How the brain is affected by Alzheimer's disease

Essentially, there's a net dysregulation of a number of genes where the additive effect of each dysregulation causes neurotoxic amyloid plaque formations, and neurofibrillary tangles of hyperphosphorylated tau protein. Not only so, these mutations induce calcium and cytokine dysregulation, and increase oxidative stress.

Specific to molecular mechanisms of amyloid beta (abeta) oligomer toxicity, a good article here makes some good descriptions. For example, abeta can reduce copper and iron ions. Oxygen reacting with these reduced metals become reactive oxygen species. They also noted that abeta reacts with many receptors, like TLR's which ended up promoting JNK-mediated apoptosis. I'd give that article a read, and I'll try to get some molecular pathology mechanisms for other facets of AD on board here.

They can't generally be repaired because the issue is with genetic mutations, and some of the mutations engage in positive feedback loops with existing conditions that make a more pronounced effect. For example, tau protein is regulated in part by O-GlcNAcylation. This is like phosphorylation, but with sugar moieties, but it becomes downregulated when glucose is low, thus increasing phosphorylation on tau (Liu et al., 2004) . Mutations that affect GSK-3, insulin resistance and/or diabetes thus can play a role in AD pathogenesis.

Some data exists to show restoration of potentially AD-causing abnormalities involving HDACs. For example, abnormal HDAC2 in AD brains hypoacetylated promoter regions for some housekeeping and plasticity genes, and they rescued the AD phenotype by knocking down HDAC2 (Gräff et al., 2012) . These are of course mouse models typically.

As for question three, I really can't say except for stochasticity. I did a review for an undergraduate course that goes over some of the recent literature involving AD genetics/pathogenesis. It might not be professional quality but it gets the message across, linked https://drive.google.com/open?id=0BwKiapIJL9T2ajc4ajhTVVRvRWc


What are the sources of molecular hydrogen in human breath?

Hydrogen in breath arises from normal intestinal bacteria, mainly in the colon, which break down (ferment) the undigested nutrients that have passed through the small intestine. Hydrogen is absorbed from the intestine into the blood and exhaled via the lungs.

Conditions in which intestinal bacteria produce hydrogen:

Normal digestion in which soluble dietary fiber is not digested in the small intestine. Examples of soluble fiber: beta-glucan (in oats and barley), pectin (in apples) fructo-oligosaccharides (in red onions), raffinose (in beans), etc.
Lactose intolerance in which lactose remains undigested due to lack of the enzyme lactase (gas is produced mainly after ingesting milk)
Fructose malabsorption in which fructose absorption is reduced due to lack of a certain molecule in the intestinal lining (gas is produced after eating foods high in fructose: apples, pears, honey, agave, etc.)
Sucrose intolerance due to lack of the enzyme that digests sucrose
Small intestinal bacterial overgrowth (SIBO) due to various malabsorptive conditions

Hydrogen breath test is an established method for diagnosing various intestinal disorders. It includes drinking a solution high in certain substance (lactose, fructose..., depending on which disorder is expected) and measuring hydrogen in the exhaled air.

To properly interpret the results of a hydrogen test you need to consider the time in which hydrogen appears in breath after ingestion of a certain substance.

Food Marble provides a relatively thin explanation of their breath test. The question is if this test can distinguish between the hydrogen produced during normal digestion of the soluble fiber and hydrogen produced in the mentioned intestinal disorders.

Business Insider made a review of FoodMarble in which they mention some other reviews...In summary: it's not proven reliable, yet.


Why do morning people have shorter biological clocks?

Circadian rhythms are entrained by light via the suprachiasmatic nucleus, a part of the brain that receives signals from special retinal ganglion cells that are directly sensitive to (mainly blue) light.

However, light is not strictly necessary: the internal circadian clock is the result of shifting gene expression that proceeds without outside stimulus. Light is only used to entrain (or "reset") the clock each day.

When people talk about the duration of an individual's circadian rhythm, they are referring to what happens in the absence of a light cycle (that is, without entrainment).

https://en.wikipedia.org/wiki/Circadian_rhythm
https://en.wikipedia.org/wiki/Suprachiasmatic_nucleus
https://en.wikipedia.org/wiki/Circadian_rhythm_sleep_disorder


A subset of pseudogenes can have a function - even if not translated: For one possibility see the official record for PTENP1, which acts as a tumor suppressor by providing a decoy for PTEN targeting miRNAs
A subset of pseudogenes can be translated. There is a selection for preserving the length of the reading frame, which suggests (but does not formally show) the presence of a translation-dependent function of (at least a subset of) those pseudogenes. - See Xu et Zhang 2016: Are human translated Pseudogenes Functional? (paywall)
As indicated by the above, it seems likely that quite some pseudogenes have a function, which just has not been discovered yet - and that the mode of action can differ between different pseudogenes.


