangle were well supported, brambles would still not be carnivorous.

Carnivorous plants release digestive enzymes to digest their prey or have other adaptations specifically to pull nutrients from the things they kill. Brambles would have to rely on something else to rot the carcass and pick up whatever trace nutrients that get released into the soil like any other plant. Brambles tendency to tangle could just as easily be a defensive adaptation meant to encourage herbivores to avoid it. Without any specific adaptations to uptake the nutrients from killed animals, classifying them as carnivorous would be premature.


Does a mydriatic drug neutralize the action of a miotic?

The iris has 2 sets of muscles:

The circular muscle (Sphincter iris) - This causes iris constriction and is supplied by the parasympathetic system - Acetyl Choline muscarinic receptors
The radial dilator muscle - This causes dilation of the iris and is supplied by the sympathetic system - The Adrenergic receptors (Alpha 1)

Theoretically speaking, there can be four sets of drugs:

Alpha 1 adrenergic stimulators - will cause midriasis
Alpha 1 adrenergic blockers/antagonists - will cause miosis
Muscarinic blockers - will cause midriasis
Muscarinic agonists/stimulators - will cause miosis

In practice,

Midriatics:

Alpha 1 agonists: Phenylephrine
Muscarinic antagonists: Atropine, Homatropine, cyclopentolate, tropicamide

Miotics (mainly used for Glaucoma):

Muscarinic agonists: Pilocarpine, carbachol, etc...
In practice alpha 1 antagonists are not usually used to effect miosis

There are two ways to achieve either midriasis:

Stimulate the Adrenergic receptors
Inhibit the Muscarinic receptors

Similarly miosis can also be achieved vice-versa.

The answer to your question is yes, when given the proper counter-acting agent, depending on the concentration of the agents and the mechanism of actions opposite effects are achieved. This is primarily because the drugs act on different sets of muscles. If a adrenergic stimulator - phenylephrine is instilled with a muscarinic stimulator - cyclopentolate, both sets of muscles will be acted upon and based on the concentration of the drugs, the decay rate and the efficacy, the iris diameter will either increase or decrease to variable degree. The point is that both the drugs will affect the final diameter of the iris (which is based on the autonomic state of the patient and the strength of drugs administered)

Now the special cases will be to administer a inhibitor of a receptor followed by an stimulator of the same receptor or vice-versa - In this scenario, the duration of action and the affinity of the given drugs to the receptor in question will play a decided role in determining the final action as both drugs act on the same muscle. If the inhibition is permanent or long-acting then inhibition of the muscle action is predominant. This may change if the stimulator has a very high affinity to the receptor - Higher affinity will result in tighter binding of stimulator and remove the chance for the inhibitor to work - i.e. increase the probability of the clearance of inhibitor. As you can see from above statement, if the clearance rate of inhibitor is slow (takes too long to metabolize), then the effect will ultimately be inhibitory effect. Similarly in case of poisonings where the stimulating effect is permanently achieved (Organo Phosphorous poisoning will cause permanent damage to acetylcholinestrase the enzyme responsible to remove acetyl choline) the reversal will depend on the affinity of the inhibitors (in this case, of acetyl choline) to the receptors (muscarinic).

Thus the question must be more specific to get a proper answer, as the effect is totally dependent on the drugs administered.


How is CO2 related to acidity in plant cells?

CO2 is a Lewis Acid.  CO2 is a double carbonyl carbon which is electron deficient, and we know that Lewis Acids readily accept electrons, so when present in H20 it forms carbonic acid (H2CO3).  Christiaan posted the balanced equation of the formation of the acid.


Do I have to use sucrose to induce a lac promoter?

You can induce the lac operon by two things: Lactose (or more precisely Allolactose a metabolite of it) and lactose analogons which are not metabolized by the bacteria.

Lactose induces the expression and is metabolized while IPTG is not a target of the $\beta$-Galactosidase and will give you a strong and permanent induction. Sucrose will not have any effect on the promoter.


