In which organs is water that we drink absorbed into the blood?

Role of the stomach in water absorption:
The absorption of much of the ingested water from a hypotonic food already starts in the stomach due to osmotic reasons.
If we study the mechanism of secretion of HCl by the oxyntic cells of the stomach, HCl secretion favours water osmosis from the blood to the lumen both for protective reasons as well as to maintain the osmotic balance of the gastric juice. This is predominantly the phenomenon in a filled stomach.
However, in the empty stomach, absorption of water is relatively more perceptible in the reverse direction upon water consumption.
Furthermore, the pyloric sphincter is usually open to the passage of water and electrolytes to empty to the duodenum. Thus, they may travel to the large intestine for absorption even before chyle. But this too is dependent on the empty or filled condition of the stomach, in which an empty stomach would pass the water and electrolytes in 5-6 minutes whereas in the filled stomach it could take 15 minutes or even more. Thus these factors may cause the early micturition to ensue.
Role of the small intestine in water absorption:
The small intestine, besides the transcellular pathway (through the cells), also facilitates water transport via the paracellular pathway. Thus it is more permeable to water osmosis than the stomach. Furthermore, the small intestinal segments duodenum, jejunum and ileum are differentially permeable to the absorption of different solutes. This facilitates the simultaneous absorption of water according to the osmotic gradient resulting from this differential absorption of the solutes, maintaining isosmoticity with the blood plasma.
However, this also has the implication that, when the digested products from the stomach (chyme) are hyperosmotic, water may flow from the blood in the villus to the intestinal lumen rather in the opposite direction until chyme is rendered isosmotic to the plasma.
Role of the large intestine in water absorption:
The large intestine is the key centre for water reabsorption rather than the stomach and the small intestine because of the following reasons:
a) It prevents most of the paracellular flow of water and electrolytes because of tight junctions, unlike in the small intestine. This prevents the back flow of electrolytes and water from the chyle to the blood.
b) The proximal colon is where most of the water reabsorption occurs as a consequence of major electrolyte intake. This region is highly active in the reabsorption of Na+ and Cl-.
c) It is mainly involved in concentrating the fecal matter, so reabsorption of water and electrolytes becomes its principle function.
For reference:
Textbook of Medical Physiology by Guyton and Hall


Is there a superterm combining "animal line" and "cell line" in disease models?

There is no super-term that I can think of but you could say genetically modified (mouse) samples/specimens?


Can emulsion test be used to detect phospholipids?

Yes, the test will still work. And you are correct about the phospholipid's process of forming 'circles' in water. The reason the test still works is because alcohol increases the permeability of the edge of these circles by making them less structurally stable. This then allows the ethanol to enter.

The hydrophilic phosphate head is not soluble in alcohol as it is not a lipid, but after the alcohol can bypass these heads, they can interact with the inner hydrophobic 'tails', which are soluble. The white emulsion/layer will then form.

This can be seen in the experiment of using alcohols to test the permeability of cell membranes. -See this investigation carried out by Westminster College.


Do mutant alleles result from mutation of the wild type?

No, not necessarily!

The terms might be confusing I agree. The most common allele (the wild type allele) might be a mutant of one other type of allele (one mutant allele) present in the population.

The reason we call the least common alleles the mutant alleles is that beneficial mutations are rare compared to neutral or deleterious mutations. If at a given locus most mutations are deleterious, then the mutant alleles will never reach a high frequency. However, if at a given locus a beneficial mutation occurs, then this beneficial mutation will likely rise quick quickly in frequency and therefore there is only a limited time frame under which the most common allele is actually a mutant of a least common allele. In consequence, we tend to call the least common alleles "mutant alleles". This name is often a good fit to the reality but not necessarily.

Note by the way that there are other sorts of selection regime occurring at a given locus that may maintain polymorphism at relatively high heterozygosity such as any form of balancing selection.


What is measured by electroencephalograms and local field potentials?

[I give this as a sketchy answer being aware that it might be nonsense. So feel free to downvote in this case. I should have mentioned - thanks to Bryan for having remembered me - that this answer has been inspired by Buzsáki/Anastassiou/Koch's article on The origin of extracellular fields and currents and just tries to sketch the mental image this article evoked in me.]

I assume that what is actually measured by an EEG electrode is an effective dipole moment in the upper cortical layers underneath the electrode (which decays with $1/r^2$). The way this dipole moment is created by "brain currents" is the matter of this answer.

There seem to be some premises under which a measurable EEG signal (= a dipole) can be detected:

The presynaptic action potentials must arrive highly synchronized. (Additive superposition.).
The apic dendrites of the pyramidal neurons that give rise to the dipole must be vertically oriented (pointing to the skull, resp. the electrode). (Orientation of the dipole.)
The sodium potassium pumps trying to restore the rest potential are unevenly distributed, i.e. mainly located at the soma. (Breaking the symmetry.)

This is the situation for the neuron (gray) at rest:

The dipole then forms as follows in three steps:

Step 1: An presynaptic action potential releases neurotransmitters that open ligand-gated ion channels causing sodium ions to enter the neuron.

Step 2: The extra sodium ions wander quickly to the soma. This happens passively, i.e. driven by repulsion and diffusion. At the end of step 2, all ions inside the neuron are distributed approximately evenly (i.e. not giving rise to an inner dipole).

Step 3: At the soma sodium ions are pumped out of the neuron. During this step equidistribution of ions is maintained inside the neuron (still no dipole inside the neuron).

In the extracellular medium, we now have an observable dipole.

Summary: What is measured by an EEG are not directly "brain currents" but an effective dipole moment that results from three different currents on different time scales:

Ions passing the membrane of apic dendrites into the neuron. (Slow.)
A net flow of ions wandering from dendrite to soma (driven by repulsion and diffusion). (Fast.)
Ions leaving the soma, e.g. by sodium pottasium pumps. (Slow.)


The cytogenetic notation seems to refer to parts of the chromosome when they're being karyotyped when the chromsomes are condensed in metaphase. If so, I think you might be able to use FISH to look for pieces of maternal or paternal genetic content on the chromosome. It looks like you can use mat and pat to refer to a maternal or paternal chromosome.


Which Enzymes are Responsible for the Biodegradation of Noladin Ether?

Noladin is an endocannabinoid. The best-characterised members of this family of molecules are Arachidonoylethanolamine (AEA; anandamide) and 2-arachidonoylglycerol (2-AG). The degradation of these endocannabinoids is reviewed in:

  Pamplona, FA et al. (2012) Psychopharmacology of the endocannabinoids: far beyond anandamide. Journal of Psychopharmacology 26:7-22

These endocannabinoids are inactivated via a reuptake system that is present in both neuronal and glial cells, although the protein responsible has apparently not been identified.

AEA is then metabolised to arachidonic acid and ethanolamine by fatty acid amide hydrolase, while 2-AG is converted to arachidonic acid and glycerol by monoacylglycerol lipase.

Because of its ether linkage, noladin cannot be a substrate for either of these enzymes. However the review also describes other possible pathways of endocannabinoid metabolism involving oxidation by cyclooxygenases, lipoxygenases and P450 cytochromes. These are the best candidates for the further metabolism of noladin, but there is apparently no direct evidence for this.


Do individual neurons communicate with the origin of thoughts?

To give a simple answer to the first part, the feedback generally happens in circuits of at least two neurons. A synapse is generally one way, transmitting information from the presynaptic neuron's axon to the postsynaptic neuron's dendrite. I'm sure there's caveats and exceptions because biology always has that, but that's the norm. A simple feedback loop might look like this: A excites B which excites C. C inhibits A as negative feedback.

The second question relies pretty heavily on the assumption that conscious thought originates from a particular part of the brain, or that one neuron is dedicated to one concept. This doesn't seem to be true. Things like memory and thought appear to be distributed, emergent properties of several circuits and areas. They might be organized or integrated by a particular part of the brain but it's not the same as having one central executive looking at all the inputs deciding what you think.

Think of it like a person working on an Excel spreadsheet. There's all the code for the OS, the software, the formulas in the spreadsheet. Those are all important parts of the process but the user doesn't need to see any of that. All they need to see is the end products of each process, and then they can figure out what to do with those products. So circuits and neurons can be involved in lower processing without connecting directly to the area that organizes and integrates information. Also, because higher level processes like thought are so distributed, there's likely to be multiple centers organizing/integrating information and all giving feedback to each other. Does that make sense?

Side note: I think you might be misunderstanding Dale's principle. When it says that neurons have the same chemical action at every synapse, that means they release the same neurotransmitter(s) but that doesn't mean they have to be connected the same way or that the neurotransmitter release has the same results. For example, say a neuron releases the excitatory neurotransmitter glutamate. If it synapses on another neuron that releases glutamate, that will promote excitation. But if it synapses on an inhibitory neuron that releases GABA, then exciting that neuron will actually result in inhibition.


Difference between rate of elimination and clearance?

Clearance is a measure of the volume of plasma from which something is removed, per unit time. For instance, it could be 2 mL/min, meaning that every minute, a two-milliliter of drug plasma is cleared. In other words, it is the rate of drug elimination divided by the plasma concentration.

Remember that the elimination rate is in units of inverse time, so dividing it by inverse volume gets you volume over time, which is the standard dimensionality of clearance.


What do the initial cell divisions look like in bird embryogenesis?

This is covered well in almost any text that talks of early embryonic development in birds. Basically, the cleavage divisions look roughly symmetrical if you look end-on from the animal pole. But, as mentioned in the question, the process is quite asymmetrical in profile, with the blastoderm being at one end and the huge yolk occupying the other.

The yolk later gets invested by a layer of cells (the splanchnopleure) to form the yolk sac while the blastoderm forms the embryo proper.

You could see this page for more details. (Not just this page, this site in general is an excellent resource for learning embryology.)


Actually, when DNA replicate in cell, there is primer exists. DNA polymerase only can add deoxyribonucleotide (dNTP) to the 3’end of a growing DNA chain, instead of creating a new strand. Here is the picture for DNA replication in legging strand, but is same principal use in leading strand. Primer is synthesized by primase in replication.