What does "substoichiometric amounts" mean in the context of molecular biology?

It possibly refers to fractional stoichiometry i.e. less than a molecule of these proteins per molecule of PRC2. Obviously, you cannot have half a molecule and this statement means that in a gross sample, the concentration ratio of these proteins with respect to PRC2 is less than 1:1. At a molecular scale, it would mean that these proteins may not be always associated with PRC2.

This is also in agreement with the known fact that PRC2 core components are EZH2, EED, SUZ12 (along with RbAp46/48) and the others are accessory factors (Margueron and Reinberg, 2011).


How to do desalt reaction by passage through a Micro Bio-spin 6 column?

Maybe you can take a look at this. I found it through google when searching for the manual as well.
http://www.bio-rad.com/webroot/web/pdf/lsr/literature/4006051.pdf


What is the smallest number of amino acids required for life?

You can divide the 22 (including selenocysteine and pyrrolysine)  proteinogenic amino acids into broad groups of similar amino acids. There are the hydrophobic amino acids like trypthophane, valine and leucine, the charged amino acids like glutamate and arginine and the polar amino acids like serine and threonine. There are some amino acids with unique features like cysteine which can form disulfide bonds.

Some amino acids are very similar, for example isoleucine and leucine, it is plausible that one of those would suffice to create most protein folds.

There are several examples of proteins designed with a smaller alphabet of amino acids, one example is the E. coli orotate phosphoribosyltransferase (Akanuma et al., 2002). The simplified enzyme consists of only 13 different amino acids and 88% of it are composed of only nine different amino acids. Even after those drastic changes the enzyme still folds correctly and has enzymatic activity.

There is one study (Fan and Wang, 2003) that tried to answer exactly the question you asked. They came to the conclusion that around 10 amino acids are necessary to create properly folding proteins:

  First, we study the minimum sequence complexity that can reserve the
  necessary structural information for detection of distantly related
  homologues. Second, we compare the ability of designing foldable model
  sequences over a wide range of reduced amino acid alphabets, which ﬁnd
  the minimum number of letters that have the similar design ability as
  20. Finally, we survey the lower bound of alphabet size of globular proteins in a non-redundant protein database. These different
  approaches give a remarkably consistent view, that the minimum number
  of letters required to fold a protein is around ten.

Akanuma, S., Kigawa, T. & Yokoyama, S. Combinatorial mutagenesis to restrict amino acid usage in an enzyme to a reduced set. Proceedings of the National Academy of Sciences 99, 13549 -13553 (2002).

Fan, K. & Wang, W. What is the minimum number of letters required to fold a protein? J. Mol. Biol. 328, 921-926 (2003).


How are CheY, CheA, CheW, CheZ pronounced in speech?

As was mentioned in the comments, these are not real words and there is no authority on their pronunciation. Given that Che is an abbreviation of chemotaxis, I would pronounce it the same as key.


Why pick just a single bacterial transformed colony

This is a matter of pragmatism in the culture process.

Taking 100 colonies instead of 1 increases the inoculation volume by a factor of 100, which then saves you perhaps 2 hours of bacterial growth time before your culture reaches the OD you want.

However, mutations and loss of plasmid in culture, while unlikely, are possible, especially if the bacteria were not cloning strains with their recombinases knocked out. In such a case, you would risk the downstream experiments being contaminated with mutants, be that protein expression, retroviral plasmid production, or something else.

Worse still, the mixture of bacteria containing mutants is less likely to be detected, since had you picked a single mutant colony, there would be absolutely no result, but a contaminated culture would produce a low but still positive result. Therefore, you may end up wasting many days or weeks troubleshooting your downstream experiments.

Therefore, picking single colonies is simply a matter of "better safe than sorry".


Why do Major and Minor grooves exist in dna strands?

It is all explained here in Wikipedia. You are referring to Watson-Crick base pairs in the B-DNA structure.


What is the biological basis for a human's ability to think clearly and be aware while "fighting/competing"?

thinking and decision making under stress or pressure is significantly reduced.  its sometimes called the 'fight or flight' condition.

