These look a lot like dust mites, a collective term to describe cosmopolitan house-dwelling mites in the Pyroglyphidae family.

The most common species in temperate regions belong to the Dermatophagoides genus, including D. pteronyssinus (the European house dust mite) and D. farinae (the American house dust mite).

 source: Wikipedia

See here for a closeup of D. pteronyssinus

Alternatively, they may be "storage mites" belonging to the Acaridae family, which are another group of common dwelling-inhabiting mites that are more often found in stored foods vs dust, upholstery, or carpeting.

Lepidoglyphus destructor is one such example but that is also found to be present in dust [Source: Juliá et al.(1995)]. Another common storage mite, Tyrophagus putrescentiae typically eats mold, and could be found outside a food setting if the mold density was prevalent enough.

 L destructor (according to M. Deml on biolib.cz)

I'll note that there are hundreds of mites in these two families of mites alone, so someone may be able to get to a more specific species for you. Knowing more about where you found them (species of plants, etc.) may or may not help narrow down more specifically. For example, the person in this forum post found a very similar looking mite on their pots as well (see here).

Description:

Both male and female adult house dust mites are globular in shape, creamy white and have a striated cuticle. The female measures approximately 420 microns in length and 320 microns in width. The male is approximately 420 microns long and 245 microns wide.  [Source: UFL.edu]

Human impact:
The genus name Dermatophagoides means "skin eater," but these mites are not parasitic. Their diet mainly consists of eating dead skin flakes from mammals (and some birds).  Human detritus is one of the primary food sources for these mites, and so it's no surprise that they are often associated with dust in human dwellings.
So these mites don't bite humans or burrow into their skin. However, they do tend to have a negative impact on humans. Specifically their digestive enzymes remain in their feces, and these dried fecal enzymes (along with their dried dead exoskeletons) cause allergic reactions in people. In fact, according to Raulf et al. (2015), 20 allergens are known from just the two species of hdust mites mentioned above!
From UF IAFS

Mite allergens are mainly present in feces of house dust mites and may become airborne and inhaled by patients, giving rise to asthma, rhinitis, or atopic dermatitis

In fact, the family name, Pyroglyphidae, which literally means "fire + carve", seems to be related to the "burning itchy" eczema that some people develop that results in lots of scratching (carving :p).

Multiple sources suggest that storage mites often have similar allergic impacts as dust mites. Fro example, this site suggests:

In Europe, Lepidoglyphus destructor has been reported to be a major source of mite allergy in rural and urban environments

The question is, how many people are impacted?

Well, according to studies cited again by Raulf et al. (2015) that examined 7000 Germans found that  ~16% had a sensitization to D. pteronyssinus. Other studies (discussed in Hossny et al. (2014)) seem to suggest much higher prevalence in certain populations -- with sensitivities found in up to 90% of people tested from certain populations.

What can you do??
According to UF IFAS:

To manage mite populations, reduce the humidity below 70% and thoroughly vacuum mattresses, carpets, sofas, and chairs. Very sensitive individuals should encase their mattresses in plastic. Use drapes that can be washed and change bed clothing frequently. Vacuuming does not always remove all the live mites and Korsgaard (1982) stresses reducing humidity over sanitation. No one method has been found for reducing mites and relieving allergy suffering. Immunotherapy, i.e., injections of mite extracts into the patients to increase antibody level, has had variable success (Munro-Ashman et al. 1976).

Final word(s):

I'll just mention that there is a ton of literature about these mites and their impacts on humans, so if you're interested, DIG IN!

The [Major Mite Taxa] key by D. E.  walter (find at idtools.org](http://idtools.org/) is an excellent online resource for digging into mite identification further!

Citations:
Hossny, E., El-Sayed, S. and Abdul-Rahman, N., 2014. Sensitivity to five types of house dust mite in a group of allergic Egyptian children. Pediatric allergy, immunology, and pulmonology, 27(3), pp.133-137.
Julia, J.C., Martorell, A., Ventas, P., Cerda, J.C., Torro, I., Carreira, J., Guinot, E., Sanz, J. and Alvarez, V., 1995. Lepidoglyphus destructor acarus in the urban house environment. Journal of investigational allergology & clinical immunology, 5(6), pp.318-321.
 Raulf, M., Bergmann, K.C., Kull, S., Sander, I., Hilger, C., Brüning, T., Jappe, U., Müsken, H., Sperl, A., Vrtala, S. and Zahradnik, E., 2015. Mites and other indoor allergens—from exposure to sensitization and treatment. Allergo journal international, 24(3), pp.68-80.


What is the evolutionary advantage with two lungs (kidneys)?

Humans and most organisms have bilateral symmetry.  Anything that is on the left side of the body will be on the right also.  Not everything can be in the middle, so ... you end up with two.  This is evolutionarily labile - for example, fish generally have one dorsal swim bladder, though it is derived from the lungs.  In a similar manner, the heart is formed by the fusion of primordia on either side during development - see UNSW for a cute video.


How does the counter current mechanism concentrate urine?

Have a look at this figure (from here):

In the descending loop the NaCl concentration is lower than in the surrounding tissue which leads to a passive water transport along the gradient, which leads to a concentration effect. In the ascending loop then NaCl is actively transported out of the loop which then prevents the diffusion of water back into the loop.

In the collecting tube water is actively transported out leading to an even higher concentration effect. A nice animation of this can be found here.


What is the course of inter auricular line?

Up front - I have never heard of this term and I could not find information on the interauricular line. The only thing I was able to dig up was the term auricular line, which is (Fig. 1):

  [The] [l]ine pass[ing] perpendicular to the anthropological baseline,
  through the cent[er] of the external auditory meatus.

Fig. 1. Auricular line. source: Radiology Key

The anthropological line being (Fig. 2):

  [The] [l]ine join[ing] the infraorbital margin to the superior border
  of the external auditory meatus.

Fig. 2. Anthropological line. source: Radiology Key


Energy coupling between two spontaneous reactions?

Points to bear in mind

That the biological coupling of an energetically favourable and unfavourable reaction (I would avoid using the term spontaneous†) is done through a composite reaction involving all the components of the two separate reactions. The reactants and products are the same as in the sum of the separate reactions — so it is valid to calculate the overall free energy change from the separate reactions — but we are talking about a different reaction or serious of reactions that occur on the enzyme. For example in the glutamate synthetase reaction that you mention there are the two reactions shown below. Gamma-glutamyl phosphate can be considered as an activated intermediate to which the free energy of hydrolysis of ATP has been transferred, rather than dissipated in heat, as would occur in the isolated reaction with inorganic phosphate as the product.

Such coupled reactions are no different from non-coupleld thermodynamically favourable reactions in a cell in that they require an enzyme to catalyse them. They do not proceed spontaneously† because there is an activation energy barrier.  If you regard this as “forcing” a reaction, then the answer to the question you pose in your comment to @VonBeche is ‘yes’. However I would describe it as an enzyme having evolved to ‘permit’ or ‘facilitate’ a reaction. It does this by providing binding sites for the substrates and (often) a different reaction pathway that involves a lower activation energy.

So why no reaction Gln + ATP ➞ Glu + NH3 + ADP + Pi ?

This can be regarded in two ways.
(1) Why hasn’t an enzyme evolved to do this sort of thing?
Either there is no selective pressure on an organism for an unneccesary enzyme to evolve, or (in this case) if the organism needs an enzyme to deaminate glutamine one evolves, but this enzyme (glutaminase) doesn’t need to involve ATP as the reaction is already thermodynamically favourable.

(2) Why doesn’t the glutamate synthetase enzyme catalyse this reaction
From your comment, this seems to be your concern. There are three binding sites on the enzyme, one for glutamate, one for ATP and one for ammonia; and I presume you are thinking why can’t glutamine bind to the glutamate site (after all it leaves from there) and react with ATP to form γ-glutamyl phosphate. The answer to this is the chemistry of the reactions shown above. The mechanism of the glutamate synthetase reaction is complex, but at the simplest level the first stage is the nucleophilic attack of the negative acid oxygen (yellow) of glutamate on the γ-phosphate of ATP:

In glutamine there is an amino group instead of the negative oxygen, so the reaction will not occur.

Furthermore, you should be aware that the enzyme is an active participant in the reaction, and the various substrates and products are oriented specifically in relation to residues at the active site of the enzyme to allow the reaction to proceed. To give a flavour of this I reproduce a portion of the summary of a paper by Liaw and Eisenberg on the mechanism of action of glutamine synthetase. I don’t expect you (or anyone else) to digest this — it merely serves to illustrate that enzymes are highly sophisticated machines in which many components participate in producing a specific product.


Understanding the strategy of Sanger DNA sequencing

If you mark the full length strand of the DNA with the fluorescent labels, you will get a lot of signals from the same nucleotide without the possibility to discriminate where the actual nucleotide is located on the strand.

Sanger sequencing doesn't end with the preparation of the terminated and labelled DNA strands, the following step is crucial in discriminating where the labelled base actually is. After labelling, the sample is run through high resolution capillary gel electrophoresis to sort them by size. The smallest fragment comes out first, then the one with one base more and so on. The detector which then identifies which fragment is coming through is located at the end of the capillary.

This works like shown in the schematic image (from here):

If you would mark a complete strand, no dicrimination by size is possible (ideally, all DNA would run on the same height of a gel) and all flourescent signals for all positions would come on the same spot. Not very helpful.


Like Mother Cape Buffalo,do remaining mammal mother species also try to protect their babies from being eaten by predative animals?

There is quite a bit of evidence showing that mothers of a number of mammalian species will sometimes kill and eat their own young.  E.g. https://www.nationalgeographic.com/news/2014/3/140328-sloth-bear-zoo-infanticide-chimps-bonobos-animals/


Hydrophobic interactions in the helix-turn-helix

To quote Sir Max Perutz, in general, the insides of proteins tend to be "waxy", while the outsides of soluble proteins tend to be "soapy."  Those two alpha helices are interacting in a space that is energetically unfavourable for a polar solvent, like water.  Since the outside of the DNA double helix tends to be highly charged, and the edges of the stacked base pairs also have H-bond acceptors and donors, the portion of the alpha helix that interacts with the DNA sequence, will also contain charged amino acid side chains.