It is also worth to mention that, looking at the last step, there is a primer there and must be removed, and DNA maybe shorter in each DNA replication time, and that is why DNA telomere mechanism is proposed. That may be a key point for aging.

So, in PCR, it also needs primers, for DNA polymerase only can only can add dNTP to the 3’end of a growing DNA chain.


Results of a complete DNA sequencing - are they 100% reusable?

A single run of sequencing won't cover the entire genome, in most cases. That's why they do multiple rounds in order to increase horizontal (covering more regions of genome) and vertical (a.k.a depth; more reads per locus so that you can be more confident) coverage.

Edit by dd3:
In the cases where "a new gene is discovered", i.e. genome reannotation, it is possible to go back and look at previously stored sequence data to find out what alleles a person has (everyone has every gene, unless they have a deletion that spans the full length of the gene). This is a bioinformatics project, and if you are interested in learning more, I would recommend searching for recent publications on genome reannotation and remapping of sequence reads.

Whole genome sequencing is generally not recommended for prognosis of a specific disease like breast cancer. The common approach is to do a PCR of the biomarker loci and if necessary do a Sanger sequencing. However, if you have the money you can get your whole genome sequencing done :P

The number of runs required to increase the depth varies for different genomic regions. This article says that CpG islands require more runs. According to this article, the depth should be >3 per genotype marker.


where does genetic material for antibody production come from?

Does our DNA in some way get modified or something else?

Yes. The DNA gets modified. VDJ recombination and somatic hypermutation are the mechanisms by which this happens.

You can find an entire book chapter/review on these topics. So I shall not elaborate further.


The enzyme phytoene synthase is the first committed step in carotenoid biosynthesis. Saccharomyces cerevisiae doesn't have this enzyme, nor does it have the rest of the relevant pathway. Other yeasts such as Rhodotorula spp and Phaffia rhodozyma can make carotenoids.

However, carotenoid biosynthesis has been engineered into S. cerevisiae.


Do telomeres appear at just one end of the chromosome?

This is a great question!  The issue- the "paradox" of replication of linear chromosomes- of trying to filling in the unreplicated region (an overhanging 3' end) should technically be an issue only for one 3' end of each chromosome on any round of replication, as one new 3' end is produced by leading stand synthesis, and the other- the one with the issue- by lagging strand synthesis. However, both ends will have telomeres, they simply trade off being the end with the issue, in each round of replication.  Or you could say, in a single round of replication, one sister will have an issue at the right end end, and the other sister will have the issue at the left hand end.


Barring Antibody-dependent enhancement (ADE), how else can vaccines enhance the infection?

Vaccines are now well-tested to make sure that they don't do make infection worse, but there are many ways they COULD.

Two early formalin-inactivated vaccines (RSV and measles) both had this effect. See this Reddit post  to understand the mechanisms.

Theoretically, a poorly-designed vaccine could worsen viral infections  in three ways:

by biasing the adaptive immune response in the wrong direction that makes it harder to effectively respond to the actual virus.  This might be by priming the wrong type of response, e.g. producing a strongly biased Th2 response when a Th1 is required); creating the right response but to the wrong epitopes, in a way that subsequent exposures can't overcome - "original antigenic sin"; or by inducing T/B cell anergy or tolerance to the virus in question.
immunopathology.  For many viruses, the immune system's attempts to kill the virus, not the virus itself's direct cytolytic effects, damage the host.  E,g, Hepatitis C has 3 broad outcomes to a natural infection:  about 20% of people create an early, strong, multi-specific CD4/8 response that clears the virus.  The rest develop chronic infection.  In most people with chronic infection, the immune response damages little - viral loads can be extremely high but liver fibrosis is minimal.  But in \~10-20%, there is a strong immune response: chronic inflammation, infiltration of lymphocytes, and constant direct killing of virally-infected hepatocytes by CTLs leads to deposition of scar tissue and, eventually, cirrhosis.  So if you created a vaccine that failed to clear the virus and instead generated a pro-inflammatory, pro-fibrotic immune response, it would be a disaster.
Increased target cells.  This was a concern with one of the experimental HIV vaccines.  It increased the number of CD4+ cells permissive to HIV infection in the female genital tract (and the rectum, but I don't remember), thus giving the virus more target cells to infect (there was also an experimental HPV vaccine that was feared to do the same).  Those vaccinated thus had increased risk of infection.


What is the technical term for when a clade on a phylogenetic tree does not have an extended branch? (see image)

The phenomenon where you have different "evolutionary clocks" of selection is called heterotachy. The branches are therefore heterotachic or simply long branches —long branch attraction is a problem with Bayesian inference for which many arguments have been had, so there is a lot of literature on it.


Just to avoid misunderstandings
Just to avoid potential misunderstandings on your side, I wanted to talk about the saying that

human [are] evolved from primates

Humans are primates, so did our common ancestor with other primates.
Our ancestors are different from modern day primates. Chimps for example (which are great apes, like us) are not our ancestor more than we are their ancestors. We just share a common ancestor (who lived about 13 millions years ago).

Spandrel, exaptation and panselectionist arguments
Your are doing two mistakes. 1) The mistake of the spandrel (named after the title of the famous and old paper Gould and Lewontin (1979)) and the exaptation and 2) a panselectionist mistake.
1. Spandrel and exaptation
Spandrel

In evolutionary biology, a spandrel is a phenotypic characteristic that is a byproduct of the evolution of some other characteristic, rather than a direct product of adaptive selection

See also What is the “Spandrels” debate about?.
Exaptation

Exaptation [..] describe[s] a shift in the function of a trait during evolution.

While the existence of a spandrel in an evolutionary process does not necessarily cause the existence of an exaptation, but I will not go into these semantics details for simplicity.
Consider for example the two following wrong statements.

Birds have feathers to fly. It is impossible that birds evolved feather to fly because early feathers would have served no purpose to flight.

Bird feather actually probably first evolved for temperature regulation. Once this was done feathers were an exaptation for early flying tools.

Humans have nose to wear glasses. It is impossible that nose would have evolved because there was no glasses before

Noses evolved for another purpose and happen to be an exaptation for wearing glasses.

Humans have a big brain for advanced mathematical skills. It is impossible that humans evolved such big brains as such mathematical skills were useless in a time where we did not invent/discover much of the most basic math concept yet.

Humans evolved a big brain, mainly for social reasons incl. social hunting and social communication and probably because it was/is under sexual selection (see wikipedia > evolution of human intelligence). It just happen that logical reasoning, abstract thinking and other cognitive skills are an exaptation for advanced math skills.
2. Panselectionist view of evolution
I just want to highlight that there is much more to evolution than just mutations and natural selection. Not every trait has been selected for (otherwise we would not have any genetic disease).
On this subject, you might want to have a look at the paragraph Did you say Natural Selection? of this answer to Why don't mammals have more than 4 limbs? and to Why do some bad traits evolve, and good ones don't?


Does the human hand have 27 degrees of freedom?

Keeping in mind that I know nothing about this, I will try to explain why the hand can be modelled with 27 degrees of freedom. This is just my interpretation of this paper, which says:

  The human hand has 27 degrees of freedom: 4 in each finger, 3 for extension and flexion and one for abduction and adduction; the thumb is more complicated and has 5 DOF, leaving 6 DOF for the rotation and translation of the wrist.

  To accurately model the hand, a complete model of the muscles, tendons, bones and a neurological control structure is necessary. The dynamics of such a complex model are still poorly understood, forcing the use of simplified models. Current models are too simplified for our purpose so we turn to recent work from the medical community to motivate assumptions used in a new model that we propose here. We use a 27 DOF model of the hand with the following sim- plifying assumptions:
  1. The thumb is independent of the other fingers.
  2. Adduction/abductionofthefingerjointsareindependent.
  3. Motion frequency does not affect joint interdependence.
  4. Both hands have the same interdependence model.
  5. The posture of the wrist and the rest of the arm do not
  affect the underlying interdependence structure.

Incidentally, this implies to me that there are different models of the hand with different assumptions that use a different number of degrees of freedom.

Anyways, take a look at this hand:

[source]

And now, follow along with your own hand!

finger (4 DOF): each finger has 2 interphalangeal joints between the distal, middle and proximal phalanges that allow for flexion/extension (2 DOF); each finger also has a metacarpophalangeal joint between the proximal phalanx and the metacarpal that allows for flexion/extension as well as abduction/adduction (2 DOF)
thumb (5 DOF): an interphalangeal joint between the distal and proximal phalanges allowing flexion/extension (1 DOF); a metacarpophalangeal joint between the proximal phalanx and metacarpal allowing flexion/extension and abduction/adduction (2 DOF); a carpometacarpal joint between the metacarpal and trapezium allowing flexion/extension and abduction/adduction (2 DOF)
wrist (6 DOF): between the carpals and radius allowing flexion/extension, abduction/adduction and supination/pronation (3 DOF); I think when the authors refer to translation of the wrist, they are simply saying that hand can be moved in all planes of 3D space (ie up/down, side to side, forward/backward - 3 DOF)

Since we have 4 fingers, they give 16 DOF. Adding the 5 DOF of the thumb and 6 of the wrist, we get 27. Please nobody question my reasoning. Thank you.


Excess copper in the body can be toxic but I'm not sure a copper blade would be especially toxic unless it was coated with something else or it remained in the wound. Copper can be acutely toxic when ingested, or chronically over a long period of exposure (like lead), but is more often associated with a failure in copper excretion. Since the body has ways of dealing with excess copper, I just don't see much merit in the super-toxic copper blade, unless it is designed to break off in the target.


Why is chronic lymphocytic leukemia (CLL) most common leukemia in the West but so rare in Asia?

This paper should help get you started. The exact reason is not yet known, but is most likely related to germline genetic differences between the two ethnic groups, as Asian immigrants to the US continue to have a low incidence of CLL.

References:

KAWAMATA N, MOREILHON C, SAITOH T, et al. Genetic differences between Asian and Caucasian chronic lymphocytic leukemia. International Journal of Oncology. 2013;43(2):561-565. DOI:10.3892/ijo.2013.1966.
American Cancer Society: What are the risk factors for chronic lymphocytic leukemia?