This is a pretty well established phenomenon.  Here's a great radiolab segment on stress response.  Psychologist John Gottman notes how our ability to have a conversation where we can even listen to what someone else has to say is practically nil when we are emotionally saturated (frustrated or upset that is).  Even a mildly stressful conversation with your own spouse can shut down most rational processes.  Gottman can predict couples who overcome this problem which is highly corellated with divorce btw - but most of these couples remove stress in conversations rather than learn to work under pressure as it were.

Jonah Lehrer wrote about how tests to rank quarterbacks in their ability to respond on the gridiron are basically non correlated.  I know there have been criticisms of Lehrer, but this is a good piece and well grounded.  The point is that its hard to tell a-priori whether someone will perform under stress and given different sorts of stress.

In the japanese space program they would screen candidates by making them do highly repetitive tasks like folding 1000 origami cranes.  NASA was just doing interviews with panels of psychologists.  That wasn't infallible.

Such a test would be valuable for fighter pilots, astronauts, maybe presidents too! but it doesn't seem to really exist at this point.

In the end you can winnow out those who break into a sweat in the interview, but to know who is going to really take the beach, I think that the only real answer is to see if they make it through a 'live fire' (or whatever) experience.

Or as Clint Eastwood summed it up: "A man's got to know his limitations."

(apologies to the ladies there - you can know your limitations too).


How quicky does dental pH change after eating?

Dental damage is mainly caused by the demineralization of the tooth enamel. Demineralization can happen due to a low pH caused either by acidic food/drinks like fruits or carbonated beverages or by bacteria producing acid while breaking down sugars.

Measurements (1, 2) have shown that food intake changes the pH (increasing or decreasing, depending on the food source), returning back to baseline after 15-30 min due to the buffering capacity of the saliva via bicarbonate and phosphate.

The drop in pH happens immediately after food intake. If teeth are not cleaned, the acid producing bacteria can have a longer-lasting effect on the pH for more than an hour. In these studies, participants are asked not to clean their teeth, so bacteria will populate the mouth. Removing bacteria or their food source as well helping the remineralization with fluoride toothpaste can counter the effects.


I am going to try answer this question.

The origine of this name came from article writen by Franz Niessl (18660-1919) and published in 1894. HE found this substance after he visualized it by nissl stainning method invented by him.

This basophilic substance was just only find in dendrites of neurons, not axones. It is composed by RNA polyribosomes.

Basicly i am tring to tell you that Niessle body is just older name from old ages of histology.

Niessel body is not diffrent with others rought endoplasmatic reticulum(RER). It same pourpose as normal RER.


Its quite simple if you look at the basics! Lets have a look at the sequence you give:

  AGWRGSDSHSR

Write that in 3-letter terms1:

  Ala-Gly-Trp-Arg-Gly-Ser-Asp-Ser-His-Ser-Arg

Pay attention to the C-terminus. The last amino acid residue in the sequence is Arginine. Now, its well established that Trypsin cleaves a polypeptide after (i.e. towards the C-terminal side of) Lysine and Arginine2.

Thus, C-terminal tryptic peptide is the peptide that remains after a polypeptide has been treated with Trypsin.


Discounting lab error and other kinds of human incompetence, there aren't very many things that can confound a paternity test. Normal DNA damage cannot, but there are kinds of genetic chimeras that get strange results.

Normal human DNA damage can't add up fast enough to change the results without killing you several times over, but there are a surprisingly large number of people who are chimeras.

The relevant particular flavor of chimerism is tetragametic chimerism, where essentially parts of your body are sibling-related to the rest. This occasionally is discovered during paternity testing, in one vivid instance when a woman was provably not the mother of the newborn that she had just given birth to. Technically I suppose the baby was her skin's niece.

The incidence of this was thought to be very low, but it's almost impossible to detect without DNA testing. We know the incidence is much higher than we thought, but we don't know how high.


What happens when the bacteria in the petri dish lack nutrients for long time?

They will die, eventually.

The requirement for energy is a thermodynamic constraint; maintaining cellular structures, repairing molecules that spontaneously damage etc takes some energy, and E. coli is not able to reach a level of quiescence sufficient to survive for years. However some cells might survive longer than expected if they enter low-metabolic activity states; that would not be enough to survive years in a petri dish, though.

Note that other species may be able to survive, through special stress-induced processes such as sporulation or cryptobiosis.


Deterministic model of lambda-phage lysis/lysogeny [MATLAB]

For homework questions, the policy is to see some work from the poster.  Since you don't know programming, I've outlined what the code is doing, beyond the simple operations (+, -, /, *, ^), to get you started.  I think you should be able to implement the models with this information, and I'd be happy to confirm your own answers.