In contrast, the portion of the alpha helix that faces inwards, towards the interior of the protein, will have largely non-polar side chains.


What is the relative power of GWAS studies in different species?

Part of the increase in power to detect a genetic association via GWAS-genotyping comes from long haplotypes. Many dog breeds went through selective breeding bottlenecks 100-200 years ago. Many lab model organisms, such as flies, worms and plants, have recombinant inbred lines that aid in GWAS discovery as well. The price one pays for this increased power, say for canine GWAS, is not being able to pinpoint the casual variant. The association SNP(s) found may be far, far away from the gene responsible for the phenotype, because of that long LD.

Another aspect not to neglect is the phenotype. In humans, there may be a 3-fold range in phenotype p, while in dog that value is just 35% (1.35x). That may mean that the phenotype is difficult to measure (accurately) and to assign to a given allele with statistical certainty.

A third aspect to consider is the effect size of the association, say on a per (risk) allele basis.

Thus, while I am not aware of any papers specifically taking such elements as haplotype length, phenotype range and effect size into an analysis of GWAS power across species, I feel that one versed in genetics of the organism of choice can readily accomplish this for the specific trait(s) of interest.


Are the intestinal microbiota substantially different within a diverticulum of the colon?

The appendix is a type of true diverticulum of the colon, although it is one that is present in everyone (unless a surgeon has removed it). There are bacteria in the gut from the mouth all the way down to the anus, and the numbers and types of bacteria change along the length of the intestinal tract. A recent review from J. Ridlon published in the Journal of Lipid Research (2006) is available online and has documented these observations from a number of investigators. In that paper the bacterial species are described as changing as well as the relative abundances of bacteria which increases along the length of the intestinal tract. Figure 1 from that paper which is open access available from the link above is below.

I think its interesting that the wiki page you're citing states that individuals without an appendix were more likely to develop a recurrent C. diff infection. One could interpret that as they did on that site that somehow the appendix is repopulating the colon and making that individual more resistant to a repeat or "Recurrent" infection. However, I don't know of any studies that have directly tested that hypothesis.

In terms of whether or not the gut flora - aka "gut microbiota" - are significantly different in the appendix is possible, but I don't think anyone has identified that just yet. One of the problems with this would be that we don't routinely remove appendices unless they are infected/inflamed which intrinsically would alter the microbiome locally.

So, is it possible that the microbiome could be significantly different in the appendix itself compared to the cecum just a few centimeters away? The answer would be - potentially, but no one has been able to address that question to date.


What could cause hairs to gray at the tips but not the roots?

Interesting question, I am not sure if I have a definite answer, but at least some ideas:
The pigment in the hair is made by specialized cells, the melanocytes. The make the pigment (eumelanin=dark and pheomelanin=red/yellowish) which is then deposited into the growing hair. They are located at the bottom of hair bulb and usually die at the end of each hair cycle. To have the hair of the next hair cycle colored as well, this melanocyte population in the hair bulb needs to be replenished. This is done by melanocate stem cells, which live in the hair bulge and which start to reproduce and differentiate in melanocyte which then migrate down to the hair bulb. There is an excellent article following this process:

Mechanisms of hair graying: incomplete melanocyte stem cell
maintenance in the niche.

The hair later gets grey (low pigment) and white (no pigment) when these melanocytes are not, or not fulley replenished in later hair cycles. Why this happens, there are a few hypothesis.

First, its possible, that with age the melanocyte stem cell population (which not only need to replenish the melanocytes, but also need to maintain its own population) is getting smaller and disappears over time. This process would explain gradually graying over time. See this reference:

Melanocyte stem cell maintenance and hair graying.

Another possibility is the presence of reactive oxigen species (ROS) which occur naturally in melanocytes. Over time, the enzyme which intercepts this ROS (catalase) is getting less active or present in the cells and thus oxidative damage is getting bigger, damaging the melanocytes and their ability to make pigment. It would actually bleach itself...

Senile hair graying: H2O2-mediated oxidative stress affects human
hair color by blunting methionine sulfoxide repair

Melanin has also an important role in intercepting ROS, so in this process less and less pigment is made (as the damage accumulates) and this also leads to hair, which is less pigmented for exogeneous oxidative stress:

Towards a "free radical theory of graying": melanocyte apoptosis in
the aging human hair follicle is an indicator of oxidative stress
induced tissue damage.

It could be possible (and this is a wild guess) that the phenomenon of the tips graying first is situated by this. Hair less protected against exogeneous oxidative stress (smoke, UV etc.) so the melanin is "used up" during this until the hair greys at the tip, since its the oldest and most exposed part of the hair. This article by Tobin gives also a nice overview:

The cell biology of human hair follicle pigmentation


Is RGB diode lighting okay for the eyes?

At a fundamental level, no, we're fine with LED lighting.  The absorption spectra of our cones are quite broad, and RGB LEDs are chosen to match our color sensitivity reasonably well.  That red+green looks the same to us as light that is actually yellow is because our eyes can't tell the difference since we don't have good enough spectral resolution in our vision.

There could be more subtle emotional or other complex effects, but to a good approximation, if it looks right it is right, and there aren't magical frequencies that we need to avoid e.g. retinal degeneration or something else awful.  (Well, large amounts of UV are bad, but RGB LEDs don't produce a significant amount of UV.)


identifying which SNPs sit in TFBS (Yeast)

I agree it can be extremely confusing sometimes to find the right data.

Do you know RSAT (Regulatory Sequences Analysis Toolkit) ?
If you go in "help & contact", and "motif databases", you'll find the Yeastract database: http://rsat-tagc.univ-mrs.fr/rsat/motif_databases/Yeastract/

I thought it would also be on JASPAR, but couldn't find it.

Then for your analysis where you look for SNPs in the motifs, there is a tool on RSAT, that unfortunately works only with the Metazoa database right now, but you might be interested to check it out, and the corresponding paper: http://rsat-tagc.univ-mrs.fr/rsat/variation-scan_form.cgi


Connect the inner and outer space of cell with a wire, will there be electricity?

Let's start with the basics.  The inside of the cell contains predominantly positive potassium ions, and negative phosphate ions, and other negative ions (e.g. from amino acids).  The outside of the cell contains predominantly positive sodium ions, and negative chloride ions.

The cell however sets up a resting membrane potential, due to the cell's semi-permeable membrane, allowing predominantly only potassium to pass through the membrane.  This causes potassium to flow along its concentration gradient towards the outside of the cell, until it is balanced by the electric potential that is consequently set up.

So we now have POSITIVE potassium ions on the outside of the cell and NEGATIVE phosphate ions (or other negative ions) on the inside of the cell, which aren't balanced.  Now as the wire is placed between the inside and the outside of the cell, electrons from the negative phosphate ions will travel through the wire, towards the positive potassium ions on the outside of the cell.

Once this occurs, the potassium from the cell's interior can now continue to flow against its concentration gradient, because the previous potassium ions in the exterior no longer contribute to an opposing electric potential.

Additional note:  As the K+ ion in the extra-cellular fluid gains electrons from the wire to form K, it will react almost immediately with water to form KOH and H2 (hydrogen gas).  The K and OH will be soluble in the extra-cellular fluid, forming K+ and OH- ions.  Over time the K+ ions will be "pumped" back into the cell's cytoplasm.  (The left over OH- ions will temporarily increase the flow of K+ down its concentration gradient, etc.)


The measured blood pressure is the radial pressure exerted by the blood column againt the arterial wall.

In a normal patient, this pressure varies between 120 mm of Hg and 80 mm of Hg.

click on the image to go to the source

When a cuff is inflated to 160 mm of Hg, the arteries collapse and circulation is temporarily suspended. As blood flow does not occur, no sound is audible.

The korotkoff sounds that are heard while measuring BP are due to disturbance in the streamlined flow of blood. When auscultating an artery without applying pressure no sounds should be heard in a normal person. Generally they are heard when blood flow occurs in spurts. This occurs when the cuff pressure is lesser than the systolic pressure but more than the diastolic pressure.


What are different firing rates in different regions in the human brain?

The article, has a classical engineering approach (might be wrong I just skimmed it), not that it's a bad thing. The general criticism of bias against sparsely coding neurons is correct, don't know how they can say its a factor of 10 or anything else though.

Average firing rate of one neuron only makes sense in relation to a different condition. For example in sensory neuroscience studies, we say a neuron likes a stimulus if the average firing rate of this neuron while the stimulus is presented is higher than in an equal period in the absence of the that stimulus. Conversely a neuron dislikes a stimulus when the average firing rate goes down.

Average firing rate across all neurons also is a weird measure as neurons have different baseline firing, different morphologies, are part of different circuits and have different functions in these circuits. It would be like saying that the average of a normal distribution is enough to describe it ignoring its variance.

Regarding the question itself a couple of things should be better defined: what is higher order thought? and medium time planning of what?

Neurons certainly do not all fire at the same rate, however rate implies a time constant and most importantly when one averages across multiple neurons one must have a criterion of selecting them which begs the question: Which neurons? How does one defines an area of the brain? Morphologically? Functionally? Genetically? Furthermore, what is its relevant time constant? These seem like basic obvious questions however they don't seem to have a clear and defined answer yet.

You seem to have a particular architecture in mind with multiple areas that have different functions, I assume you are modeling it. All models are wrong (yeah yeah I know its a cliche) which is to say that every model has a particular set of more or less valid assumptions. You just have to know what these assumptions are and what you can conclude given these assumptions. So basically there isn't really an answer to your question from the biology side we're still blind scientists in a dark room looking for the brain dead cat that is hiding the light switch.

Once I figure out the function of an arbitrarily defined brain area I'll let you know its time constant, then again it is arbitrarily defined and I cannot possibly figure out its function in all possible conditions without having assumptions of my own of how things should work...


Why are certain aneuploidies more common?

I thought it was just that the other aneuploidies were fatal. They occur as often but miscarry earlier in the term therefore you don't see them. So basically there are only three that are viable 21,18 and the sex chromosome with a number of combinations: XO, XXY, XYY and XXX.