Do all humans experience flatus regardless of their diet?

Eventhough food contributes the most to flatulance, it can also be caused by swallowing air when you chew gum or smoke. It can also be caused by health conditions like coeliac disease and gastroenteritis (reference). So it is indeed hard to believe when people claim that they never fart.


If you use pre-staining, the stain migrates as well in the electric field and this can lead to some parts of the gel being unstained. This would look pretty much like you describe, the ladder being invisible as well points strongly to that part of the gel just being no stained properly.

It sounds a bit unlikely with your running parameters, I've only seen that with a very long running gel, but I also haven't used pre-staining for quite a while now. Ethidium bromide is positively charged and migrates in the opposite direction as the DNA, I have no experience with Sybr-Safe though and don't know if it behaves the same as EtBr in this regard.


How does the inability to produce vitamin C helped weight gain?

The effect comes indirectly since lower levels of ascorbate increases urate levels, according to

  Arthritis Rheum. 2005 Jun;52(6):1843-7.

  The effects of vitamin C supplementation on serum concentrations of
  uric acid: results of a randomized controlled trial.

  Huang HY1, Appel
  LJ, Choi MJ, Gelber AC, Charleston J, Norkus EP, Miller ER 3rd.

So the direct weight gain effect is due to increased levels of uric acid.

Further in the chain of events is that

  Recent studies show that fructose-induced uric acid generation causes
  mitochondrial oxidative stress that stimulates fat accumulation
  independent of excessive caloric intake.

according to

  Diabetes 2013 Oct; 62(10): 3307-3315.

  Sugar, Uric Acid, and the Etiology of Diabetes and Obesity

  Richard J. Johnson1,2⇑, Takahiko Nakagawa1,3, L. Gabriela Sanchez-Lozada4, Mohamed Shafiu5, Shikha Sundaram6, Myphuong Le1, Takuji Ishimoto1, Yuri Y. Sautin7 and Miguel A. Lanaspa1


What does static electricity generated by plastic combs do to our hair?

The motion of the comb against your hair remove electrons from the hair and deposits them on the comb. The positively charged hair and negatively charge comb now attract each other due to their opposite charges. You can read about this is any introductory Physics text, the topic is "static electricity". I doubt any harm is done to your hair, the issue is that it may be difficult to get your hair lying perfectly flat because of this attraction. This effect is more pronounced in low humidity.

If you want to see an exaggerated example of this, rub an inflated rubber balloon several times, quickly in the same direction, against your hair. Then bring it back near your hair while observing in a mirror.

Edit: I hesitated adding this because folks on this particular SE are sticklers for references. My source for the following is a workshop I attended at Chico State University circa 1990. This workshop was taught by a couple PhD Physics professors to enrich Physics teachers in electircity and magnetism.

When you dry clothes in a drier, static electricity is generated resulting in "static cling". But the cling that persists after a load is done is only part of the story. Constantly, at least once clothes are sufficiently dry, electrons are being stripped from one type of material by another. These electrons snap back from where they accumulate to where they were removed. This results in microscopic "sparking" that causes an ever-so-sight amount of wear on the cloth. So, the professors went on, the use of fabric softening anti-cling tissues minimizes this and prolongs the life of clothes. My take is that this is subtle and is more likely to be evidenced by the quality of appearance of the surface of a garment after many washings than it prematurely falling apart. I don't know for sure how significant this is, especially if you replenish your wardrobe regularly.

So, this may also apply to hair. But, unlike a particular garment, hair is constantly replenishing itself. (Well, not on my head.) So I seriously doubt this static discharge damages hair to any measurable extent. Perhaps if you were to run a comb through your hair for a couple hours every day you might see an effect. Bottom line for me, I use anti-static tissues, fragrance free; typically I get 20 years of use from my washable items and consider the tissues cheep insurance.  But I use plastic combs on what remains of my hair without any worry.


I have this issue too with data from a Partec PAS III. I don't consider it a problem, as it's really just the x-axis which is one order of magnitude higher. At the end, all values coming from the machine are arbitrary values, so as long as the change is systematic, there's no problem.


Can Listeria monocytogenes endotoxin act as an A-B toxin?

Considering great research we did after the answer was accepted, I should add important information about the topic. The old (and accepted) answer follows in "" marks for the sake of clarity.

We found that in spite of the earlier reports, the newest ones failed to find endotoxin-like structure in the Listeria born material. Most academic discussions about the issue say there is no such thing called "listeric endotoxin", thus I gave a right answer to a "compromised" question.

I should say that question is still brilliant because it promoted great research and should be an important source for everyone looking for information about listeric "endotoxin"

  Listeria endotoxin is not a protein. Thus, is lacks enzymatic activity
  and acts indirectly by binding to sensitive receptors on macrophages.
  Thus, it can not cause lysis itself.

  Considering AB-exotoxins, A-subunit is a protein that has enzymatic
  activity (responsible for toxin action)  and subunit B has no
  enzymatic activity (protein responsible for binding to receptors).

  Thus, the answer to your brilliant question is NO, Listeria endotoxin
  cannot act as AB-exotoxin being nonprotein and non enzymatic
  substance.

  Also, don't be confused with Listeriolysin O, which is listeria's
  eXotoxin protein which is pore-creating protein.


If an ethnic group holds nearly 100% of a particular haplogroup, does it means that people who have this haplogroup are their descendants?

Short answer:
No.

If populations A and B share a haplogroup it does not imply that population A is B's ancestor, or population B is A's ancestor. No present-day population is the descendant of any present-day population, though both populations may share common ancestors. The common haplogroup is probably inherited from common ancestors.

Long answer:
No.

When you say "Egyptians" or "Vietnamese", in genomic studies you generally mean present-day people. People living in present-day Egypt or Vietnam may be related to each other, but they cannot as groups be each others' descendants. It is more likely that there is some ancestral population that is the common ancestor of both groups that carried the genetic variant. The only exception I can imagine is a VERY recent colonization (assuming there were no indigenous people in the colonized country, which is effectively never the case).

To take this specific example, it would be most likely that at some point in ancient human history the expanding human population (from e.g. out of Africa) had people carrying a haplogroup that settled Egypt, Anatolia, and Vietnam in independent events.

Therefore none of those groups would be descended from one another. Each population was founded by the people who stayed in that region, not the related people who left and colonized other regions.

Sampling of ancient DNA makes the question more interesting, if you for example found 20,000 year old bones sharing the haplogroup. Maybe that is a descendant of one or both populations. But again the relationship of that ancient individual to present-day geopolitical borders would still be fairly meaningless without a lot of supporting data.

It is additionally possible that the haplogroup arose independently in two different populations. This is sometimes called parallel evolution or convergent evolution. In this case there is actually no relationship at all between the populations. While this is much less likely than common descent, it is nonetheless a hypothesis that you need to reject before you claim that one group are the descendants of another group.

I hope that this helps!


I have read that the unique amino acid sequence of the VH and VL domains of a given antibody can function not only as an antigen-binding site but also as a set of antigenic determinants. the idiotypic determinants are generated by the confomation of the heavy- and light-chain variable region. Each individual antigenic determinant of the variable region is referred to as an idiotope. In some cases an idiotope may be the actual antigen-binding site (The paratope), and in some cases an idiotope may comprise variable region sequences OUTSIDE of the antigen-binding site. Therefore, each antibody will present multiple idiotopes, and the sum of the individual idiotopes is called the IDIOTYPE of the antibody.

I hope that had been helpful


Advantages of Monogamy over Polygamy and Vice Versa In Nature?

Polygamy spreads genetics further, but usually you trade that spread for care of the offspring.

Monogamy means less genetic diversity, but the offspring usually get more attention and care, meaning they're more likely to survive.

So it's more babies where more will die, or less babies that take more energy to grow and nurture but more likely to survive.


This question is closely related, and the fascinating link posted by @JohnSmith is a good read.

In short, with a four-base system, and a codon size of 1, you get four possible amino acids.  Silly system.  A codon size of 2 gives 16.  Not too shabby, but not a lot of room for growth, and not enough for those 20 amino acids.  Codons of size 3 gives 64 - plenty of room to work with and it covers all your forseeable amino acids, and then some, without being too wasteful.

The redundancy, known as degeneracy, is pretty straightforward.  There's room to expand, and any redundancy/degeneracy will only reduce the likelihood of errors.  That's a huge benefit.  For some amino acids, the first two bases are enough.  That third position can be quite tolerant to mutation, which is very beneficial to organisms.  It appears to be even more fine-tuned, to the degree that redundancy often not only reduces the likelihood of mutation but also reduces the damage caused when a base does mutate.  Swapping a hydrophobic AA for another hydrophobic one is less likely to cause aberrant protein function, and anything with a U in the middle is probably hydrophobic.  Convenient!  I'll also note that, while it's not perfect or even a significant correlation, the more popular amino acids tend to get more redundancy; tryptophan is traditionally the least common AA.

Finally, there are a few non-proteinogenic amino acids, so, as the linked question/answer above points out, maybe in the future there will be more amino acids.


Does the order of amino acids matter in making up a protein?

Yes.

The 'order' of amino acids is the protein sequence, also known as the primary structure. A peptide (short protein) with sequence XYXYXYXYX is very different from XXXXXXXYYYYYYY.

Your example is a bit trickier, since it seems like AB should be roughly equal to BA. However, each amino acid has two ends - the amino and carboxyl - and so a dipeptide like this is more like NH2-A-CONH-B-COOH with a peptide bond in between.

The really tricky question is : are two sequences 'the same' if they are different by just one or two letters. In other words is AAAAAABAAAAAA different from AAAAAACAAAAAA - and this is the study of mutations of proteins.

There is a lot more to say on this topic, of course.


Dopamine is one of many neurotransmitters which modulate information passage between one brain area to another. Dopamine is thought to play important role in  pleasure, addiction,
and learning.Massive increase in the
amount of dopamine released in the brain during video game play, the releasing of dopamine
are in areas thought to control reward and learning.