If action potential is "all or nothing" then how are finely tuned signals sent from one neuron to another?

how is one type of neurotransmitter secreted rather than another

Most neurons release a single major neurotransmitter. JM97 commented a link about cells releasing more than one, but that is talking about "extra" neurotransmitters are short peptides, different from the major neurotransmitters like glutamate, GABA, acetylcholine, dopamine, norepinephrine, etc - I think that link is very misleading in the context of your question. Those cells don't choose one or the other, they release their primary neurotransmitter plus the peptide.

However, there are lots of different neurons and lots of different TYPES of neurons, so some release one type of neurotransmitter, others release another. Typically this is denoted by refering to cells as "___ergic": GABAergic cells release GABA, glutamatergic cells release glutamate, etc. Those specific cell types express the proteins necessary to synthesize their neurotransmitters and transport them into synaptic vesicles, ready to release. The actual signalling cascade that results in vesicle release is pretty much the same across different neurons: the difference is in what is packaged into those synaptic vesicles.

  if a neuron received an excitatory post synaptic potential that initiated a graded potential that initiated an action potential what specific signaling cascade or mechanism would denote the release of one excitatory neurotransmitter (say nor-epinephrine) over another (say dopamine) ?

Simple: if the action potential is fired by a noradrenergic cell, that cell will release norepinephrine on all of its targets. If the action potential is fired by a dopaminergic cell, that cell will release dopamine on all of its targets. They are different cells.

In contrast to outputs, which use a single primary neurotransmitter, individual cells can receive inputs from many types of neurotransmitter. So a dopaminergic cell could receive GABAergic inhibitory inputs and also receive glutamatergic excitatory inputs, but it will only release dopamine on its targets.

If you have a network, and you wanted that network to release more dopamine on average, you would increase the synaptic weights of the excitatory inputs to dopaminergic cells: that is, increase the amplitude of EPSPs in those cells (you could possibly also reduce the inhibition).

In the title of your question, you asked how "finely tuned signals" can be sent. Tuning of signals isn't just about which neurotransmitter is released, but rather which cells that neurotransmitter is released on to. Individual cells can both receive 1000s of inputs and send outputs to 1000s of other cells. The patterns of those connections and the patterns of active cells are what determine the "message" - this is called "encoding".


How likely is it that a person's progeny has an inheritable disorder based on this pedigree?

This is a very rough draft about the case, not verified, and should not be used for any medical conditions. Ask your own doctor. It is just for demonstrating some Mathematics and genetic passing generally.

Condition: Muscular atrophy
Differential conditions: TODO
Support: history of genetic passing in -1 and -3 generations

Disease

Muscular atrophy as a condition jumps over a generation. The environment/living of your greatgreatgrandfathers determine your grandfathers future, as a rough estimate.
The disease's common feature is recessive autosomality.
Assumptions

Autosomal recessive disease because everyone who exhibits symptoms is not be able to reproduce due to their early death.
TODO genetic passing
What is the genetic profile? Is there any other autosomal recessive diseases in the gene map?

Proposed probabilities where the random variables $X = disease$ and $Y = carrier$ such that the subscript 0, -1, -2 and -3 is about new children's, John's, parents' and grandparents' status, respectively.
Both of John's grandparents must have been carriers
\begin{equation}
P(Y_{-3}) = 100\%
\end{equation}

The probability of John's dad and any aunts and uncles having the disorder is (TODO think this again with the correct genetic passing)
\begin{equation}
P(X_{-2}) = 25\%
\end{equation}

The probability of being a carrier is for dad, aunts and uncles (TODO think this gain with the appropriate genetic passing)
\begin{equation}
P(Y_{-1}) = 50\%
\end{equation}

Disease as a process

$X \sim P_{i}(\mu, \sigma)$, $i = -3, -1, 1, ...$  where I propose the mean $\mu$ and the variance $\sigma^2$.

To understand this better, we should know how the generation $-5$ lived.
Can you get it?

Assumptions

Assume the events of individual probabilities independent i.e. (-3) events do not affect (-1) events in the series.
...

Test if the two independent statistics $X_{-3}$ and $X_{-1}$ are from the same population.
If you assume it, put it to assumptions.

Probability Density Functions in Generations -3, -1, 1, ...

Probability density function

At $X_{-3}$, the 3 aunts of 4 died. The mean $m = 0.75$ (=3/4).
You cannot use Binomial because sampling is not with replacement, not Poisson because occurrence probability is not less than 10%, ...
...