More information here:
http://www.nature.com/scitable/topicpage/chromosomal-abnormalities-aneuploidies-290

With regard to the frequency for each chromosome:

For males (i.e., sperm; source):

  The mean disomy frequency is 0.15% for each of the autosomes and 0.26%
  for the sex chromosomes. Most chromosomes analyzed have an equal
  distribution of disomy with the exception of chromosomes 14, 21, 22
  and the sex chromosomes, which display significantly higher disomy
  frequencies.

Size of the chromosome is frequently reported as a factor in the frequency.

For females (i.e., eggs; source):

  The data is obviously harder to attain. One study from IVF treatments
  show differences in the frequency of different chromosomes at
  different stages in meiosis.


What is the role of pyrophosphatase in RNA polymerization?

This question can be answered by considerations of chemical equilibrium. For any chemical reaction:
$$\ce{A + B <=> C + D}$$
It is a property of nature that removal of product ($C$ or $D$) from the reaction mixture drives the reaction in the forward direction. This is an example of le Chatelier's principle and can be explained as follows:
In a reaction mixture containing $A$, $B$, $C$ and $D$, the rate of forward reaction ($A + B \rightarrow C + D$) depends on the frequency of collision of $A$ and $B$ molecules. Similarly, the rate of backward reaction ($C + D \rightarrow A + B$) depends on the rate of collision of $C$ and $D$ molecules. The collision frequencies, in turn, increase with concentration of the relevant species. An abrupt reduction in the concentration of $C$ hinders the backward reaction while leaving the forward reaction unchanged. Thus the forward reaction begins to dominate.
The reaction catalysed by RNA polymerase is:
$$\ce{RNA + NTP <=> Longer \ RNA + PP_i}$$
By removing $\text{PP}_i$ from the reaction mixture, pyrophosphatase does exactly that and drives the reaction in favour of RNA polymerisation. Note that hydrolysis of pyrophosphate is favoured because of the negative free energy change associated with it (thanks to David for pointing that out).


Are there fundamental differences between the adaptive immune systems of higher primates and other mammals?

I am not aware of a discriminatory feature between primates and all other mammals. However, there are significant differences for some animals. For example, the anti bodies of camelids and sharks consist of the heavy chain only, or the antibodies of sea lampreys are not of the immunoglobulin protein family.

Those differences have been exploited for biotechnology.

consider this review: http://www.nature.com/nbt/journal/v23/n10/full/nbt1127.html


when does an erythrocyte start carrying oxygen molecules and what is the binding capacity

Erythrocytes contain many hemoglobin proteins. Each protein has 4 haem groups, and oxygen molecules bind to in porrin ring inside these haem groups. The binding capacity is the affinity each haem group has for oxygen. This changes depending on the external conditions, for example PH.

For example, when the ph is quite low (acidic), this is often due to CO2 build up in the local area, dissolving in the blood to form carbonic acid. This means that there is anaerobic activity happening in the area so it needs more oxygen. The oxygen associated with the hemoglobin will disassociate making it available for the surrounding tissue. It is important to remember that the process is not concrete and is always fluctuating. There are many curves that show the likelihood of association and disassociation. I would recommend looking at these disassociation curves to understand.

Erythrocytes are typically oxygenated in the lungs (supplied by the pulmonary artery from the heart). After oxygenation, the blood goes back to the heart via the pulmonary vein in order to be sent round the body. Reticulocytes are immature erythrocytes and will be carrying increased amounts of haemoglobin as they develop it. The following link leads to a paper which approximates haemoglobin content in reticulocytes.

  https://www.ncbi.nlm.nih.gov/pubmed/18027835


High intracellular glucose.

Affects: all cells that do not depend on insulin to take in glucose. Examples: neurons [1], kidney cells, retina cells.

Causes: high extracellular glucose (in most cases hyperglycemia)

Effects: promoting necrotic cell death through $H_2O_2$ (peroxide) formation, which may participate in the development of diabetic vasculopathies and associated disease [2].

High extracellular glucose.

Affects: extracellular matrix, cardiac muscle

Causes: lack of / low levels of insulin, insulin resistance

Effects: enhances collagen production thus affecting kidney by thickening glomerular basal membrane [3, 4]. It promotes cardiomyocyte metabolic stress and altered glucose handling [5]. It is also a potential mechanism involved in cardiac glycogen accumulation [5].

Diabetes mellitus involves:

high extracellular glucose, leading to:
high intracellular glucose in cells that do not depend on insulin to uptake glucose;
low intracellular glucose in cells that depend on insulin (muscle and fat tissue).

References:

David R. Tomlinson and Natalie J. Gardiner. Glucose neurotoxicity (2008). Available from http://didattica.uniroma2.it/assets/uploads/corsi/140868/Glucose_Neurotoxicity_-NATURE_Reviews-Neuro,_Jan_2008.pdf (accessed 27.07.2014)
RnCeus.com. Glucose Homeostasis (2012). Available from http://www.rnceus.com/dmeds/glucose.html (accessed 27.07.2014)
Takeuchi A, Throckmorton DC, Brogden AP, Yoshizawa N, Rasmussen H, Kashgarian M. Periodic high extracellular glucose enhances production of collagens III and IV by mesangial cells. Am. J. Physiol. 1995 Jan;268(1 Pt 2):F13-9. PubMed PMID: 7840239.
Ayo SH, Radnik RA, Garoni JA, Glass WF, Kreisberg JI. High glucose causes an increase in extracellular matrix proteins in cultured mesangial cells. Am. J. Pathol. 1990 Jun;136(6):1339-48. PubMed PMID: 2356864.
Kimberley M. Mellor , Upasna Varma , David I. Stapleton , Lea M. D. Delbridge. Cardiomyocyte glycophagy is regulated by insulin and exposure to high extracellular glucose. American Journal of Physiology - Heart and Circulatory PhysiologyPublished 15 April 2014Vol. 306no. H1240-H1245DOI: 10.1152/ajpheart.00059.2014


Which viruses still present today caused a deadly pandemic/epidemic in the past?

There are a few viruses which are around for a long time and have caused recurring episodes of disease. Most of these where not pandemic, which is probably more of a problem for modern times due to fast travel/exchange of people and are also a problem of "modern" cities where many people come together in a limited space.
Among theses viruses are:

Measles: This virus is around since at least 400 BC, profiting from the first big cities. (see reference 1 and 2 for more details)

Polio: This virus has been described already in ancient Egypt, although major outbreaks didn't happen before the early 20th century. There is a nice article in Wikipedia about it, see reference 3.

Smallpox: These are only not threat anymore because mankind successfully eradicated them. They have been described first around 1500BC in India, later also in China and Egypt. See reference 4 and 5.

Not viruses but also pathogens which caused historic epidemics: Typhoid fever, Cholera and the Yersinia Pestis (also known as The Plague or the Black Death).
References:

The history of measles: from a 1912 genome to an antique origin
Measles may have emerged when large cities rose, 1500 years earlier
than thought
History of Polio
Emergence and reemergence of smallpox: the need for development of a
new generation smallpox vaccine
History of Smallpox


Why are there multiple sequences for the same segment for an individual "strain" of influenza?

It looks to me that the website you're looking at is mostly taking publicly available data from Genebank (the NCBI repository for sequence data) an collects it to form an overview.

For your question this means that there are 4 available sequence datasets for the A/Michigan/45/2015 influenza strain - they are likely very similar but based on the reported segment length not quite identical.

  Or is it that they are including both positive and negative sense of the virus?

If you mean the positive and negative strand of the DNA, then no - since the sequence of these two is always complementary the Genebank repositories only stores the forward sequence.

You can also see that the 4 different datasets have similar Acession numbers:
KY117020 - 27 (Passage M1/C3)
KU509700 - 07 (Passage E1)
KU933490 - 07 (Passage E3)
KY090607 - 14 (Passage M1/IR)

You can look up more details for these accessions on the genebank website:

It seems that all 4 datasets came from the same publication
... which apparently was never published (so it's not available online), but it might be part of some WHO program?
The main difference of the 4 datasets I can find is the passage of the strain. I'm no virologist, so I'm not quite sure what it means, but in cell biology passage describes the time a certain cell line has been in (in vitro) culture.


Bionomics is indeed the 'thorough' study of living organisms and their relationship with the environment/ niche they thrive in.

Aim of Bionomics is mainly to decipher the driving factors for an organism to prefer a given niche. Given this key goal, it is apparent that one needs to focus on all aspects of an organism's life cycle and community dynamics.

So the answer to your question would be: Yes, one will need to focus on all the five points pertaining to Anopheles sp. (the 5th point i.e diseases caused) will more be an information resulting out of the study of its interactions with other living/ non-living forms), than a specific focal point for Bionomics.

References:

A good article on Bionomics

An amazing and detailed report on Bionomics of Entomophagous Coleoptera

Other references:

The dominant Anopheles vectors of human malaria in Africa, Europe and the Middle East: occurrence data, distribution maps and bionomic précis. Sinka et al., 2010

Description and Bionomics of Anopheles (Cellia) ovengensis (Diptera: Culicidae), a New Malaria Vector Species of the Anopheles nili Group from South Cameroon. Awono-ambene et al., 2004


Should hydrogen peroxide be applied on a bloody nose?

No, I don't think oxygenated water does anything to stop bloody noses. But holding a wet cotton swab with pressure to the inside of the nose might.

The vast majority of bloody noses in healthy individuals arise from one specific area in the nose (on either side):

In the mucosa of the nasal septum (the cartilagenous structure separating the nose into two sides), there is an area where several arteries "meet", giving it an exceptionally rich vascular supply, called Kiesselbach's plexus. It is on the anterior surface, and exposed to dry air and trauma (even such as might be sustained by a bad cold). Bleeding typically occurs when the mucosa erodes for any reason, and the capillaries and venules (and sometimes arterioles) become exposed and subsequently break. The result is the familiar bloody dripping of a nosebleed.

The most common treatment is direct pressure (squeezing the sides of the nose together) for 5-10 minutes. This works because putting direct pressure on any bleed stops the blood flow long enough for a clot to form and the arteriole to close down.
If needed, more aggressive control can be achieved by a professional.