So the best way to figure out what any line of code means, in any language, is to type it and see what happens. To help you get started with programming in MATLAB:

Any text following a % (on the same line) is a comment: it does nothing in the program, and is only there for you to write notes to yourself.

The first two sections, Time-Related Constants and Simulation Constants, are just setting variables. It's like saying x = 3, so that later on you can do other operations with x.

The semicolon at the end of a line (in MATLAB) suppresses the output of the line. See what happens if you type x = 3; versus x = 3 at the command prompt.

In iteration constants, length is just a function that tells you the length of the vector.  X_rna_0 was previously initialized to go from 0 to 1.4 in steps of 0.2: the syntax is vector_name = start:step:end.

The simulation variables section is creating xyz-matrices, with all values initialized to zero.  The length in x is xr_max, and so on.  The idea is that, later on, at each step in Euler's method and each value of xr_max and xp_max, you'll save the value of X_rna.

The initial conditions are being set using meshgrid, which is best explained here.  The : means all of the rows/columns, corresponding to position: say you had a 3 x 3 matrix called apple.  apple[:,1]  gives you all the first column (1) of all three rows.  apple[1,:] gives you the first row (1) of all three columns. The .' means that the matrix is being transposed: again, the best way to see what's going on is to create a matrix of your own, perform the operation, and see if what you get is what you thought it would be.

For loops, you can read about here, for a start.  I do not think understanding this loop requires more information than that page.

Dot before ^2 means that each element of the matrix is being squared; you are not multiplying the matrix by itself.

That should decipher most of the code for you.  If you have further questions, feel free to comment here.

EDIT: Question 2 asks you to make a plot.  A plot of y vs. x would be made by typing plot(x,y)

Also, help on a particular MATLAB function can be accessed by typing help name_of_function.


Can you help identify this bird in Louisville Kentucky?

To me that sounds like the distinctive "who cooks for you" call of the Barred owl.

Compare with the recordings available from the Audubon Society, Cornell's All About Birds, and many others such as this YouTube video from a Cornell Lab Bird Cam of a Barred owl calling from its nest.


How long might a tick be on a body before biting?

They wander the body for 30 minutes to an hour before inserting their feeding parts into the skin. Source.
It entirely depends what material you are wearing, i.e. fluffy wool is difficult for them to climb on. They can fall off somewhere in the home and bite another day.
2mm nymphs climb on human skin at about 10cm per minute, so it could find the back of the knee in about 5 minutes and search for a bite site. tick attachment site distribution is: 9% head-neck, 5% arm,
24% stomach-groin, 7% back, 18% chest-shoulder, 25% leg-foot, and 12% hip.


Can human survive falling from 30,000 ft without a chute?

Summary: A fall from "any height" may be survivable, depending on what you hit, but with an expectation of severe injuries. A water impact at terminal velocity will in all likelyhood result in immediate death.

The Serbian Flight attendant Vesna Vulović holds the Guiness World Record for surviving a fall without a parchute with an estimated fall height 10,160 metres. However, some doubts have been cast on the accuracy of the record, with claims that the fall was actually only several hundred meters. Vulovic was found partly in the wreckage of the plane, so it can be discussed whether she had a truly "free fall" for the purposes of this question. However, several other persons have been known to survive completely "free" falls from great heights. Although it is hard to verify the exact altitudes, the WW2 aviators Alan Magee, Nicholas Alkemade and Ivan Chisov are reported to have survived falls of about 6700 m, 5500 m and 7000 m, respectively.

The exact altitudes are in any case not necessarily of interest, as it can be assumed that all persons falling from a height of more than about 500 meters will reach terminal velocity, the velocity where air resistance prevents the fall speed from increasing, before hitting the ground. As such, above a certain height, other factors become determining for the survivability of a fall. As has been demonstrated by the listed examples, it is clearly possible to survive a fall at terminal velocity. However, this requires favorable conditions at the site of impact, and will likely result in severe injuries.

Due to the flat surface and the surface tension of water, it is hard to imagine an unprotected impact with water being survivable at terminal velocity. The best chances for survival will likely be in areas with foliage, snow and/or a hilly landscape allowing the kinetic energy to be dissipated through rolling downhill. Of the listed aviators above, Nicholas Alkemade appears to have been the least injured. About him, it is reported that

  His fall was broken by pine trees and a soft snow cover on the ground.
  He was able to move his arms and legs and suffered only a sprained leg


What do Illumina HiSeq/MiSeq paired end reads look like?