Reference

Certain neural structures, called the reward system, are critically involved in mediating the effects of reinforcement. A reward is an appetitive stimulus given to a human or some other animal to alter its behavior. Rewards typically serve as reinforcers. A reinforcer is something that, when presented after a behavior, causes the probability of that behavior's occurrence to increase. Note that, just because something is labelled as a reward, it does not necessarily imply that it is a reinforcer. A reward can be defined as reinforcer only if its delivery increases the probability of a behavior.

The reason why we are happy when we get these decorative items is because they are things which we can possess. Reward system is responsible for this kind of behavior, when we gain or achieve something in life its usually gets rewarded in the form of a pleasure. Foraging ants and bees are provided with these reward systems and which in turn makes these animals to derive a pleasure out of their daily achievements. Whether in life, video game or stack exchange or anything, an achievement is something brain thinks relevant and rewards it with a pleasure in mind.
Considering badges in stack exchange, really badges are an analogy to reputation. When we have more badges usually our charisma increases like in the case of reputation. Also levels and scores in games,achievements in office, stack exchange badges and hats all fall under the same analogy. So when we have more badges we are meant to be more successful and brain will reward us to attain more badges and also people like hats too.

References
Digital Media: Transformations in Human Communication - Paul Messaris, Lee Humphreys
Cyber Junkie: Escape the Gaming and Internet Trap - Kevin Roberts


What does "each pathway define an independent genotype" mean?

This is somewhat outside my field, but basically it seems they're defining the independence of the three hypothetical metabolic pathways in two different ways:

Mathematically the pathways are not independent since P₃ is a combination of P₁ and P₂.
Biologically the pathways are independent since each requires a different combination of enzymes and therefore genes (the genotype). This is the method used in MPS.

Does that answer your question?


I know pretty much nothing in medicine!

Fever is an abnormally high body temperature. Fever is a symptom and not a disease per se. Different medical conditions (incl. various infectious diseases) causes a patient to have fever.

Note that fever might be in some/most situations an adaptive response to a disease. In other words, for infectious disease causing fever, fever might be good for the host and not for the parasite. However this issue remains controversial (see the post linked in the OP's question for more info).

As GoodGravy said in the comments, many people get confused and consider fever as a disease instead of what it really is; a symptom. One likely reason for this confusion is that when one has fever, (s)he very often treat fever directly (taking drugs like Aspirin for example) rather than treating the underlying cause (the virus for example) of the fever.


Why is GTP, rather than ATP, used in nuclear transport?

Disclaimer

Although this question appears to be either unclear or unanswerable (or both), and shows no evidence of research on the poster’s part, I have chosen to address one aspect of it to emphasize a general concept. This, despite the fact that my knowledge of nuclear transport processes is minimal.

Brief Answer

GTP, rather than ATP, is used for nuclear–cytoplasmic transport via importins and exportins, because this process involves one of a large family of ‘G proteins’ that — as their name implies — operate through the use of GTP. Whereas ATP is generally used to drive endergonic molecular reactions, the hydrolysis of GTP in G-protein cycles can be thought as a device to terminate a molecular process. Whether G proteins adopted GTP rather than ATP merely by chance or for a biological reason is a matter of speculation.

NTP hydrolysis — for fun or profit?

It would appear that the question relates to protein-transporting ‘importins and exportins’, which I learn from the Wikipedia article on nuclear transport are regulated by the small G protein, Ran. When complexed to GTP, Ran facilitates the export of proteins by exportins, a process that is terminated by hydrolysis of GTP to GDP. The GDP-bound form facilitates the import of proteins by importins, a process that is terminated by GTP displacing the GDP.

So if we consider the role of the hydrolysis of the nucleotide triphosphate — here GTP — it is clearly not to supply thermodynamic energy for an endergonic process such as muscle contraction, light generation or a chemical reaction with a +ve ΔG:

Rather, it is to produce a conformational change in a protein which allows the termination of a process. This termination is generally through the GDP-bound form of the G protein (grey) interacting with some other protein (black):

This diagram is deliberately simplistic so that the general features of G-protein action can be seen. However, I think it illustrates the same point made in Berg et al. Section 15.6. Other examples are signal transduction of hormone action via cyclic AMP and binding of aminoacyl-tRNA to the ribosome.

Why do G proteins use GTP?

This ‘choice’ of GTP in the original ancestral G protein could have been mere chance, that was subsequently reflected in other G proteins that arose through gene duplication and divergence. That would imply that, at least, it was not disadvantageous. Or as the oldest G proteins are perhaps those involved in protein biosynthesis — a process still catalysed by a ribozyme — the choice of GTP might have reflected an RNA base-pairing interaction in the ‘RNA world’.

Alternatively one might suggest a biological rationale for separating two types of energy-requiring processes — perhaps by regulation of the enzyme that catalyses the conversion of ATP to GTP, dinucleoside-phosphate kinase. However I am not aware of any evidence to support this idea.

Hydrolysis of GTP in other contexts

As mentioned in a comment by @Roland, there are instances where GTP is used to drive endergonic reactions (phosphoenolpyruvate carboxykinase) in a manner analogous to the use of ATP, but this is quite different from hydrolysis of GTP in G proteins. I do not believe that any convincing rationale for this has been propounded, nor for the similar exceptional use of UTP in glycogen synthesis and CTP in phospholipid synthesis. This question has been discussed in another post.


HOW is the Gallbladder attached to the liver

1. Gallbladder attachement to the liver

In this video (check from 55 sec on), you can see that the gallbladder is covered by a thin sheath that wraps the gallbladder; the sheath extends to the liver and intestine and thus keeps the gallbladder in place. The sheath is a part of the abdominal membrane (peritoneum) that covers most of the abdominal organs. You can see that the surgeon is cutting the sheath.

2. The Cystic Vein: The Significance of a Forgotten Anatomic Landmark (PubMed Central)

  ...there is no cystic vein per se, but the venous drainage is
  through the bed of the liver [between the attachment surfaces of the
  gallbladder and liver]...however..Gray's
  Anatomy of the Human Body...describes cystic veins which join at the
  neck of the gallbladder to form either single or double cystic veins
  which flow along the cystic duct and upward along the hepatic
  ducts.


Diffusion is always a passive process that doesn't require energy.  Therefore it would seem that A is correct, B doesn't really make a whole lot of sense.  In the case of the cell membrane diffusion will often be in the form of 'facilitated diffusion' through carrier proteins, however the transport is still not active.


Why were dinosaur skeletons so light compared to mammal skeletons?

I have also heard the claim that dinosaur bones were lighter than mammal bones of equivalent  size, and at the moment I do not believe it.  I will not believe it until somebody explains it to me how that is possible.

If you have a structure that you want to add more weight to, to support that weight, you want to ADD structural elements, not subtract them.  If the structure could support itself before adding more weight, then adding structural elements will make it stronger (unless it's already at the absolute limit).  Otherwise, the structure does not stand at all.

If you google about the weight of bird bones, you can find recent research saying that bird bones are actually not lighter than mammal bones.  Their weight is just distributed differently (more densely on the outside of the bone, as opposed to more evenly spread throughout the bone as in mammals) to resist bending and twisting better at the cost of being weaker to impacts.  Birds arguably have a much stronger reason to lose weight than dinosaurs, but their bones are still just as heavy as ours.  Since birds are dinosaurs, I find it very unlikely that ancient terrestrial dinosaurs had magic bones lighter than both mammals and birds.

Also, I'm aware that the internal structure of our bones is very efficient.  As I understand it, the bone on the inside of a bone grows thicker where it is more stressed.  If you train a computer to calculate the ideal lattice structure to support the stresses of a given bone shape, the computer calculates pretty much the exact same lattice as what actually exists in our bones.  So, if the internal structure of our bones adapts to better handle the stresses we experience in life, and if the bones of vertebrates can evolve into any external shape whatever, I cannot imagine how dinosaur bones could be stronger than ours unless they were made of a different material.  I am not aware that this is the case.


Petrides, 1950, writes:

  Male skunks have tiny nipples which are considerably smaller than those of juvenile females.

and also:

  Female skunks which had bred could easily be distinguished from those which had not by differences in the size of the teats

So it sounds like the mere presence of teats is not sufficient to sex skunks, but the size is sexually dimorphic and is probably a reasonable guide with practice, though the differences may be more subtle for female juveniles vs. males.

For pelts, Petrides recommends sexing based on the presence of a penis scar; I presume that genitalia is likely a more reliable guideline than teats.

For roadkill where damage might make it hard to sex animals based on genitalia, Fuller et al found canine size to be highly predictive, though they suggest that a comparison group of sizes from animals of known sex be used for a particular region, so that might not be too helpful for sporadic sexing.

Casey & Webster 1975 discuss sex identification based on presence of Barr bodies in the hippocampus, but their technique would probably not be applicable to your use case.

Casey, G. A., & Webster, W. A. (1975). Age and sex determination of striped skunks (Mephitis mephitis) from Ontario, Manitoba, and Quebec. Canadian journal of zoology, 53(3), 223-226.

Fuller, T. K., Hobson, D. P., Gunson, J. R., & Schowalter, D. B. (1984). Sexual dimorphism in mandibular canines of striped skunks. The Journal of wildlife management, 48(4), 1444-1446.

Petrides, G. A. (1950). The determination of sex and age ratios in fur animals. American Midland Naturalist, 355-382.


Can an influenza virus carry other infectors with it?

I wouldn't call influenza a vector here, but yes, an infection with the flu virus which results in a full infection can have secondary infections as complications. There are often caused by bacteria which usually live in the respiratory pathway and kept under control by the immune system.

This includes pneumonia (either viral or bacterial), inflammation of muscles and the heart muscle (myositis and myocarditis) as well as pericarditis. Less severe complications include infections like ear infections and sinusitis.

See the references for more details:

References:

Complications of Viral Influenza
Double trouble: Bacterial super-infection after the flu
A Mouse Model of Lethal Synergism Between Influenza Virus and
Haemophilus influenzae


I use the term "X-inactivation" instead of "lyonization". Anyway, X-inactivation is a very specific process by which an entire X chromosome (or equivalent sex chromosome) in a female mammal is completely silenced.