If you happen to apply pressure with the wet cotton swab to a large enough part of the plexus (or somewhere near the spot from which your nose is bleeding), your nosebleed will stop. But it really doesn't matter what you use to wet the cotton swab (plain water, oxygenated water, carbonated water (ouch!), or other. (Noted: OP added that the liquid is hydrogen peroxide. This is not a good idea as it is an irritant and actually can cause mucosal damage.) Sufficient pressure and clot formation (and subsequent tenderness with the nose) is all that is needed.*

What doesn't work:

icepacks to the neck
leaning your head forward (increases blood flow) or back (may cause the blood to flow into your throat)
lying down (increases blood flow)
frequent 'peeking' to see if bleeding has stopped
a dry object placed against the area of bleeding (it will break up the clot when pulled away from the septum)

Aftercare and prevention is another subject.

Note: The safest way to end a common nosebleed is by squeezing as much of the 'rubbery' portion of the nose together for up to 30 minutes if necessary. Putting something into your nose poses the risk of infection.

*more serious or recurrent bleeding needs medical attention


What gene targets associated with the new coronavirus (SARS-CoV-2) have been identified so far?

This is an interesting question. A recent study published on bioRxiv by researchers from Xi'an, China (pre-print) argues that CD147 can also be an entry receptor for the virus. They showed virus entry can be blocked by an antibody to human CD147.


How long does it take for E. coli to shift feedstocks?

This must depend upon the conditions in question, but I think it would not be very long.
The length of a generation for e coli can be 12 minutes or 24 hours, so that gives some idea of a typical time.

I did find this interesting case in the literature. They found that even as you subject e coli to minimal nutrients they are expressing genes that prepare them for a richer nutrient mix.  The bacteria are primed for a flood of carbohydrates succinate or amino acids.

This study incubated the e coli overnight before taking their readings, so this puts an upper bound of about 12 hours.  The implication is that if you are moving the bacteria to rich media it might be just a short time before they are in log phase growth.

In practice moving from LB plates to log phase growth is usually just like 4 hours.  This paper interestingly shows that cold adapted E coli moving to other media react in a few hours, but can show behavioral changes days out.

I would say that 4 hours might be a typical expectation. 12 is typically used in the literature.


Comparing gene expression levels between control and disease at different time points

The gene expression profile may change at different time points between the two groups; you should decide what you actually want to measure. If you want to see if the diseased group is different from the control then you should compare them at every time point. For most situations you would need to compare just their steady state behaviour.

Imagine a diseased individual who shows some physiological differences at certain developmental stages compared to the control but in the end turns out to be perfectly normal. So what matters in most cases is the steady state and not the transients.

However if you are interested in the change in expression then you should compare ([D1] - [D0]) with ([C1] - [C0]). This will tell you if the dynamics of the diseased and the control samples are similar or not.

There are issues with fold changes. Though they are decent measures, you cannot really apply a t-test with fold changes (normalizing to 1 is a different thing).

You can do another t-test between [C1] and [C0] (similarly for D). This would tell you if the diseased or control population changes its expression at time t=1 or not.

AFAIK you cannot compare the dynamics and the values simulatenously. What you should test depends on what you are interested in.


Why PPD test in patients without M.tuberculosis often slightly positive?

The question asks PPD test in patients without M.tuberculosis.
It does not say if the patient has previously had infection with M.tuberculosis.
I think this question implies that the patient has never had before infection with M.tuberculosis.
I am not sure how it can be in reality possible for adults, since M.tuberculosis spreads in air.

The reason for false positiveness can be that assays that use PPD use unspecific antigens, in contrast to IFN-gamma and second-generation assays.

The other reason is that once you get infected you always have some degree positive skin test reaction.
So to say patient without M.tuberculosis is faulty in a way because I think most people get exposured to this bacteria at least little in life.


Assuming that you know the amount of NADH and FADH$_2$ produced by glycolysis and TCA cycle, you can determine the reducing equivalent produced: for each NADH or FADH$_2$ produced, two reducing equivalents are produced. It means that the re-oxidation of NADH and FADH$_2$ will release 2 electrons. Here are the corresponding half-reactions:

$\textrm{NADH} = \textrm{NAD}^+ + \textrm{H}^+ + 2~\textrm{e}^-$

$\textrm{FADH}_2 = \textrm{FAD} + 2~\textrm{H}^+ + 2~\textrm{e}^-$

Knowing the total reducing equivalent produced, divide it by four in order to obtain dioxygen consumption: O$_2$ is reduced into 2 H$_2$O by accepting four electrons. Here is the corresponding half-reaction:

$\textrm{O}_2 + 4~\textrm{e}^- + 4~\textrm{H}^+ =  2~\textrm{H}_2\textrm{O}$

Of course this only applies to aerobic organisms: some microbes are able to use other electron acceptors than O2.


What if Staphylococcus Aureus are extinct?

It is almost entirely parasitic and has not physiological or ecological effects that could not be replaced easily by another bacterium. It is responsible for immeasurably more infections that protections of humans, therefore it is a disease vector, not a beneficial bacterium.

If it went extinct, humans may suffer from increased population pressure, that would be the only worry.


Is ovum + ovum fertilization possible for human?

Using a somatic cell in an a ovum is what is typically done in the process of cloning.  It was the same process used to create Dolly the Sheep. What you're asking about is something very different:

Consider that somatic cells are properly diploid.  Whereas an ovum itself just contains a haploid number of chromosomes. In typical sexual reproduction the sperm fertilizes the ovum which would than bring the chromosome number to to correct tally.  So combining the genetic material in two ovum should bring the chromosome count to the correct tally as well, but scientists would need to somehow motivate the  activities that happen when typical  sexual reproduction occurs. It's likely very challenging to do that if not highly improbable. Should it work, this process could only produce female children.


Can the sensory neuron network and the motor neuron network be considered separate networks?

The sensory and motor pathways can indeed be considered separately both in concept and physically. Of course the nervous systems is a single network of neurons, but that doesn't stop it from having separate components.

One can indeed often simplify neural pathways as "IN (sensory) ===> (black box with decision-making magic) ===> OUT (motor)"

Reflexes

Reflex arcs are a great way of demonstrating this separation because they do not involve the more complicated integration of the brain. Let's take the knee-bend (patellar) reflex as an example: https://en.wikipedia.org/wiki/Patellar_reflex

The diagram is correct in concept but let me add the anatomical detail to illustrate how sensory and motor pathways are separate, yet connected: When the reflex is triggered, the signal travels up from the sensory neuron ends located under the knee cap (these are dendrites) to the sensory neuron's body in the spinal chord. The sensory cell relays the signal via its axon, which then synapses with a motor neuron's body also in the spinal chord. The motor neuron then sends a motor impulse via its axon back down to the leg, where it triggers muscle contraction.

Physically, in this case there will be a separation also in nerves (at least if I may trust Wikipedia for now), where the sensory reflex neurons' dendrites travel from the leg to the spinal chord through an afferent nerve and the motor neurons' axons travel in the reverse direction through an efferent nerve. The only physical and conceptual connection between the sensory pathway and the motor pathway is the synapse between the sensory and the motor neurons in the spinal chord.

More complex sensorimotor pathways might include interneurons or integration with various circuits in the brain, but it is usually possible to define discreet separate parts of the pathway, one sensory and one motor, with the only connection being those interneurons.

Sensory and motor separation in the CNS

The central nervous system (CNS, which includes the brain and the spinal chord) is actually surprisingly organised in this regard, with quite strict separation of motor and sensory pathway components. For example, the cortex of the brain has distinct regions which contain sensory neurons for evaluation of various types of peripheral skin sensation. Separate from these are regions which contain motor neurons for movement of skeletal (voluntary-control) muscle. The interaction of these is of course more complex given that it involves skin sensation and conscious decision making in regards to movement.

Likewise, the spinal chord is structured into sensory and motor regions. In summary, the spinal chord consists of: 1) cell bodies (motor, sensory, inter; grey in the picture), 2) ascending axons (blue), 3) descending axons (red). Similar to nerves, axons going up or down the spinal chord are bundled into "tracts". Sensory axons are never bundled with motor axons, making it possible to create a map of the spinal chord in cross-section.

The tracts' names might be a bit confusing at first, but on second look are actually pretty self-explanatory. They usually contain where the axons come from and where they are going in order to synapse with other neurons. E.g. the spinocerebellar tract is formed of axons coming from the spine and going to the cerebellum. Given that the cerebellum is near the brain and the spine is further down, this is obviously an ascending tract - and ascending tracts are always sensory (because sensory information never needs to be carried downwards due to the brain being at the top).

Where it gets blurry

The sensory/motor separation isn't always as clear as I've described above. In fact, nerves (bundles of axons anywhere in the body outside of the CNS) will usually contain both sensory and motor pipelines. In particular, the cranial nerves (12 of the most important nerves) all include sensory and motor components for the respective part of the body that they manage. E.g. the facial nerve contains both the sensory connections for parts of the tongue and the motor connections that control facial muscles.

Another more complex example is pain sensation, where interneurons in the spinal chord can feed back onto sensory neurons and inhibit their signals, or axons can inhibit those packed in the same nerve bundle simply due to electrical effects.


Going by an e-value or bitscore cutoff will give you possible homologs, but it sound like you want to remove redundant sequences. If you want to cluster and combine similar sequences to make a smaller database, you could just go via sequence identity using something like CD-HIT. This, for example, is what's done to produce the UniRef set from the UniProt database.


Short answer
Technologically yes, but practically no, because there would be no surrogate mother available to bring the artificial XX zygote to term.

Background
Theoretically a cell with two male Xs can be generated, given that it is technically possible to shuttle single chromosomes between cells (Paulis, 2011).

However, assuming that in your future world oocytes are available from oocyte banks and sperm from sperm banks just like they are today, then the artificial combination of two Xs from male cells wouldn't be necessary in the first place, as regular IVF could be used.

Note that in both the chromosome transfer and IVF scenario, a female would still be necessary to implant the zygote. Until artificial wombs become available (they are not), it is impossible to generate females without females.

Reference
- Paulis, Methods Mol Biol (2011); 738: 57-67


Why does a "cascade" of events happen during signal transduction?