Conditional probability and Bayes theorem

Consider the conditional probability $P(X | Y)$ that is what is the probability of getting the disease for the generation when given the carriers ...
...

You propose 25% probability for generations series $-3, -1, 1, ...$.
You can test this. Select the statistical significance $\alpha = 0.05\%$. Select the appropriate probability density function or teach neural network to it.

False assumptions

John, his dad, and his wife must all be carriers of the disorder. Why wife should be a carrier?

Literature

Blythe, Peter.  Mathematics for the international student Mathematics HL (Options). Haesa & Harris Publications. I recommend this for beginners.
TI-84 and TI-86 have good manuals about the statistics.
Some publications about teaching a neural network doing some of the genetic analysis.
...


What's the cause of the scars on these cherries?

Are they coming from a disease?

No, this appears to be a combination of rain damage and pests. If a disease were present, much more of the cherry would suffer, there would be signs of rotting, and, the damage wouldn't solely be so superficial, as is the case in your posted images.

Consider the next few images which demonstrate the effects that various diseases have on a cherry, and notice how much more detrimental [and different] the impact.

Bitter Rot (Colletrotrichum gloeosporioides & C. acutatum)

Brown Rot (Monolinia fructicola)

Alternaria Rot (Alternaria sp.)

There are other [equally common] diseases of cherry trees (Prunus sp.), including cherry spot leaf, black knot, silver leaf, and PNRSV, however, in pretty much all of these cases too, there's no modification to the cherry fruit (excluding extreme circumstances, as is the case with spot leaf, I believe).

Instead, as mentioned, one major cause of the damage is rain. Just before harvest, when the cherry is at it's greatest [and possibly maximum] volume, rain that's absorbed through the surface of the cherry causes the cherry to further enlarge, which ultimately splits the cuticle (skin). The result is the following:

For more information on cherry splitting/cracking:

Fruit Splitting (Cracking) – What causes it and can we do anything about it?
Fruit Split In Cherries: Learn Why Cherry Fruits Split Open
A Review of Cherry Fruit Cracking
Story: Stone fruit and the summerfruit industry
Cherry Weather Worries

Given the irregularities of scarring on some of the cherries, I also suggest that insects and/or birds scratched/ate away at them. Consider the following images that illustrate the kind of damage that birds & wasps cause when feeding on cherries, and notice the similarities to those in your images.

bird damage

wasp damage

This, in combination with the rain, is most likely what caused damage to your cherries.

  Is it correct to call them "Cherry scabs"?

I just call it scarring, and I believe many other people do too. I'm not sure if there's a specific term for fruit damage that's then been "scabbed" over. If someone knows of a term for this, please provide in a comment and I will supplement my response with it. Thank you.

While continuing to research this topic, specifically when attempting to find alternative reasons that could explain this kind of damage, I did ran across this article which talks about wind damage, and provides an image that slightly resembles the markings on your cherries. I'm still heavily convinced though that your cherries suffered their damage from rain & pests.


What does "kcal/mol" mean when speaking of enzyme catalysis?

The reaction barrier (also termed activation energy) is the energy that is needed for the reaction to take place. An enzyme is "only" a catalysator which lowers the necessary energy (and/or makes the reaction possible under the conditions) but some energy to start a chemical reaction is still needed. See this image (from here):

To your questions: A and B are essentially the same - but the reaction time necessary with small amounts of enzyme is much longer than when 1 mole of enzyme is present. The amount of energy needed to catalyze the production of 1 mole of product stays the same.


Reason for seeing grid-like patterns when strobing a solid black-white image?

Seeing in animals is at some level using Gabor wavelets (Marčelja 1980 and later authors). Your images reminds of a combination of two low frequency Gabor basis vectors. Apparently the nervous system does not have time to model the incoming image into Gabor components of other frequencies.

Here is a picture of two low frequency Gabor basis vectors added. (In this image rotated 45 degrees compared to your image.)
http://medicalxpress.com/news/2013-01-feature-combination-perceptual-identification.html

This is a signal processing or a linear algebra question as much as a biology question.

One could argue that even lower frequency Gabor vectors would model the original images even better.