"Imprinting" is typically applied to single genes, wherein genes inherited from a specific parent are always epigenetically silenced. The genes are usually autosomal. Thus, we're talking about scales : entire sex chromosome composed of thousands of genes (x-inactivation) vs single genes (imprinting)

The choice for which X-chromosome is inactivated is sporadic and different in different cells within the body. It is controlled by opposing expression of different non-coding RNAs (XIST on the inactive X and TSIX on the active X).

Imprinting is very specific to the allele that is inherited from a specific parent (for example, some genes are paternally imprinted, while others can be maternally imprinted).

Males with aberrant X-inactivation will lack any expression of genes carried on their single X-chromosome, a condition that will not result in a viable fetus. However, whether there are aberrant X-inactivations in single cells or tissues of ageing adult males....perhaps likely yes, given all the other aberrant somatic mutation events that occur over the course of life.


Help ID this plant, quite possibly a weed

I presume it is Cleome viscosa, the Asian spiderflower.

It is commonly found in rainy season.

Medicinal uses:

The crushed leaves have been investigated as a treatment on stored seeds of cowpea, to prevent weevil infestation.
The leaves are use as external application to wounds and ulcers. The seed are anrhelmintic and carminative Juice of leaves is used as remedy against discharge of puss from the ear.

Identified by the following features-

Palmate leaves

Colour of flower especially the brown part at the base

Herbaceous habit

References:

Wikipedia
Flowersofindia.net


Who would win in a fight: an amoeba or a leukocyte?

Assuming you don't mean a single leukocyte as I doubt That a lone leukocyte could do much. Macrophages and neutrophils can release their lytic/degrading enzymes spewing them on to the amoeba. Antibodies produced by BCells, particularly the IgE type can coat amoeba and cause histamine release from mast cells recruiting more neutrophils and macrophages. Eosinophils are also important. Finally one must not forget the complement system, a series of proteins that could kill by making pores in the amoeba membrane. Amoeba have however developed many techniques for immune evasion, such as diverting the immune system via cell signalling (cytokines) such as IL10 which dampens the immune system or coating themselves or activating the "wrong" immune system.


What does the point in the middle between two numbers mean?

Short answer

It's a decimal point.

Longer answer

A point in the 'middle' of the neighboring characters is called an interpunct, and was the standard in UK typography for marking a decimal at one point in time (possibly elsewhere as well). You're most likely to encounter it in older issues in UK and UK-inspired journals, and no doubt some have lagged behind the trends for reasons of tradition/stubbornness or whatever else and still use it.

Note that you will also encounter countries that use the comma as a decimal separator; Wikipedia has a list that includes most of mainland Europe and South America, for example.


Animals with substantial five-fold symmetry besides starfish? Any land animals?

Many (if not most) of the Echinoderms (to which starfish belong as well) have five-fold symmetry, such as many sea liliy (Crinoidea) and sea urchin (Echinodea) species.

Five-fold symmetrical sea lilly:

Sand dollar (type of sea urchin):


Why does uterus have to be prepared every month for fertilization?

A quick search through the Internet, as well as any textbook, will reveal that the lining of the uterus (endometrium) created thickened during every menstruation cycle is rich in nutrients, and requires a constant blood supply, in order to accommodate a fetus.

Therefore, maintaining the lining would be more costly to the body than rebuilding it every month; in fact, as part of the lining is reabsorbed, rather than destroyed and expelled, thus conserving energy and nutrients. The reason a part of the endometrium is not reabsorbed is its thickness, which prevents its total reabsorption.

Also, the menstrual pain is, in fact, caused by the breaking down of the endometrium, although not directly, but by muscular contractions (cramps) and the contraction of blood vessels, which happen to prevent blood loss and help with the expelling of the endometrium.


What are the possible reasons to get extra unrecognized band in agarose gel electrophoresis?

Looks like genomic DNA contamination to me.

More importantly, does it really matter? I certainly appreciate the curiosity but, if your objective is cloning, I would just keep going and then do some diagnostic cuts of your plasmid after transformation. You can clearly see your vector or insert in the gel.


Can mitochondria be regenerated by the cell?

If we were to suppose, as in the question, that all the mitochondria in a cell 'died' ('were irreparably damaged' would be better, as they are not independently alive) without any other consequences the cell would have no way of regenerating them. Even if the cell had another source of ATP (see @another 'Homo sapien' comment) such as anaerobic glycolysis, one very clear reason is that the mitochondrial DNA could not be replaced (there are no copies of it in the nucleus). If the mitochondrial DNA were not replaced, then there would be no way of making the mitochondrial proteins it encodes.
The cell would die for a more immediate reason than suggested in the comment, and one that should be of interest in relation to a less well-known function of mitochondria. Mitochondria play a key role in the process of programmed cell death — apoptosis. In this process signals cause the mitochondrial membrane to become permeable and allow the efflux of cytochrome c, which is a signal for activating the apoptopic pathway. Presumably if mitochondria were damaged by other means the leaching out of cytochrome c would have the same effect, causing the death of the cell.
If you think of the overall economy of an organism, it's often easier to make new cells rather than trying to repair ones that are beyond redemption.
Further Information

Mitochondrial DNA: http://www.ncbi.nlm.nih.gov/books/NBK26924/
Apoptosis and mitochondria: https://en.wikipedia.org/wiki/Apoptosis#Activation_mechanisms


How do fully dioecious plants determine sex?

The short answer is that in dioecious plants the sex of an individual plant is determined by its chromosomes.

Several familiar crop plants are dioecious: asparagus, kiwi, hop, papaya, spinach and yam. The evidence indicates that dioecy has evolved independently in different plant families. I refer you to

  Matsunuga & Kawano (2001) Sex determination by sex chromosomes in dioecius plants. Plant Biol 3: 481-488.

I have summarised below some of the introductory information in this review.

First some background for context: In mammals there is an XY system in which maleness is determined by an active Y chromosome i.e. the Y chromosome carries male sex determination gene(s). Males are said to be heterogametic. In Drosophila there is also an XY system, with heterogametic males, but in this case what determines sex is the ratio of X chromosomes to autosomes. This ratio exerts its effects through the Sxl gene. In this system the Y chromosome does not carry male-determining genes.

In flowering plants, in dioecious species, the usual situation is that males are heterogametic. However, there is variability in the underlying mechanism of sex determination.  So for example in hop (Humulus lupulus) there is a pair of sex chromosomes that can be distinguished by their appearance. However there is no active male determination but rather the X to autosomal ratio determines sex (as in Drosophila). Conversely, in asparagus (Asparagus officinalis), sex is determined by a pair of chromosomes designated pair 5. The two chromosomes are morphologically indistinguishable but genetic evidence indicates that there is active sex determination in this species - one member of pair 5 acts like the mammalian Y chromosome.


This would most likely come under the category of Proprioception - the sense of how our bodies are arranged in the world, and how much effort each part of our body is expending.

From Wikipedia, 'In humans, it is provided by proprioceptors in skeletal striated muscles (muscle spindles) and tendons (Golgi tendon organ) and the fibrous membrane in joint capsules. '.

So our brain receives signals from muscles, tendons and joints, and integrates these into an internal sense of how we are arranged and what our bodies are busy doing.


What kind of detergent should I use in cell culture laboratory for cleaning purposes?

I can't tell if you're asking about glassware or work surfaces (hoods, benches etc), but...

We use regular old dawn dish soap in my lab because what's more important than the soap you use to wash you're glassware is the water you use to rinse it.  We teach our undergrads the 3-rinse-rule.  After soaping, every item gets 3 rinses with normal tapwater (or until no more suds forms- whichever comes last) followed by 3 rinses with deionized water.  We have DI water on tap which makes things easier.  I remember rinsing some glassware with acetone or other solvents in organic chem lab, but you shouldn't need to do anything like that for TC.

The same principle holds true for work surfaces.  After cleaning, decontaminate with 70% ethanol, 10% bleach, envirocide or any other BSL2 recommended cleaner.


That's not an insect but a crustacean (it has more than 6 legs).

It is a woodlouse (plural woodlice). A woodlouse is one of the few terrestrial isopode crustacean. There are about 5000 known species of woodlice. I have no idea which one is the one you captured!

Woodlice are generally appreciated in gardens as they control pests. They sometimes get inside searching for moisture. While it may not be pleasant to have woodlice at home (just because they look disgusting to many, me including), they do not spread disease or cause much damage.


Various Genetic Loads and their Definitions

The genetic load is a population construct, a way of quantifying the fitness reduction in a population due deviations from the optimal genotype.

One type of load comprises all the others, namely genetic load.

  Genetic load is just the loss of mean fitness relative to the ideal fitness.

You forgot to include substitution load in your list, but otherwise I think you included all the main ones.

  Substitution load is the total loss of mean fitness caused because favorable alleles substitute gradually by selection rather than
  instantaneously.

As for the ones you mentioned:

  Mutational load is just the accumulation of deleterious alleles in a population.
  Segregating load is the decrease in fitness in a population due to homozygotes being less fit.
  Drift load is the fixation of deleterious alleles due to small population size. The smaller the population, the greater the risk of
  this happening.
  Lag load is the loss of fitness due to a change in environment.

Another type, mentioned by rg255:

  Gender load, which is the deviation from the optimum due to an allele drifting back and forth because the version that is optimal in one sex is not the one that is optimal in another.


The ODEs for the Goodwin oscillator are:

$$\begin{align}
\frac{dX}{dt}=&\ k_1\frac{K_i^n}{K_i^n+Z^n} -k_2X\\[1em]
\frac{dY}{dt}=&\ k_3X-k_4Y\\[1em]
\frac{dZ}{dt}=&\ k_5Y-k_6Z\end{align}$$

If you assume $X$ to be mRNA and $Y$to be protein then $Z$ can be thought of as an activated form of the protein (lets for instance assume a phosphorylated form).

The Hill coefficient, $n$ roughly tells you how many monomers of the activated protein co-operatively bind to the promoter or the number of protein monomers that form a multimeric repressor complex which inhibits the production of $X$. $K_i$ is a measure of how strongly would $X$ be inhibited by $Z$. To be precise it is equal to the concentration of $Z$ at which the production of $X$ is half its maximum rate. (Similar to Michaelis constant)

What the model says is that at higher values of $n$ (>8) there are sustained oscillations (which are called limit cycles). At lower values the oscillations damp. Note that even for low values of $n$ sustained oscillations (but not limit cycle types) can arise if there is substantial delay in the loop. However these oscillations are not as stable as limit cycles to perturbations.