There is one main reason: Amplification of the signal. You can start a signal downwards the cascade with relatively few receptors which need to be activated which allows even for weak signals to be translated into the nucleus.

This figure shows this for G protein coupled receptors (from here):

For example one molecule of cAMP can activate many molecules of pKA until it's hydrolysed which in turn can phosphorylate many other protein molecules.

For more information you can read the references articles (at least the introduction) and follow the references in them.

References:

Ultrasensitivity in the mitogen-activated protein kinase cascade
Noisy signal amplification in ultrasensitive signal transduction


You are right that the membrane doesn't stop everything.  Its main purpose is to separate the inside of the cell from the outside so that you can accumulate resources in it.  Your potassium ions, proteins, sugars, RNA (and DNA, behind another membrane) have to stay inside the cell because they can't dissolve through it.  There are indeed channels and transporters from some hydrophilic substances as you say, but they are usually very specific about what chemicals they will transport.*
The membrane is actually very delicate but it is reinforced by a cytoskeleton, and proteins are embedded in it to transmit force to features outside the membrane (such as desmosomes and hemidesmosomes connecting to other cells or extracellular matrix) so that the membrane itself is never put under strain.  Think of it like a thin plastic bag that can hold water because you put it inside a much stronger container - even though the stronger container is not waterproof.
Many harmful chemicals would not be harmful if they could not get into your cells, so you should not be surprised if they are often hydrophobic and dissolve freely through the membrane.  Some cells have other defense mechanisms (pumps to try to expel the toxins or enzymes to try to break them down), but ultimately any true toxin is defined as the one for which nothing works well enough.
Many pathogens have evolved methods of crossing the cell membrane.  Bacteriophages famously break a hole in the membrane with a special injection apparatus, while many human viruses fuse a cell membrane section they carry around themselves with the victim cell membrane, using proteins that have evolved the right hydrophobic features.  It is hard to defend against such things because our cellular membranes need to be able to fuse with themselves for purposes such as releasing vesicles of neurotransmitter.  The same "no true pathogen..." argument applies - we only get sick from the pathogens that can infect us.  If we lacked these protections, we would be even more vulnerable than we are.

Exceptions, perforins and granzymes, prove the rule:  they are meant to kill the cell affected.


CD4+ as Monocytes cell surface receptors

Macrophages and monocytic cells can express CD4, CD8 or even co-express them. The CD4 and CD8 molecules interact with MHC complexes on neighboring cells, and as you can imagine elicit varying effect in a cell type-dependent manner.

Plainly enough, Zhen et al. demonstrated that monocytic CD4 ligation to MHC-II molecules on other cells, such as activated endothelium, induced an expression pattern conducive to macrophage differentiation (1). Gibbings et al. also demonstrated that CD8 associates with FcyR on the monocyte's surface similar to CD8/TCR associations, and stimulates the secretion of cytokines (2).

I'll try to find a model source, but CD8a on dendritic cells can associate with MHC-II molecules on T cells like HLA-DR and aid in cross-priming the T cells.

Now what CD4 does on functional, differentiated macrophages is less clear to me, and I need to review the literature on that a bit more. It could just be expression imprinted because they're monocyte-derived cells, or it could also elicit an effect like CD8/FcryR above. I do not know.

There are more cases, so these serve as selected examples.


How to interpret the simple sequence repeat (SSR) on the coding sequence, but not the related protein sequence?

SSR searching tools have generally no idea about CDSs: they consider DNA/RNA sequences as strings and search for tandemly repeated patterns, nothing else. It is also important to remember that in many real-life cases different programs with different settings will reports differing results.

[Knowing that you always have two strands in the genomic DNA, one has to bear in mind that also SSRs can be "read" in either direction, such that for a stretch ACCACCACC the unit can be reported as ACC or GGT. Some programs by default will report SSR units sorted according to alphabet: ACC in this case. Now with coding sequences the story is a bit different: RNA has only one strand, i.e. it has a direction, which means that you cannot "flip" RNA sequences.]

mRNA besides having a direction, codes for protein with the protein sequences sometimes showing their own repeated patterns. SSRs in mRNA are mostly tri-nucleotides or with unit lengths divisible by three and coincide with the tandem aminoacid repeats. So, from the functional point it is a ACC|ACC|ACC|ACC|ACC|ACC|ACA (note that the last element is ACA) repeat, which codes for the respective T|T|T|T|T|T|T aminoacid repeat. To formalize this idea you search for SSRs in the RNA sequence and in the protein sequence and try to find the overlap.

From the point of view of the DNA-polymerase [the enzyme which changes the SSR length] it is a perfect CCACCACCACCACCACCACCA repeat: within these limits the fragment is prone to slippage. But for an actual slippage event the unit boundary does not matter. Imagine that the polymerase "skipped" a CAC unit in the middle: CCACCAC[CAC]CACCACCACCA. The outcome for the protein sequence will be the same: minus one threonine.


At what point is a picked flower considered dead?

This is very much analogous to your "limb" suggestion, or, since the flower is a reproductive organ, one can ask,

  At exactly what point is the uterus considered dead after a hysterectomy?

or,

  At exactly what point are the testicles considered dead after a male dog is castrated?

The organism (woman and dog respectively) does not die. Tissue dies. Tissue dies all the time. Red Blood cells die after about 120 days, give or take. Skin cells die faster than that.

It depends on the definition of death. If one of the requirements for "life" is the ability to reproduce, are both the woman and the dog now dead? Of course not. They had the potential, or perhaps they already reproduced.

If one of the requirements for "life" is the ability to grow, well, the uterus and the testicles are dead immediately upon removal. But we stop "growing", and we don't die.

If one of the requirements for "life" is the ability to respond to its environment, the uterus and the testicles are not dead. They are "alive" for a time, though the environment is toxic to them if thrown away. If placed in nutritious media, they will "live" a bit longer.

Common sense, which often isn't reliable in science, would dictate that the flower dies when it can no longer maintain cell turgor, i.e. can no longer absorb fluids. But the argument can be made that it is only "dying" at that point.

Basically your question depends entirely on the definition of life. And that has not been agreed upon.


Spread of malaria from an infected person

With humans infected with malaria, the parasite load in the blood can be quite high. It ranges from 10 to 108 Plasmodium falciparum parasites per ml .

When a female Anopheles mosquito bites an infected human, they take in infected blood, not just the parasite. They take in a few micro liters of blood, which in usually enough to get themselves infected, and the next time they bite a human (about one week later), the infection is spread.

You can learn more at the CDC malaria FAQ and their overview of the malaria transmission cycle.


Is there a scientific explanation for male and female fragrance preferences?

The idea that males and females react differentially to various smells in the context of “hard science” alludes to the concept of sexual dimorphism in olfactory signaling, which has been investigated:

  Stowers & Logan. Sexual dimorphism in olfactory signaling. Current Opinion in Neurobiology. 2010. 20,770-775.

    What makes males and females behave differently? Although genetic master-regulators commonly underlie physical differences, sexually dimorphic behavior is additionally influenced by sensory input such as olfactory cues. Olfaction requires both ligands for signaling and sensory neural circuits for detection. Specialized subsets of each interact to generate gender-dimorphic behavior. It has long been accepted that males and females emit sex-specific odor compounds that function as pheromones to promote stereotypic behavior. Significant advances have now been made in purifying and isolating several of these sex-specific olfactory ligands. In contrast, the neural mechanisms that enable a gender- dimorphic response to these odors remain largely unknown. However, first progress has been made in identifying components of sexually dimorphic olfactory circuits in both Drosophila and the mouse.

You’re right that most research in humans (like this paper) on this subject includes elements relating to sexual orientation or sexual selection, but I did find one article that is more relevant to your question:

  Lindqvist. Preference and Gender Associations of Perfumes Applied on Human Skin. Journal of Sensory Studies. 2012. 27,490-497.

    Abstract

      The perception of fragrances has been a growing field of interest, where perfumes classified as either typically feminine or typically masculine primarily have been used as stimuli. The current study explored gender associations and preferences of more “unisex” perfumes found in the middle of a gender continuum of fragrances, both when the fragrances were applied on humans, and when they were presented in glass bottles. Blindfolded participants indicated if they wanted to use the fragrances themselves, if they wanted their partner to use the perfumes, scaled gender associations (femininity and masculinity) for each perfume and tried to guess the gender of the person each perfume was applied on when not presented in a bottle. Results show that the gender of the person that the perfume was applied on did not affect the participants' preference or their gender scaling. Moreover, the preference did not differ between female and male participants, indicating that the commercial gender categorization is less important to the perfume consumers.

    Practical Implications

      On the commercial market, most perfumes are classified as either feminine or masculine, although the odor quality of feminine and masculine odors are overlapping and constitute a continuum rather than two separate clusters of odors. Earlier research has shown that participants tend to prefer perfumes positioned in the middle of this gender continuum. The current study investigates gender associations and preferences of perfumes from the middle of the gender continuum while these are applied on humans. When blindfolded participants evaluated their perception of the perfumes in this study, it became clear that neither the gender of the humans that the perfumes were applied on, nor the commercial gender labeling of the perfumes were important to their perception. Consequently, the commercial gender categorization does not seem to be sufficient for all perfumes. Instead, the classification of perfumes could be according to other aspects, e.g., according to odor quality.


Do decibels matter if the sound is outside human hearing?

Your dog training device produces what is called ultrasonic noise. Children can hear in the 25 kHz range, though they may not develop that ability until they are school aged.

This review has a good overview of the literature around ultrasonic noise. They draw the conclusion that it's hard to isolate the effect of a particular frequency or frequencies exactly, but there is some inconclusive evidence that noise at the frequency and dB of your dog training device could cause hearing damage and have other negative effects. In several countries, you're above the admissible range, but this is for longer term exposure.


How does the cell regulate different metabolic pathways?

I heard somewhere that cells ………………………… so they regulate where they use up the energy.

Yes NADP/H is primarily employed in anabolic pathways such as fatty acid synthesis, while NAD/H is employed in catabolic pathways such as glycolysis.

I don't think there is a general rule for other "energy-currency" molecules (pyrimidine triphosphates are not used except in some rare cases such as glycogenesis).