Detection of bacteria to measure quality of water

IF you are looking at a much faster technique but don't mind spending a bit and have some research equipment access, there are ways by which bacterial contamination can be detected by measuring ATP (Adenosine tri-phosphate). See this research publication. There are commercial kits available which you can use: Here is one of them by Thermofisher.

Again, this is only if you have access to the research equipments and funds.


How does alum help in blood coagulation?

I will answer the three questions one at a time. Lets begin with the first one:

  Do people actually use alum to stop bleeding, or only as a disinfectant? Does alum have any disinfectant effects?

Yes, alum is also used as a disinfectant, and it works in the same way as it does in blood coagulation. In aqueous solution, potash alum dissociates as:

$K_2SO_4.Al_2(SO_4)_3.24H_2O \rightarrow 2~K^+ + 2~Al^{3+} + 4~SO_4^{2-} + 24~H_2O$

Now, as is known, blood is a colloidal solution, in which the plasma proteins are charged (see Rügheimer et al, 2008). These ions from alum neutralize the charges on plasma proteins, causing the blood to coagulate. Similar effect is observed in disinfectant where these ions react with the free organic acid and thiol groups of proteins on microbes and free proteins, resulting in their precipitation (Williams, 2001). Thus alum can act as disinfectant.

  Does precipitation of proteins in blood help clotting?

Coagulation of both plasma proteins and RBCs takes place on application of alum, since both of them are charged (Fernandes et al, 2011) as is discussed in next point. However, it is difficult to say whether coagulation of plasma proteins plays a significant role in clot formation or not.

  Does alum contribute in any way to the process of blood clotting?

Yes, alum does contribute in the process of clotting: it makes clotting faster. Although the term 'clotting' is generally used for formation of what is called as platelet plug, the actual process of clotting also depends on coagulation of colloidal particles in blood. When the blood is exposed to the extracellular matrix (due to damage to blood vessel), platelets activate and, via a cascade of reactions, lead to formation of a platelet plug. Red Blood Cells get tapped in this plug (which is actually a fibrin meshwork) and lead to formation of clot. A nice and simple representation of this process is below (from here):

Without alum, RBCs would take longer to coagulate due to mutual repulsion. By neutralizing them, alum makes this process easier and faster. Hence, alum helps in the formation of blood clot via coagulation of red blood cells.

I hope this helps.


Is there any other possibilities for the disease?
Yes.  At 37°C, Histoplasma capsulatum usually doesn't form hyphae.

Were the hyphae branching, like this?

If "conidia with spores in radiating columns" means the pictures below,
We have enough to say that this is not a case of Histoplasma capsulatum and there is definitely another possibility for this disease.
Conidia with radiating chains of spores is pathognomonic for aspergillosis.


What are the major steps of follicular B cell development

According to Basic Immunology - Functions and Disorders of the Immune System (3rd Ed.) by Abbas and Lichtman (Copyright © 2011 by Saunders), p.133:

  A majority of B cells are called follicular B cells because they
  reside in the follicles of lymphoid organs. These follicular B cells
  make the bulk of T-dependent, class-switched, and high-affinity
  antibody responses to protein antigens and give rise to long-lived
  plasma cells.

and in the caption for FIGURE 7-2:

  Subsets of B cells. Follicular B cells make T-dependent responses to protein antigens, and marginal zone and B-1 B cells account for
  most of the T-independent antibody responses. In mice it has been
  shown that B-1 B cells arise earlier in development, from progenitors
  in the fetal liver, and follicular and marginal zone B cells arise
  later, from bone marrow precursors. Comparable differences in the
  origins of these subsets have not been defined in humans. Note also
  that the distinctions in the type of response are not
  absolute—follicular B cells can make T-independent responses and
  marginal zone B cells can make some T-dependent responses. Ig,
  immunoglobulin.

(emphasis not in original)

From the sentence I emphasized, it seems to me that as of 02011, there is still a great deal that is not well-understood about the origins (and perhaps also development?) of human follicular B cells.