Have a look at this post.

These are some advanced concepts and you may start by reading this book by Steven Strogatz called Non-linear Dynamics and Chaos*.

*Strogatz, Steven H. Nonlinear dynamics and chaos: with applications to physics, biology, chemistry, and engineering. Westview press, 2014. (latest edition);  ISBN-13: 978-0813349107; ISBN-10: 0813349109


Difference between flexion and contraction?

Flexion: the movement that decreases the angle between two parts [1]. Examples: clenching the hand into fist, sitting down.

Contraction: the property of muscle to generate tension when actin and myosin filaments are crossing. There are a few types of contractions. The isometric contraction is when the muscle generates tension but its length doesn't change (for example when you try to lift something that you can't). The isotonic contraction is when the muscle changes its length [2]. This kind of contraction leads to movements and can lead to flexion too.

References:

Wikipedia contributors, "Anatomical terms of motion," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Anatomical_terms_of_motion&oldid=612679254 (accessed June 26, 2014).
Wikipedia contributors, "Muscle contraction," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Muscle_contraction&oldid=609265714 (accessed June 26, 2014).


RNA polymerase Sigma subunit: transcription factor, coenzyme, or what?

No.
I don’t think anybody would call the sigma factor of bacterial RNA polymerase — or indeed any other protein — a cofactor or a coenzyme, the subset of cofactors that are organic (the original poster is wrong in his declaration about cofactors, or at least one reputable text book disagrees with him).
I could justify this statement by quoting a definition from the section linked above:

“The catalytic activity of many enzymes depends on the presence of small molecules termed cofactors, although the precise role varies with the cofactor and the enzyme.”

by saying proteins like the sigma factor are not small.
However it is more interesting to me, and more useful to the naive reader, to make some general remarks about definitions in biochemistry and molecular biology.
What are definitions good for?
Definitions of terms are useful for scientific discussion or argument to enable those involved to be sure they are talking about the same thing. They often arise at the stage of a field of science when things are crystallizing after a period of uncertainty or lack of clarity. Even so they may lack precision. Cofactor just means “something else that is needed for certain enzymes to work” — biology is not physics.
Definitions are also useful for students and their teachers. They allow students to try to build a rational picture of a subject that is new to them. They allow teachers to systematize a subject (or lazily set rote-learning type MCQs instead of asking students to explain things).
The student new to the subject might find it helpful to consult glossaries such as those in Molecular Cell Biology, Molecular Biology of the Cell and Pearson’s Biological Glossary.
What are the limits of definitions?
The problem in a fast-growing field like modern molecular biology is that the period of resolution — when old men can form committees to give names to things — seldom lasts. Biology is anarchic, and new things come along that don’t fit into the neat pigeon holes that have been so carefully assembled. Nor do the anarchists or revolutionaries care. They find new things, describe them, and then get on with the next experiment. Why spend one’s time reading yesterday’s newspaper?
But the problem for the student comes when he discovers that everything does not fit into the neat categories he’s been taught, that there is a world beyond lactate dehydrogenase and metal proteases.
Sigma factors — what’s the problem in categorizing them?
The “classic enzymes” studied in early biochemistry catalysed simple chemical reactions between small molecules. However catalysis also occurs in more complex polymerization processes like nucleic acid and protein synthesis, that have the complexity of repetition along a polymeric substrate, and the necessity of having a specific start and stop along that substrate. It turns out to do that, that rather than enzymes such as RNA polymerase being a single catalytic protein they are complexed with other proteins that are necessary for certain of these functions. In the case of proteins like the sigma factor(s), this is complicated by the fact that these accessory proteins do not remain permanently associated with the catalytic protein subunit.
The poster, in his title, asks whether the sigma factor is a transcription factor. The answer to this is yes… and no. And calling it a transcription factor doesn’t really help much. Yes, it is a transcription factor because it is necessary for transcription and different sigma factors can impart a certain specificity to bacterial transcription. No, because the term transcription factor is mainly used for the much more specific proteins in eukaryotes that work in a rather different way.
What to call it? A subunit of the enzyme, is sufficient for Berg et al.. An accessory protein might perhaps add something. But don‘t worry too much about naming it, learn how it works.
Postscript: Other fruitless terminological disputes you may wish to avoid

Why is NAD regarded as a coenzyme and ATP a co-substrate?
Why is it epidermal growth factor, not epidermal growth hormone?
Why is it called vitamin D when it’s actually a hormone?
Should the term, molecule, be applied to double-stranded DNA or the individual chains?
How long must an oligopeptide be before it is called a polypeptide or protein?

No doubt there are others that I have missed that can be found in the list archives.


Identify this unusually-shaped, orange-colored fruit that grows in pairs?

The seed pods reminded me of the Apocynaceae, so I searched for "apocynaceae china" and found this University of Hawaii page where it is identified as Stemmadenia litoralis.  However, a little more looking it seems Tabernaemontana litoralis may be the preferred name.  There is some debate here.  This book may hold the final answer regarding the genus.

Your picture of the fruit is one of the best one I could find on the internet. There is another good one here with other pictures of the plant.

You were also correct that as a planted tree it might not be native.  This plant comes from Central America.


Is there a difference in the energy produced from the hydrolysis of GTP and ATP?

As @WYSIWYG said in comments, there is no effect of change in nitrogenous base on the third phosphate. Why? Simple, they are too far to directly influence each other's stability. See the diagram (of ATP) below from wikipedia:

and of GTP from here:

What one can clearly interpret from these diagrams is that there would be no effect on the energy released by hydrolysis of the third phosphate by the nitogenous base present. It will remain -30.5 kJ/mol(1) in both cases.


How do viruses such as COVID-9 and flu return in the winter if they disappear in the summer?

I think the first step in answering your question, is correcting part of it. Influenza does not disappear in the Summer. Infection rates decline, but people can still become infected in the off season. Remember, we live in a globally connected society. Summer in the Northern Hemisphere is winter in the Southern Hemisphere. Influenza also has a number of animal reservoirs and intermediate hosts, which can contribute to persistant survival.

As far as the seasonality of infection rates, there are a number of contributing factors. This article from Harvard University discusses a few factors:

  "1) During the winter, people spend more time indoors with the windows sealed, so they are more likely to breathe the same air as someone who has the flu and thus contract the virus.

  2) Days are shorter during the winter, and lack of sunlight leads to  low levels of vitamin D and melatonin, both of which require sunlight for their generation. This compromises our immune systems, which in turn decreases ability to fight the virus.

  3) The influenza virus may survive better in colder, drier climates, and therefore be able to infect more people."

For a more exhaustive discussion of the underlying causes of influenza seasonality, here's an open access review article on the subject.

Some researchers suspect that the SARS-CoV-2 virus, the causitive agent of COVID-19 infections, may have a similar patern of seasonality, but it's probably too early to know for sure how influential each of these factors will be in the long term.


Where’s the flaw in my proposed TB Treatment?

High oxygen concentration can be deleterious; it can induce oxidative
damage.
The systemic blood circulation would supply oxygen to the
"oxygen-deprived" lung.
Moreover, Mycobacteria can survive in anaerobic conditions.

And what if both lungs are infected? There are many flaws in the proposed therapy.

Adding this point from one of the comments below:

There are several cases of extrapulmonary tuberculosis and in these cases treating just the lung would not make sense.


Can undigested food proteins enter the bloodstream?

Sort of.

Proteins can enter the body through the intestines by exploiting a few transport mechanisms, They are not truly crossing the cell membrane but are transported across the cell in vesicles. Though not into the bloodstream but into the lymph system.

M cells in particular will move antigens across the intestinal wall, a few more durable proteins (like prions) have been shown to piggyback on this system to cross in tiny quantities. Some viruses also exploit it. Collagen definitely does not enter this way but there are likely egg antigens that may.

Note this is very rare for non-antigens, the vast majority of food you eat will not contain anything that can exploit this although they may contain antigens that get passed to the immune system.

Source

Source 2


Why are tree rings the same if rainfall is different from place to place?

The rings are not only affected by time but also by location. So no, the patterns are not always the same depending where you are. Climate do affect the rings.

Typically a major factor affecting ring patterns is the seasonality. Depending on the number of rainy season, you might observe one or two rings per year.

If interested, here is an introduction to dendrochronology (from the University of Victoria).


Is there a genetic reason explaining the difference of the height of male and female?

Short answer:

There is strong evidence that height is a heritable trait with a strong genetic component. The genetic mechanism could be higher expression of an X-chromosome gene that, expressed in high levels, inhibits cartilage development, perhaps causing lower height. The increased expression seems to be caused by incomplete X inactivation in females. Furthermore, there is differential selection for height between human males and females likely causing the differences we see in modern human populations.

Long Answer:

Genetic basis of height

The genetic variants analysed by Wood et al. (2014) account for ~29% of the phenotypic variance and 60% of the heritability of height.

Due to this high heritabilty (and the fact that there are still expected to be more unknown variants affecting height) there most likely is a genetic reason explaining the difference of height in human males and females. Thinking about the nature of this difference is a bit difficult. It is good to know that the trait has a high heritability and therefore a strong genetic component as this allows us to have a look at how natural selection affects height.

Selection on height

Height is a polygenic trait that is under recent and strong natural selection (Field et al., 2016 - preprint) leading to height increase in both human males and females (Fig. 3D in Field et al. (2016)):

What does this tell us in terms of the genetics underlying the height differences in human males and females? First, we have to understand that natural selection (at least mainly) affects individuals, not species. Then, we can understand that natural selection can affect males and females of a species differently. And Field et al. (2016) have shown exactly that for height. In their analyses, you can see that male and female height show (mildly) differing signals of natural selection (Fig. 4C in Field et al. (2016)):

But selection needs heritable genetic variation that allows this differentiation between the sexes. So what is the mechanism?