  I mean is there a simple map which contains the main processes and the energy carrier and regulatory compounds?

You can search for the term "metabolic network". It would be too huge so it is better to look at specific sub-networks. KEGG is a good site for finding metabolic networks. There are other representations like hive plots, to visualize very huge graphs.


What do cells do when they aren't creating proteins?

As indicated in the comments there are several non-coding (untranslated) RNAs, that the cell produces. Most of these perform gene regulatory functions.
However, widespread transcription is known to take place throughout the genome (pervasive transcription), but the functions of these RNAs are not clearly understood. It has been suggested that in certain cases the event of transcription, rather than its product, is responsible for chromatin regulation.


The fraction of the genome that is evolutionarily conserved through purifying selection is less than 10%?

I will try to tackle the terminology first

Conserved: That remains identical (or at least very similar) across species.

Purifying selection: Is one of the possible forces that lead to conservation of important sequences of DNA, by removing deleterious alleles.

So, the phrase simply means that the proportion of the genome that is very similar in sequence with the genome of other species (i.e. evolutionarily conserved) is less than 10%.
This is the answer to you question. Then, I just want to add that I share David's view on the abstract.


Meaning of ‘NC number’ associated with a gene?‘

This particular ID represent RefSeq accession number.
NC_ stands for a genomic molecule representing complete genomic molecule, usually reference assembly. Every sequence has a stable accession number, a version number, and an integer identifier (gi) assigned to it. RefSeq records can be distinguished from INSDC records by the inclusion of an underscore (“_”) at the third position of the accession number.


It's a Queen's Wreath Vine, aka:  Purple Wreath, Bluebird Vine, Sandpiper Vine

  This native Central American flower, which blooms in the dry season, is striking in its unusual blue violet color.  Gracefully arched sprays of delicate flowers contrast with the crisp, sandpaper-like leaves.  The flowers are five deep purple petals about 2 cm across in the middle of five slender, blue or lavender sepals that create a distinctive star shape.  Although the flowers last only a few days, the star-like sepals in the cascading clusters persist for many days, gradually becoming lighter.  They are very attractive to butterflies.


By definition, polyploidy just means that a cell or organism contains more than 2 pairs of homologous chromosomes (or is more than 2n). This is more common in plants than it is in animals. The plant, as shown below, undergoes failed meiosis, which means that the diploid (2n) cells never become haploid (n). As a result, a plant ends up with more than 2n when it self-polinates. The shown result is tetraploidy (4n), but there are other possible results (3n, 5n, etc).

Multiple plants within a population can end up with the same polyploidy number. They can then reproduce with each other but not with the original plants or any other plants. As a result, they become biologically isolated from the original group of plants and are considered a different species. It is a type of sympatric speciation, which means that it occurs without geographic isolation.


How well supported is the hypothesis that aging is mainly caused by the number of mutations in tissues?

I think telomere shortening largely accounts for the replicative cell aging.
http://www.ncbi.nlm.nih.gov/pubmed/22901253
The increase in no. of mutations with age surely does affect the tissue/organism survival too. There's a recent study that I'd like to share here. It is quite interesting and informative.
http://www.iflscience.com/health-and-medicine/mutations-found-115-year-old-womans-blood-could-help-unlock-secrets-aging


As you mentioned, the resulting impairment depends on the level of the injury: nuclear, fascicular, central / peripheral. So, you should differentiate lesions inside the brain tissue (which can be at nucleus, at any location of a tract, before crossing or after, and outside. From this, the first thing we should explain is the normal anatomy.  From normal anatomy we can understand the pathology.

One interesting fact you probably wanted to know is that Optic Nerve it not a real nerve in a classic definition, because it begins outside the brain as grouping axons of RGCs (retinal ganglion cells) and after leaving the eye becomes a “nerve”. From this, you can understand its damage better, because the damage to the visual fields depends on the level of insult.

IV nerve is the only cranial nerve that completely crossed (decussated). Thus, the lesion before the crossing/decussation (you were right mentioning the nucleus, but we extend the “region” until the decussation) will cause palsy and consequent atrophy contralaterally to the lesion. After the decussation the palsy and atrophy will be ipsilateral.

Considering cranial nerve XII we should speak about nuclear-infranuclear and supranuclear damage and with this notion supranuclear damage will cause contralateral transient tongue paresis. Nuclear-infranuclear damage will cause more permanent palsy, which is mostly bilateral because the nuclei are close to each other.

Considering VII pair, nuclear-intranuclear damage (“peripheral”) will cause ipsilateral hemifacial palsy including the brow and eyelid, while supranuclear (“central”) lesion will cause contralateral facial palsy with brow/eyelid sparing.


Circulating Tumor Cell vs Circulating Tumor DNA

I'm not sure the relationship you are trying to build between EMT and cancer cells.

Yes some "healthy" cells undergoing EMT could (due to specific underlying mutations) result in cancer cells but such a phenomenon is not a "hard and fast" rule.

The majority of ctDNA would likely be (as you suggest) from lysed cells, however, should mutations occur that allow for the aberrant export of DNA, then the latter could occur (I would assume this is rare but based on the currently available literature this possibility cannot be discounted).

Thus your "new hypothesis" seems to be the most likely.


When does one decide to refer to a virus as a new variant?

We use them as synonyms. However, variant is, in my view, more colloquial than scientific. Strains are in the literature often defined by their distinct genome compared to other strains of the same species (might be one base-pair substitution or more). In microbiology, including viruses, we often think of a strain as the proliferation of a single distinct DNA/RNA molecule.
https://www.sciencelearn.org.nz/resources/184-virus-strains


What is the main difference in chromatin fiber and chromonema?

10nm fibres are seen only by electron microscopy,while chromonema fibres refer to chromatin fibres visible by light microscopy. See this paper. 10nm or 30nm fibres are thus much, much smaller than chromenema fibres. There are likely several layers of organization (like 100nm and 200nm fibres) before you get all the way up to chromenema fibres.


None of them can be directly use for energy. We all talk about aerobic oxidation, which is the major process for metabolism.

They all need to go into the tricarboxylic acid cycle (TCA cycle) and oxidation phosphorylation to produce ATP, which is the energy used in organism.

For glucose, they can break down into two pyruvate and enter the TCA cycle. That is the fastest pathway organism use to produce energy.

For fat, since they have long carbon skeleton chain, they cut off 2 carbon compounds from the fatty acid every time. And under a series of process, it become pyruvate and go into the TCA cycle. So it really takes long time and complicated pathway to oxidate the whole fatty acid molecules.

For protein, it is much more complicated. Since protein is not energy store form, it need to become a energy store form first. First it need to be degraded into amino acid, and different amino acids takes different procedure to go into the TCA cycle. Here is the picture I found on the book  by John L. Tymoczko, Jeremy M. Berg and Lubert Stryer.

In sum, glucose is the fastest energy form that body can use to take metabolism, oxidate fatty acid or proteins take much more complicated pathway.


It is almost impossible for following reasons:

For photosynthesis you need chloroplasts
To maintain chloroplasts you need many genes in the nucleus that will support its endosymbiosis

I said almost impossible because there are some natural examples of what you are asking. A sea slug called Elysia  acquires choloplasts from green algae on which it feeds. However, it cannot maintain the chloroplasts and pass them on to the next generation but it acquires enough to appear green and survive on photosynthesis when there is no food.
Another example is that of the protist, Rhopalodia gibba, which acquired a cyanobacteria like organism. This protist already had a red alga derived secondary plastid before it acquired a "green" cyanobacteria. This acquisition gave the host the ability to fix nitrogen in the presence of light.
The case of Paulinella chromatophora is very interesting because the acquisition of an endosymbiont happened very recently. The endosymbiont is close to Synechococcus clade of cyanobacteria.
Intuitively, it can be understood that these kinds of acquisitions would be quite difficult for a multicellular organism.
ADDENDUM
Photosynthesis is a complex reaction which requires a dedicated compartment which not only harvests light and produces ATP but also has enzyme complexes required for anabolism (carbon fixation etc).
For now we can accept the hypothesis that it would not be possible for a huge eukaryotic cell to perform these functions in absence of a dedicated organelle. For a discussion on why this is so, you can refer this post.
Having said that, there is an easy way to impart partial photosynthetic ability to a eukaryotic cell. Some archaea and bacteria employ rhodopsin to pump out protons against its gradient, in the presence of light; this is coupled with ATP-synthase just like the complexes of ETC in mitochondria. In this study, Hara et al have expressed delta-rhodopsin in mammalian mitochondia which now makes the mitochondria generate ATP in presence of light. Furthermore, these cells were immune to mitochondrial toxins that affect complex-I activity.
PS: thanks biogirl. I almost forgot about this and I just remembered when I was reading about something else


Why is the strength of genetic drift inversely proportional to the population size?

Plane Crash Analogy

4 people in a plane crash

In a small aeroplane, there are 2 people that wear a blue shirt and 2 people that wear a green shirt. The plane crashes, half of the people died. The 2 survivors are those wearing the green shirt… well, nothing so surprising!

400 people in a plane crash

In a very big aeroplane, there are 200 people that wear a blue shirt and 200 people that wear a green shirt. The plane crashes, half of the people died. The 200 survivors are those wearing green shirt… This is quite surprising!

Genetic Drift

The same logic applies to genetic drift. Genetic drift is caused by events that modify the reproductive success of individuals in a random way (independently of their genotype). We usually referred to this as random sampling. At each generation, individuals are randomly chosen to reproduce and some genotypes might just happen to be chosen more often than others at a given draw (=at a given generation). Genetic drift pushes the frequency of allele slightly away from what would be predicted. According to the Wright-Fisher model, the frequency of alleles (of a bi-allelic gene) in a haploid population (to make it easier) in the next time step is given by:

$$p' = \frac{p \cdot WA}{p \cdot WA + (1-p) \cdot Wa}$$

where $p$ is there frequency of an allele at time = $t$ and $p'$ is the frequency at time = $t+1$. $WA$ is the fitness of the genotype which frequency is $p$ and $Wa$ is the fitness of the genotype which frequency is $1-p$. If the population is infinite, the predictions of this equation are exactly correct.