Interestingly, in the 4th edition of this textbook (Copyright © 2015 by Saunders), the details have changed slightly (as below):

  Subsets of B cells. Follicular B cells make T-dependent responses to protein antigens, and marginal-zone and B-1 cells account for most
  of the T-independent antibody responses. In mice, B-1 cells arise
  earlier in development, from progenitors in the fetal liver, and
  follicular and marginal-zone B cells arise later, from bone marrow
  precursors. Note also that the distinctions in the type of response
  are not absolute; follicular B cells can make T-independent responses,
  and marginal-zone B cells can make some T-dependent responses. Ig,
  Immunoglobulin.

Most interesting to me is the removal of the 3ed sentence: "Comparable differences in the origins of these subsets have not been defined in humans." Which leads me to believe that comparable differences in the origins of these subsets have now been defined in humans (in the past 4 years).

So I have a definition and description of follicular B cells, but I am unable to find anything else in either edition of this book on the development of follicular B cells (in either mouse or human).

Another reference in my course resources is Cellular and Molecular Immunology, 8th ed., 2014, by Abbas, Lichtman, and Pillai.

In it (Chapter 12: B cell activation and Antibody Production), I find the following about follicular B cells:

  Distinct subsets of B cells respond preferentially to different types of antigens ( Fig. 12-3 ). Follicular B cells in peripheral
  lymphoid organs primarily make antibody responses to protein antigens
  that require collaboration with helper T cells.

Which strikes me as yet another description of follicular B cells, but not a list of steps in their development (which is my learning objective).

The same textbook makes several other mentions of follicular B cells, but does not address their development. Although I should probably already know this (and this may be in some of my lectures but these are not universally searchable and I have precious little time to read), I do not know about either their progenitors or their progeny, and I think this is what is meant by this learning objective: the major steps in their development.

In the same chapter of the same textbook, I also see:

  Most mature naive B lymphocytes are follicular B cells (sometimes also
  called recirculating B cells) that constantly recirculate in the blood
  and migrate from one secondary lymphoid organ to the next in search of
  antigen. Follicular B cells enter secondary lymphoid tissues (spleen,
  lymph nodes, mucosal lymphoid tissues) through blood vessels located
  in the T cell zones, and then they migrate into the follicles, the B
  cell zones of these tissues. The movement into lymphoid follicles is
  guided by the chemokine CXCL13 secreted by follicular dendritic cells,
  the major stromal cell type in the follicle, as well as by other
  stromal cells. CXCL13 binds to the CXCR5 chemokine receptor on the
  recirculating naive B cells and attracts these cells into the
  follicles. As we will discuss later, the same chemokine-receptor pair
  is also important during immune responses because it can attract a
  subset of activated T cells to the follicle.

This seems like a great description of the follicular B cell that also delves into its function, but seems to include nothing about its development.

The same chapter of the same textbook also includes:

  Naive follicular B cells survive for limited periods until they
  encounter antigen (see Chapter 2 ). Follicular B cell survival depends
  on signals from the BCR as well as on inputs received from a tumor
  necrosis factor (TNF) superfamily cytokine called BAFF (B
  cell–activating factor of the TNF family, also known as BLyS, for B
  lymphocyte stimulator), which provides maturation and survival signals
  through the BAFF receptor. BAFF and a related ligand, APRIL, can
  activate two other receptors, TACI and BCMA, which participate in
  later stages of B cell activation and differentiation (and will be
  discussed later). These cytokines are produced mainly by myeloid cells
  in lymphoid follicles and in the bone marrow.

This paragraph briefly address a little bit of what seems like the development of the follicular B cell ("Follicular B cell survival depends on..."). And in chapter 2 I see that follicular B cells are a class of B lymphocytes (along with Marginal zone B cells), but I interpret this learning objective as about the development of follicular B cells after they become follicular B cells, not before this point in their development.

So this is the best answer I can find on my own after many hours of searching and reading relevant passages in recent textbooks on the subject. Yet this answer also seems incomplete to me. After all this reading, I still have no "steps (per se) of follicular B cell development."

So I could really use a more complete answer.


Book/source for learning bioinformatics, focused on genomics?

Unix and Perl to the Rescue by Keith Bradnam and Ian Korf is an excellent introductory book and guide for bioinformatics (Linux and Perl) in genomics. It includes exercises and starts with the very fundamentals. You will still need some basic understanding of genetics and biology though.