Genetic mechanism of height differences between human males and females

As pointed out by @tsttst in the comment differences between sexes are usually caused by genes on the X and Y allosomes. There is evidence that the height differences between human males and females are related to the X-chromosome (which also explains some of the missing heritability of the GWAS study by Wood et al. (2014)), reported by Tukiainen et al. (2014). They write

  In one of these three associated regions, the region near ITM2A, we observed that there is a sex difference in the genetic effects on height in a manner consistent with a lack of dosage compensation in this locus. Further supporting this observation, ITM2A has been shown to be among those chrX genes where the X chromosome inactivation is incomplete.

They also give a molecular mechanism how this hypothesised increased expression of ITM2A can cause the height difference. They report that the ITM2A gene is
involved in cartilage development (van den Plas et al., 2004) and that the height-associated ITM2A variants change expression of the ITM2A protein. This is interesting as increased ITM2A expression in mesenchymal stem cells of adipose tissue seems to inhibit cartilage development (Boeuf et al., 2009). Tukiainen et al. (2014) conclude:

  As the allele associated with shorter stature associated with increased expression of ITM2A (sic), this suggests the allelic effect to height could be mediated through the capacity to generate cartilage and bone.

Finally, how can this be interpreted from an evolutionary point of view?

Evolutionary interpretation of height differences in human males and females

Differences in height (but also other traits) between sexes of a species are refered to as sexual dimorphisms. Sexual dimorphism (at least in primates) in height is strongly related to differences in mating behaviour and a sign of aggression and/or dominance-based mating patterns (Wynn and Coolidge (2011, p.82), sorry for that poor referenc link). The counterpart to this is pair-bonding, or in human terms marriage: a primate example is our pretty close relative, the Gibbon, that is (at least socially) monogamous and as expected does not have a height-related sexual dimorphism. Great apes including humans do have this polymorphism even though pair-bonding in humans is widely spread. Therefore, it was not surprising to find a reduction in height dimorphism from Australopithecus over Homo erectus to Homo sapiens (Wynn and Coolidge, 2011, p. 83, see also this, especially the last paragraph of this chapter).

Update on the main source

One of the papers I mainly used for this answer - to illustrate selection on height - was a preprint. It is now published in Science: Field et al. (2016).


How fast do cancer cells divide (compared to normal cells)?

Tumors can be benign (they don't bother you at all eg: a mole which does not change) and malignant (also called cancer).

The difference is based on:-

Degree of differentiation - How much the tumor cells resemble the normal cells
Rate of growth - In general (over generalised) benign tumors are slow growing while malignant tumors are fast growing
Spread to nearby tissues - Benign growth don't cross tissue planes as defined by basement membranes/fascias, while malignant tumors invade across tissue planes
Metastasis - Spread to a remote location in the body through blood, lymph vessels, transcoelomic (peritoneal, pleural, pericardial spaces) routes - This is ONLY seen in malignant tumors.

Coming specifically to rate of growth, these factors must be considered:

What is stated above in 2 is the general case:

Malignant tumors a.k.a cancers grow fast
Benign tumors are slow growing
That being said some benign tumors grow faster that malignant tumors. Eg: Fibroid - grows very rapid under the influence of estrogen as in pregnancy

The rate of growth of malignant cancers depend on their degree of differentiation (look point 1 above).

Well differentiated cancers grow slow - Cancers that are very similar to normal cells are considered to be well differentiated
Poorly differentiated cancers grow faster based on the "poorness" of differentiation,i.e. the worse the degree of differentiation, the faster the growth. Totally undifferentiated (unidentifiable as any tissue type) are called anaplastic cancers and these grow the fastest

The rate of growth of cancers may vary over time

Due to excessive division probability of mutation is high and a sub-clone may emerge with faster rate of division thus a previously slow growing cancer could suddenly start growing fast
Due to the same process some cancers may suddenly decrease in their growth rate and may eventually even vanish! (become necrotic and get cleared away)

This is taken from Robbin's Text book of Pathology,Ed.8, chapter 6

Edit 1:
To know the numbers you need, you have to find out the rate of increase in volume (by measuring size at two points in time) and divide it by the approximate volume of one cell. This will give you the number of cells that has newly divided within the two measured points (growth in interval). Which can then be converted to cell divisions per second.

As pointed out, the rate is going to vary extremely, based on the cancer type.


There are many websites which describe this phenomenon. They all seem to confirm the basic premise of the question: in tropical rain forests most of the minerals are held in the biomass and rapid decomposition contributes to the recycling of these nutrients for new growth. One example is here.

  Tropical rainforests are noted for the rapid nutrient cycling that occurs on the ground.  In the tropics, leaves fall and decompose rapidly.  The roots of the trees are on the surface of the soil, and form a thick mat which absorbs the nutrients before they reach the soil (or before the rain can carry them away).  The presence of roots on the surface is a common phenomenon in all mature forests; trees that come along later in succession win out in competition for nutrients by placing their roots over top of the competitors, and this pattern is seen in the temperate rainforest as well.  What does not occur in the temperate rainforest, however, is a rapid cycling of nutrients.  Because of the cold conditions and the acidity released by decomposing coniferous needles on the forest floor, decomposition is much slower.  More of the nutrients are found in the soil here than would be the case in a tropical forest, although like the tropical forest most of the nutrients are held in the plants and animals themselves.

I looked for actual evidence of these differences in rates of decomposition and I found this:

  Salinas, N. et al. (2011) The sensitivity of tropical leaf litter decomposition to temperature: results from a large-scale leaf translocation experiment along an elevation gradient in Peruvian forests. New Phytologist 189: 967-977

These authors reported a comparison of rates of decomposition at various elevations in Peruvian forest. The parameter k is the decay rate of dry mass, year-1. The following data are taken from Table 3.

site          elevation (m)   mean k (yr-1; 15 species)
Tambopata     210             1.753
Tono          1000            1.424
San Pedro     1500            0.968
Trocha Union  2720            0.546
Wayquecha     3025            0.424

and this:

  Jacob, M. et al. (2010) Leaf litter decomposition in temperate deciduous forest stands with a decreasing fraction of beech (Fagus sylvatica) Oecologia 164:1083–1094

These authors studied leaf decomposition in a deciduous forest in Germany, with emphasis on the effect of proportion of beech trees upon overall rates of decomposition. Using data from Table 1 and Figure 2 (values converted from mg-1 g-1 day-1 to yr-1)

% beech yr-1
  96    0.2555
  67    0.657
  21    1.022

My Conclusion

Rates of decomposition can be much higher in tropical rainforest (k=1.753 yr-1 for the Tambopata site in Peru, k=0.256 yr-1 for a beech-rich forest in Germany). However, at higher elevations tropical rain forests are characterised by much lower rates of decomposition (Wayquecha k=0.424 yr-1), comparable to those in deciduous forests.

These are all measurements of loss of dry mass from leaf litter. This will be dominated by loss of carbon, and I would expect that minerals will leach from the decaying litter more rapidly than these values. Nevertheless it seems plausible that relative rates of mineral recycling will reflect these k values.


how many spores are needed to "infect" a wall?

Yes, the box likely had many fungal spores attached to it since it smelled “moldy”. This doesn’t mean that your room will definitely be contaminated because spores often wait for ideal conditions to germinate. There are fungal spores in the air we breathe all the time, so if those haven’t already colonized your wall then adding the ones from the box are unlikely to cause any problems.

If you do see spots appear, they can be easily removed with a damp paper towel, generic home cleaner, or diluted bleach.


"producer cell line" vs. "host cell line" in biopharmacology

I would lean towards staying with "producer cell line". In my mind, a host cell line is hosting something, like a virus, while a producer produces something. The non-transformed cell line would be the parent cell line.

On the other hand, "host cell line" also implies hosting the recombinant protein product that is later purified, so there's an argument to be made for either phrase. I still prefer producer, though, as I think it's more directly descriptive of what the cells are actually doing - producing the protein of interest.


Improving DNA quality and yield from stool samples

Expected photometric ratios for pure DNA are around 1.8 (A260/A280) and 2.0-2.2 (A260/A230). For reference, if you are extracting pure RNA, its ratio is ideally 2.0 (A260/A280).

Often, lower ratios usually indicate low purity due to contaminants or simply a very low amount of DNA.

EDTA, carbs and phenol among other chemicals all have absorbance at 230nm. If you used TRIzol reagent to extract DNA, you may also get some absorbance from this reagent at 270nm if you incorrectly pipetted some of the phenol phase (pink stuff) or the interface (white cloudy stuff between the aqueous phase and the pink phase). If you measure a low ratio, like you did, it probably means that in your final DNA extract, you seem to have (a) things that are not DNA in your solution, and/or (b) a very low concentration of DNA.

If you suspect you have enough DNA, you can purify to try to remove non-nucleic acids. However, with ratios that low, I suspect you should extract DNA from scratch; it does not appear that you have enough to rescue simply by purifying again.

Which method did you use to extract your DNA? What do you mean by filtering?


How does the immune system distinguish own and foreign antibodies?

The short answer is that antibodies are proteins like any other, and if an antibody from a foreign source is injected it can result in an immune response. This is, of course, exploited in the production of secondary antibodies for use in research (e.g. goat anti-rabbit IgG is a goat  antibody that recognises rabbit IgG).

Because of this, therapeutic antibodies are "humanised" and this is the case with Rituximab which is derived from a mouse monoclonal IgG:

  Rituxan is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. The antibody is an IgG1 kappa immunoglobulin containing murine light- and heavy-chain variable region sequences and human constant region sequences. Rituximab is composed of two heavy chains of 451 amino acids and two light chains of 213 amino acids

Presumably it would be possible for the remaining mouse-derived variable regions to be recognised as foreign by the human immune system, and this possibility is hinted at in the abstract of an early paper on rituximab (McLaughlin et al. (1998) Rituximab chimeric anti-CD20 monoclonal antibody therapy for relapsed indolent lymphoma: half of patients respond to a four-dose treatment program. J Clin Oncol.16:2825-33.) My emphasis...

  A chimeric monoclonal antibody more effectively mediates host effector functions and is itself less immunogenic than are murine antibodies.