Now if we say that meteorites fall and half of the individual get killed. The probability of getting killed by a meteorite obviously does not depend on genetic predisposition, it is a question of chance! If you look at a population of 1 million individuals, half of them having the genotype $A$, the other half having the genotype $a$. It is very unlikely that more than 60% of all individuals that get killed are of the same genotype. Therefore, the meteorites won't change much the frequency of the genotypes. If you look at a population of 4 individuals 2 are $a$ and 2 are $A$, 2 of them get killed by a meteorite. Well, you have a probability of one half that the two survivors are of the same genotype and that the genotypes frequency would have changed drastically.

Genetic drift refers to these changes in allele frequency which are due to random events (such as meteorites) and the strength of genetic drift indeed depends on the population size for probabilistic reasons. The greatest the population size, the lowest is the strength (or the relative importance) of genetic drift.

How to model genetic drift

There are three famous models of genetic drift that all lead to very similar expectations. I shall just name them here but I will not develop the underlying mathematics.

Wright-Fisher model of genetic drift

Not to confuse with the Wright-Fisher model of selection written above
It models genetic drift as a random sample of the previous generation and hence uses a binomial distribution.

Moran model

It is based on a birth-death model (a type of Markov model).

Kimura's diffusion equation model

It is an extension of the above two models for a case of continuous time.


Why do boys sweat more than girls during exercise?

Your assumption seems to be true that Males sweat more than Females, but, not necessarily because of muscle mass.  The jury is still out as to the reasons.  However, in a 2010 study, it was concluded that…

  … training improved the sweating response, and a sex difference was
  observed in the degree of improvement in the sweating response due to
  physical training. This sex difference became more pronounced with
  increasing exercise intensity. A sex difference was observed in the
  control of sweating rate to an increase in exercise intensity, i.e.
  the maximal activated sweat gland responses of untrained females
  required a higher body temperature or work intensity than the other
  groups.

So, there does seem to be something different in the way males and females sweat.  Recent research suggests

  that when we're under heat stress from high temperatures or an intense
  workout -- regardless of what shape we're in or how much body fat we
  have -- women consistently sweat less than men but tend to have a
  higher skin temperature.

(http://health.howstuffworks.com/wellness/men/sweating-odor/men-sweat-more-than-women.htm)

In a nutshell, the cause(s) for the differences in how men and women sweat is still unknown.  Some think it may have to do with body composition.  While others think more research is required to determine

  how efficiently we use the sweat we produce, but also to our capacity
  for making sweat, hormonal fluctuations, sex hormone differences and
  how our bodies regulate water as possible reasons why men sweat more
  than women.


In binary fission, the fully grown parent cell splits into two halves, producing two new cells. After replicating its genetic material, the cell divides into two nearly equal sized daughter cells. The genetic material is also equally split. The daughter cells are genetically identical (unless a mutation occurs during replication).

Source: Binary Fission - Wikipedia

This corroborates with what I was taught in school as well.

A quick Google Image Search also shows that most diagrams on the subject involve one parent producing 2 daughter cells.


How many possible human genotypes are there that produce distinct phenotypes?

Is my reasoning correct?

I can see at least five major problems in your reasoning.
Do most genes have two alleles?
The claim that most genes have two alleles is wrong. Actually, the entire top answer in the linked quora post is wrong. The person answering confounds simplified cases used to teach intro genetics class with what nature really looks like.
As about one every 100 nucleotides is a SNP (bionumbers) and given that a gene is on average about 30k sites (bionumbers), the average number of alleles is probably closer to 300 although that would be counting synonymous mutations which is a bit unfair. About 20% of substitutions are synonymous (bionumbers), which would lead to an estimate of 240 alleles per gene on average. Even if you consider that 90% of these mutations have no effect on the phenotype (which is maybe an overestimation, bionumbers), you're left with 24 alleles per gene. Of course, this is a very vague estimate but it is, I think, much better than 2.
Non-coding sequences
Also, the majority of phenotypic distinction is caused by non-coding (non - gene) sequences such as regulatory sequences. You cannot ignore them in the calculation.
According to this pie chart (not sure if we can trust this chart though), 5% of the genome is made of regulatory sequences (against 1.5% of the genome that is coding).
One genotype ≠ one phenotype
If you have in mind that one genotype = one phenotype, then it would be very wrong too. There is environmental variance, epigenetic variance and other sources of variance (e.g. developmental noise) that underly phenotypic variance (see this post to understand the sources of phenotypic variance in populations).
indels and CNV
You are only considering substitutions. There are plenty of indels and ohter CNV too.
The existence of this variation does not only complicate the question, it actually renders the question a bit undefined because if you allow the genome to take any size, then number of possibilities is necessarily infinite.
Diploidy
Your calculations assume individuals are haploids. But humans are diplontic.
Gene are not atomic
Genes are not units that cannot be split. Recombination do happen in genes and it would be wrong to take the number of variants at genes (or at any other type of sequences) as basis for your calculation
Attempt at a calculation
So, ignoring many of the problems, here is my attempt at a calculation.
There are about $1.5 \cdot 10^7$ SNPs in the human genome (bionumbers). Based on this pie chart (not sure if we can trust this chart though), I will assume that about 6.5% of them are in coding or regulatory regions and I will assume (based on that paper) that 90% of them have no fitness effect and by extension I will assume it also mean no phenotypic effect (although the actually percentage should been increased). This will result in $1.5 \cdot 10^7 \cdot 0.065 \cdot 0.1 = 97500$  SNPs of interest. It results into $2^{97500} ≈ 10^{32500}$ possible haplotypes of interest. The number of possible genotypes of interest is therefore $\left(10^{32500}\right)^2 = 10^{65000}$. I also assumed absence of epistatic interactions otherwise the number would become so fantastically closer to infinity!
Interest in the calculation
I fail to find much interest in making such calculation because it entirely depends upon the model we want to consider. There is no offense against the OP's question here (and in fact the OP shows that he understands the importance of the considered model), I just want to make sure readers understand that these calculations are based on a very arbitrary model and one cannot make any sense of the given result without understanding the model.
The calculations from the Quora post that OP linked assumes that every SNP could be polymorphic. As long as the intention behind the calculation is not clearly stated, this is a perfectly reasonable model. Here, in my attempt, I assume that the number of SNPs is fixed, but any combination of it is possible. This can or cannot be a fine assumptions. Also, the estimates of the number of SNPs are of course, estimates of the number of SNPs that are at a frequency that is not too low to be detected! So, if we were, for some reason, to consider all the SNPs (by assuming some drift-mutation equilibrium), then the result would differ quite a bit. But again, it all depends upon the specific model one wants to consider.


Any superresolution techniques relying on stochastic sampling (e.g. PALM, STORM) is extremely difficult to accomplish in vivo, as the tissue would be moving (e.g. due to respiration) and this would hinder a lot the reconstruction of the image.

Apparently it may be possible to do it with STED but I could not find the related paper*, although the same authors recently published some interesting work on living brain slices.

* Note that the images in that article come from this paper, which is not done in vivo.

Thanks to @vkehayas for pointing out that in vivo STED has been done for instance here Nanoscopy in a living mouse brain


Fe in bacteria light-harvesting system Reaction Center

After reading the comments in the first answer, I believe OP's question is this:

  What kind of bond occurs in the Fe of the reaction center of bacteria light-harvesting system?

Before continuing, it's worth mentioning that an ionic bond is a kind of bond, and that atom would not be considered free (whatever that means) even if its bonds were only ionic ones.

However, to make things here even more unequivocal, the bonds of that Fe are covalent bonds (thus, that atom is not free under any definition...).

According to the Protein Data Bank in Europe, this is the x-ray high resolution structure of the photosynthetic reaction center from Rhodobacter sphaeroides at pH 10, zoomed at the portion that contains the Fe (link here):

You can see that the Fe has 5 bonds, thus summarised:

  [SQUARE_PYRAMIDAL] - HIS 190L - HIS 219M - HIS 230L - GLU 234M - HIS 266M

And what kind of bond are those?

According to the same PDBE entry, they are covalent. Have a look at the color code in this page: http://www.ebi.ac.uk/pdbe-site/pdbemotif/?tab=boundmolecule&pdb=2uxj&ligandCode3letter=FE

Here is a screenshot, in case the link above doesn't work. Have a look at the 5 red bonds (red represents covalent... not very legible, I know):

Source: Protein Data Bank in Europe


To "conjugate" means to join or couple something together. Deoxyribonucleotides are the "letters" of DNA - A, T, C, and G. In biology/biochemistry, when you conjugate something you chemically modify it by adding something to it. Given the context of your question, the conjugated deoxyribonucleotides are fluorescently-labeled — a fluorescent dye has been covalently attached to it.


This is an insect in the order Neuroptera, definitely neither a dragonfly (order Odonata) nor a grasshopper (Order Orthoptera).  The name of that order means "nerve-wing", which referes to the intricate network of veins throughout the wings, which have a very different appearance and pattern than the wings of either dragonflies or grasshoppers.  I'm not familiar with Indian fauna per se, but the long antennae with slightly curved/hooked tips make it look more like an antlion (family Myrmeleontidae within the Neuroptera) than an owlfly (family Ascalaphidae within the Neuroptera; their antennae have small clubs at the ends), though it's a bit hard to tell from the photo.


Data Bias in protein-protein interactions data

I'm one of the STRING maintainers, so I hope I can clear things up a bit.

Gene co-occurrence: genomic context methods are very useful for bacterial genomes, but not so much for eukaryotes. However, they are actually the most unbiased data we have, since there's no human influence (beyond selecting species for sequencing).

Benchmarking: Interactions predicted from text-mining etc. are benchmarked against the KEGG database. However, this doesn't necessarily lead to biases, as this benchmarking is basically a calibration step.

Actual biases: For eukaryotes, most interaction data comes from the experimental, database and text-mining channel. All of these are biased in various ways: e.g. there are study biases (disease genes will get more attention) and technical biases (some proteins are hard to work with)

As we don't know the actual set of protein-protein interactions, we can probably not test for biases in the data.