However, I'm not aware of any evidence that simple immune responses to Rituximab actually occur.


Can storing food in a de-pressurized container result in anaerobic bacteria growth?

Any sealed container can become anaerobic relatively quickly if there are oxygen consuming organisms inside (which there probably are if it's not sterilized). So, growth of anaerobes should always be a concern when using a sealed container for food storage, and proper temperatures for such storage should be considered.

A container like the one you describe would probably be good for extending the shelf life of dry foods that are sensitive to oxidation (coffee, spices, or your soy lecithin powder), and might even help stave off aerobic spoilage organisms (like molds), but it probably won't do anything to prevent growth of anaerobes like C. bolulinum or C. perfringins.


In humans, the coelom forms by the splitting of the lateral plate mesoderm, which occurs during weeks 4-5 (Sweeney, 1998).

Sweeney, LJ. 1998. Basic Concepts in Embryology. McGraw-Hill.


No bands show up in gel electrophoresis, not even marker

What I can quickly think of is that you were running the gel incorrectly: instead of from - to + direction,  You ran it the other way around and your DNA went out of the gel. Another thing might be that the UV light was not turned on or is broken.


Why do redheads tend to sunburn more easily?

You should have a look at wikipedia > melanin.

  Melanin is a broad term for a group of natural pigments found in most organisms. [..] Melanin is an effective absorber of light; the pigment is able to dissipate over 99.9% of absorbed UV radiation.1 Because of this property, melanin is thought to protect skin cells from UVB radiation damage, reducing the risk of cancer. Furthermore, though exposure to UV radiation is associated with increased risk of malignant melanoma, a cancer of the melanocytes, studies have shown a lower incidence for skin cancer in individuals with more concentrated melanin, i.e. darker skin tone. Nonetheless, the relationship between skin pigmentation and photoprotection is still being clarified.

Most of the variation in skin color among humans is caused by differential levels of melanism. People with red hair have a low level of melanism (almost by definition) and therefore suffers more from sunburn than people with more pigmented skin.


A doctor might give bicarbonate (HCO₃¯) to a patient who is breathing very rapidly. What is the doctor assuming about the patient’s blood chemistry?

if a person is both (1) hyperventilating and (2) has a low blood pH then this is a case of metabolic acidosis... in metabolic acidosis the patient compensates by breathing heavy... why? because hydrogen ions are captured by bicarbonate (the conjugate base of carbonic acid) which is then exhaled as carbon dioxide...

metabolic acidosis is not caused by excess carbon dioxide... this is the case of respiratory acidosis... but under respiratory acidosis the breathing is supressed, however tachypnea with frequent shallow breaths could lead to poor removal of carbon dioxide...

here are some causes of metabolic acidosis:
http://en.wikipedia.org/wiki/Metabolic_acidosis#Causes


Can P. falciparum and other malaria parasites be cultured and genetically engineered?

Yes it is possible to culture plasmodia but they don't grow in a simple constituted medium. Usually RPMI supplemented with serum and erythrocytes is used for growing plasmodia ex-vivo. This article discusses the issues related to plasmodial culture in detail. The authors say that sometimes a certain growth stage (in particular gametocyte) is lost on prolonged cultivation.
In the same paper it is discussed that the exo-erythrocytic (liver stage) plasmodia can be grown on cultured hepatoma cell lines.

Several transfection methods also exist. However, culturing is not a mandatory prerequisite for transfection. Usual methods like electroporation work for a wide spectrum of cell types (in-vivo electroporation is also becoming popular). You can refer to this article for a summary on different transfection methods for plasmodia.

A major limitation, in my opinion would be that the different life stages may not be reproduced in a single culture (as you can see that each stage thrives in a very different type of milieu).


What causes spontaneous muscle twitches?

Short answer
Spontaneous muscle twitches are thought to be caused by spontaneous activation of motoneurons controlling the muscles.

Background
Spontaneous muscle activity (twitching) is referred to as muscle fasciculations. Most commonly, they are benign, but they can be associated with certain pathologies too, such as ALS.

Fasciculations are thought to originate due to spontaneous activation of muscle fibers due to processes in the motoneurons. At the axonal endings there are synapses that junction onto the muscle. The axonal tips of motoneurons are thought to be highly sensitive to depolarization (electrical firing), which is what triggers acetylcholine release and muscle contraction.  The complicated process itself takes a small fraction of a second.  If any of this happens involuntarily, then the muscle fiber contracts spontaneously (source: ALS Association).

Specifically, it is thought that spontaneous depolarization of motoneurons are the cause of fasciculations. This decreased firing threshold can be the cause of disease, disrupted ion homeostasis in the body, fatigue, drugs and other causes (Blum & Rutkove, 2007).

Note that spontaneous / random activity in neurons is not only possible, it is quite common. Especially in neurons close to firing threshold, such as the motoneurons responsible for muscle activity, slight perturbations in ion concentrations inside or outside the cell can trigger an action potential. Further, channel opening is a stochastic process, meaning that even voltage-gated Na+ channels can open without a depolarization being present; although the chance is slim that will happen, it can statistically still happen. Stochastic processes like this can cause neurons to fire spontaneously, without a stimulus being present.

Reference
- Blum & Rutkove, The Clinical Neurophysiology Primer, Springer (2007)


You could have easily find these using a simple google search, however I will point several out:

See figure 1 of this article for an ultrasound image of a trigger point. Really interesting!
See figure 1 of this article for a schematic representation, and figure 2 for a real image. Although you did not ask for a deeper understanding of this topic, if you want to read more about it I would recommend reading this paper as it covers a lot of aspects (such as pain signals to the brain).
This article covers different imaging techniques and facilitates interpretation by using arrows to point out the trigger points.

If this is not what you are looking for please specify what you mean with "pictures"? (vibration sonoelastography, schematic, ultrasound, etc.) I cannot point you in a direction for real life images (if these even exist).


Beetle with long, slender iridescent green body and orange legs

I'm going to guess it's an Plinthocoelium suaveolens, based on the image found here, which I show below:

I found this link through a Texas beetle page here and is the best I can do from the image provided.


What are the positive effects of wrongful antibiotic use on a viral infection?

There are indeed antibiotics which have immunomodulatory side-effects, these are mostly from the class of macrolide antibiotics (erythromycin, clarithromycin, roxithromycin, azithromycin) and to some degree from the tetracyclines. Beta-lactam antibiotics (as Penicillin or Ampicillin) have not been shown to be immunomodulatory, but they are among the most commonly used. See reference 1 for more details.

The biggest effect has been shown on pulmonary diseases such as cystic fibrosis or diffuse panbrochiolitis (see reference 2).

Although the exact mechanism of action is not known, Macrolides are know to downregulate the inflammatory cascade and that the reduce the strong cytokine expression of some viral infections. However, these regulatory effects are relatively weak if you compare them to the anti-inflammatory properties of corticosteroids. So the question here is if the advantages are really sufficient compared to the problems, which an unnecessary use of antibiotics may cause. See reference 3 and the references in the paper for more details here.

Antibiotics may be useful to fight bacterial secondary or superinfections which accompany a virus infection.

References:

Immunomodulatory Properties of Antibiotics
Macrolide activities beyond their antimicrobial effects: macrolides
in diffuse panbronchiolitis and cystic fibrosis
Macrolide Therapy in Respiratory Viral Infections


What is this unusual structure inside this banana?

It looks like some species of Nigrospora genus took over the inside of that banana. According to Wikipedia, N. sphaerica was first isolated from bananas. The other species that you will find referenced online is N. oryzae. In the articles I
cite below the colonies are grown in potato dextrose, though.

Here is a picture of the red fungus inside a banana (from the Canadian Food Inspection Agency):

Googling 'Nigrosporia banana' also returns lots of similar pictures.

To get a better answer, a sample could be taken from the banana and then cross-check what you see under the microscope with the oryzae morphology images seen in the researchgate article.


How could this fossil's soft tissue be preserved so well?

You're right that the authors don't comment on how they think the fossilization occurred. Since that process isn't the point of their article, my guess is that any discussion of it would have detracted from their research focus.

There are some ways that soft tissue fossilization can occur, but to specifically answer your question as it relates to this case, you'd have to know more about the geological conditions in which the fossils were found, which I don't see in the article. This article provides a nice review of soft-tissue preservation processes.

The main points to consider in soft-tissue fossilization, according to the linked article, are pressure, time, charge and chemistry.

Pressure: How much pressure was the fossil under? The higher the pressure, the less oxygen and fewer organisms can access it and degrade biological tissue.

Time: How quickly did the fossil become inaccessible to degrading organisms? The faster this occurs, the less likely that any soft tissue will rot away.

Charge: Does the sediment in which the fossil found carry a charge? Electrical charge acts both as an selective barrier to some organisms and chemical compounds that can hurry biological decay and provides a means for reaction with biochemical compounds, which brings us to the last point:

Chemistry: Can components of the biological soft tissue react with their surrounding minerals? If so, then the inorganic compounds present may be able to reduce lipids and other complex carbohydrates to molecular carbon and minerals in the form of the biological organism.

So say, for instance, that this organism was suddenly encased in a thick layer of clay. As the review states:

  In clay-rich environments, the large surface area and charge of clay
  grains are thought to contribute to preservation in one of two ways.
  First, enzymes produced either through autolysis or by invading
  microbes are adsorbed to the surface of the clay grains and
  inactivated, slowing or preventing degradation (Butterfield 1990,
  Garwood et al. 1983). Second, molecules directly adsorbed to clay
  grains are resistant to degradation (Stotzky 1980), whereas
  protein-protein layers are readily degraded. This mechanism may
  explain the exquisite preservation of thin carbon films in impression
  fossils such as the feathered dinosaurs of the Jehol Biota (see
  discussion below). As tissues interact with surrounding clay grains,
  only the molecules in direct contact with clays are preserved as
  monolayers, whereas the rest are degraded normally. Thus, surface
  morphology is preserved, and original carbon might be preserved as
  well

Who knows if this process explains these particular fossils. ¯_(ツ)_/¯  As I said earlier, we'd need more information. The section quoted above, though, seems (to me) to provide a plausible hypothesis.

I hope this helps!