People are doing small molecule screens with stem cells right now (albeit embryonic stem cells). Probably a lot more screens of that kind are in progress behind closed doors in the pharmaceutical industry, and we can expect iPSC culturing to get better and cheaper, so sometime in the next decade we'll see them become a common model.

iPSCs will probably be an improvement on existing cell culture models, and will also allow things like the creation of cell lines for specific genetic diseases, but they wont' be a quantum leap forward for drug discovery in general.


By 'human estrus', I take it to mean that the female shows some increased desire when they are fertile.

At the height of fertility, which coincides with estrus, female behavior changes a stronger interest in sexual activity is exhibited.  In many primates in general, the female may give of a strong scent or even physically show color or swelling that indicates even to observers of other species that they are fertile, also engendering sexual behavior in the males.

For instance, baboons are well known for reddening of the female's rump and they also emit a strong scent.  Non - primates also show estrus - most of us know how dogs and cats can change their behavior.

Human signs of Estrus is of great interest to primatologists, evolutionary biologists and psychologists as it influences the biology and the social nature of people.  It has been proposed that humans do not exhibit estrus and this is still an influential idea. Certainly its difficult to look at a woman and tell whether she is ovulating and most women themselves cannot tell when that is happening.

Still, examination of behavior and appearance have shown that womens appearance does change over their monthly fertility cycle.  Women's faces may become thinner at higher fertility and this and other cues make them more desirable on the average.  While their sexual desire is not clearly higher, female perception of men's faces changes too.

While this is quite different than the typical definition of estrus, the biochemical cycle of fertility does affect human social behavior and preferences, perceptions.  The evolutionary reasons for these changes are probably adapted to the highly social nature of human existence and the fact that offspring are such a large investment.


If bacterial resistance randomly occur, then why limit broad-spectrum antibiotic use?

You're correct, this is extremely relevant, and it's unfortunate that your medical education didn't include good instruction about evolution.

You point to some very useful and interesting studies. I'm particularly fond of the studies that demonstrate the early existence of antibacterial resistance genes, e.g., in ancient permafrost.

Now to your question

  Is it a scientific fact that emergence of bacterial resistance through mutations is always random, i.e. in the sense that it is not a directed response to exposure of the population to that antibiotic?

I think the issue here is a conflation of two separate concepts. Mutation is one mechanism for producing variation. Mutation can be understood as a stochastic process, causing changes in the genome of an individual by chance.

Evolution occurs because of existing variation. Evolution is not a stochastic process. It is a biased process, a change in the distribution of existing variation.

The emergence of antibacterial resistance is evolution that results from selection acting on existing variation. Emergence here refers to emergence of a resistant variant within a population. Selective pressure (application of antibiotics) causes a predictable change in the frequency of genes that would allow reproduction in that environment, the frequency of existing resistance genes increases in the bacterial population.

Though there is evidence for important antibacterial resistance mutations pre-dating the use of antibiotics, this does not rule out the occurrence of spontaneous mutations, as demonstrated in the article you linked. The production of genetic variation by random mutation can be followed by a rapid increase in the frequency of a new genetic variation that is selected for in a given environment. This can be particularly likely in organisms with high error rates, short generation times, and large numbers of individuals. The spontaneous mutation isn't directed, as you say. It is random. The selection of that particular random mutation is directed, though.  Once the random mutation occured, then we can say the variation exists. Then selective pressure acts on existing variation, allowing evolution, a change in the frequency of the, in this case, gene for resistance.

Goodman & Gilman, one of my go to pharmacology references, actually has an excellent discussion of these concepts as they relate to antibacterial resistance, in Ch. 48, under the subsection EMERGENCE. There is a good discussion of the various mechanisms of emergence, but this general statement is helpful:

  Mutations are not caused by drug exposure per se. They are random events that confer a survival advantage when drug is present. Any large population of drug susceptible bacteria is likely to contain rare mutants that are only slightly less susceptible than the parent. However, suboptimal dosing strategies lead to selective kill of the more susceptible population, which leaves the resistant isolates to flourish.


By what mechanism does Risperidone swell breast tissue?

Risperidone prevents dopamine from acting on the pituitary gland by blocking dopamine type 2 receptors. One of dopamine's effects on the pituitary is to suppress prolactin production. In patients taking risperidone, prolactin production thus increases and prolactin levels in the body are higher than normal. In younger males, this can result in abnormal growth of breast tissue and even milk production.

See e.g. Melkersson, K. I. (2006). Prolactin elevation of the antipsychotic risperidone is predominantly related to its 9‐hydroxy metabolite. Human Psychopharmacology: Clinical and Experimental, 21(8), 529-532.


The oldest common ancesstor of all human beings

You are talking about the mitochondrial eve and the chromosome Y adam.  At some point there must be just one pair, though historically the evidence can be lost if there is a near complete extinction event.  Current evidence for eve points to SE Africa.


Does Sirtuin protein family Sir2 work in low-calorie diet mostly?

Does sirtuin 1 (SIRT1/SIR1) function to mediate the effects of a low calorie diet? Perhaps, but its really not clear.  Is the function of SIRT1 primarily to mediate low calorie response? Absolutely not.  What does that mean for SIRT2/SIR2 - its probably not more closely associated with calorie restriction signals, though it might be connected in a similar ambiguous way... but see below.

Firstly SIRT1 has also been shown to have many influences in many studies of conditions such as Alzheimers, anxiety and other neuro-functions.  SIRT1 modifies p53 - a bottleneck in cellular reproduction and a key regulator in cancer prevention, but which also an important aspect as to why it is active in calorie restriction conditions.

When reading reference like the one you have here its important to remember that correlation is not causality.  Very few genes in animals function only when specific behavior or conditions are experienced, especially signaling genes.

Examining the OMIM report (see link above) there has been a close examination of the possible role of SIRT1 in calorie restriction since the early 2000s in knockout mice.

SIRT1 would seem to play an important role in embryonic development for instance - cell growth is so important at that point and 80% of mice who are homozygous SIRT1 (-/-) knockouts die before they are born and even more die in the early natal period.  The mice who do survive have problems generating red blood cells which is another important case of cellular reproduction.

Yet the relationship of the knockout mice to calorie restriction has been debated - its been difficult to interpret the activity and the weight loss or gain of the knockout mice compared to wild type mice since the SIRT1 knockouts are smaller.  They may also have genetic traits that compensate for the absence SIRT1 in order to have survived.

More recently mice where SIRT1 expression in the brain have been produced, but the result has been anxiety or anxiousness as opposed to specific calorie restriction diet.

This reminds me of the story of leptin, in the early 90s they found that leptin deficient mice became quite fat, but despite this obvious linkage to obesity, leptin turned out to mediate a lot of other psychological factors as well - it only caused obesity when its function was blocked.  It did not turn out to be an appetite signal.

SIRT2 seems to have similar roles in calorie restriction.

  Rogina et al (2002) found that under 2 life-extending conditions, Rpd3 (601241) mutants fed normal food and wildtype flies fed low calorie food, Sir2 expression was increased 2-fold.

But also has similar relationships to Alzheimers.  SIRT2 has not been followed up on as much as SIRT1.  This correlation might not be causal or should be nuanced in a similar way.


Identification of Insect found on beach in Maharashtra

This appears to be a Lychee Shield Bug, Commonly found in India, formerly considered a beetle, but now classified as a True Bug.


sounds like a mongoose or a civet, which species is hard to guess there are several species of both in India, and they come in a variety of colors and sizes. In the mongooses the color can vary a lot even in the same species. One easy way to tell the difference is civets have cat like ears while mongoose have short rounded ears.

But here is a picture one at least one species of each, since their body plant does not vary much even if their color and size does.

Indian Brown Mongoose,

Sri-Lanka Mongoose

Asian Palm Civet


Depolarization and hyperpolarization in stereocilia of the inner ear

There are roughly two modes of pitch coding in the cochlea: place-coding and temporal coding. The place-theory is the most prevalent accepted model of how the cochlea realizes pitch coding (e.g., Zwislocki, 1991). Basically, it is based on a frequency-to-place Fourier transformation on the incoming sound, where each frequency is coded on a different place on the basilar membrane, as described accurately in the question.

However, there is another, much overlooked way of coding pitch, namely temporal coding. Up until about 1 kHz, spiral ganglion cells in the auditory nerve and acoustical brain stem regions (such as the inferior colliculus) have been found to respond in a phase-locked pattern (Du et al., 2011). Electrophysiology in auditory nerve fibers illustrates the phase-locked activity in response to low-frequency sounds (Fig. 1). This phase-locking behavior of neurons in the auditory system is called the frequency-following response (FFR).

fig. 1. FFR in auditory nerve fibers. Upper trace shows the stimulus, middle trace a single fiber, and the lower trace the compound activity of many fibers. The group-response faithfully codes the stimulus waveform. Source: New York University.

However, as you rightfully state in your question - why would inhibition of auditory nerve fibers (ANFs) be helpful? Figure 1 illustrates nicely that the auditory nerve FFR is rectified, i.e. only the upper half is coded, while negative action potential counts obviously don't exist; ANFs fire, or they don't, they don't fire negative action potentials. However, one has to realize that a relatively large proportion of ANFs in healthy ears spontaneously fire, i.e., in the absence of sound the auditory nerve is still remarkably active. Spontaneous firing rates vary from 0 to more than 100 spikes/s (Jackson & Carney, 2005). Hence, suppression of spontaneous activity codes pitch too.

Moreover, as a theoretical and un-referenced side note - the auditory system processes acoustic information on the sub-millisecond level. Left/right sound localization is performed by the auditory system by resolving inter-aural time differences (ITDs). By analyzing the delay at which sound arrives in one ear with respect to the other, the localization in the horizontal plane can be estimated. ITDs do not exceed 0.8 ms, given the speed of sound and the size of the human head. This is well below the time it takes for any action potential to develop(!). Hence, by deploying both phases of the sound, one phase being excitatory, the other inhibitory at the ANF level, no time is lost when a sound wave happens to enter the cochlea with its inhibitory flanking phase first.

References
- Du et al., Neurosci Biobehav Rev (2011)
- Jackson & Carney, JARO (2005); 6: 148–59
- Zwislocki, Acta Otolaryngol (1991); 111(2): 256-62