Where the reads found in R2 are the reverse complement of those found
  in R1.

This statement seems incorrect.

Paired-end reads comes from opposite ends of a fragment (you could learn the reason it happens from Illumina's video). If insert size is 150bp, read length usually is ~60bp as quality score after 60th bp is unacceptably low. In this case, R1 length is ~60bp, and it is 5'3', R2 length is ~60bp, and it is 3'5'. When a number of reads are enough to cover the gap, they form a contig.

Here's an illustration from Illumina's website:


This condition is also known as "lactic acidosis" and can be pretty dangerous, since it influences the pH of the blood.
When we metabolize glucose to produce ATP and NADH it is metabolized finally to pyruvate in a process called glyolysis (I am not going into detail here since this is nicely explained in the Wikipedia). Pyruvate can then be used further in the body in the Gluconeogenesis, the Citric acid cycle and other pathways.
If a lot of energy is needed Pyruvate is converted by the pyruvate dehydrogenase into acetyl-CoA.

The problem with diabetes is that the pyruvate dehydrogenase can be inhibited in diabetes. If the body then needs a lot of energy pyruvate will be converted into lactate which is released by the cells into the bloodstream.
Gluconeogenesis cannot be activated since this needs either Pyruvate, Acetyl-CoA or Oxaloacetate as starting material. The other problem with this process is that this happens in the liver and when the glucose is released into the bloodstream, it cannot be taken up by the cells due to the lack of insulin.

The conversion from Pyruvate to Lactate is katalysed by the Lactate dehydrogenase and needs NADH + H+ as a co-factor. The image below is from the Wikipedia article on Lactate dehydrogenase.

This reaction is highly exergonic which means its preferred direction is to the right side. To change this and make Pyruvate from Lactate you need an excess of NAD+ which usually only happens in the liver.

There is also an epidimiologic study available showing a strong correlation between elevated blood lactate levels and diabetes type II: "Association of blood lactate with type 2 diabetes: the Atherosclerosis Risk in Communities Carotid MRI Study."


For birds you can start by searching 18s in http://birdgenenames.org/cgnc/

But generally NCBI Nucleotide database, should provide you with all information and accession numbers. See this broad search: http://www.ncbi.nlm.nih.gov/nuccore/?term=18S+ribosomal+RNA+gene

Adding species specification and other parameters, you might find what you are looking for. For example, see chicken 18S ribosomal RNA gene


Why did high A+T content create problems for the Plasmodium falciparum genome project?

The sequencing technologies that were developed in the last 20 years have a range of optimal use at an average A+T/G+C rate. Both highly AT-rich and GC-rich regions are complicated to process by the different sequencing technologies. Each technology has different ranges of usage, but to name one, Illumina technology prefers sequences in the middle range. If you try to sequence an AT-rich genome with the Illumina standard protocol, you will sequence an incomplete genome, the fragments of which are not a perfect reflection of the original complete genome. Other technologies claim to be completely unbiased to nucleotide content. Pacific Biosciences is one of them, and people seem to agree on that claim, after having analyzed the data that is produced by their machines. Oxford Nanopore Technologies claims that they have almost no biases, but as of today (2012-06-13), there is no confirmation of that by external analyses.

Beyond sequencing problems, the software used to assemble and annotate the sequences may also be prone to errors in AT-rich and GC-rich regions. But many of those problems stem from the incompleteness of the sequencing.


Why does dissociation of carbonic acid cause a decrease in pH?

Any acid that releases a proton when it dissociates in water will also produce a conjugate base. We can conceptualize this as $\ce{HA <=> H+ + A-} $. In this particular example, $\ce{HCO3-}$ is $\ce{A-}$.  The strength of the acid is determined by the extent to which the acid, $\ce{HA}$, dissociates. This can be expressed using the equilibrium constant for this reaction, which has a particular name, $\ce{K_a = \frac{[H^+][A^-]}{[HA]}}$, (where $\ce{[X]}$ is the concentration of $\ce{X}$ at equilibrium). The larger $\ce{K_a}$ is, the further the reaction moves to the right (or, as it is often expressed, the smaller the $\ce{pK_a}$, which is $\mathrm{-log_{10}}$  $\ce{K_a}$).

Here, the addition of any $\ce{HA}$ will produce $\ce{H^+}$ and $\ce{A^-}$ in an aqueous solution (the blood), and decrease the $\ce{pH}$. $\ce{A^-}$ is only a base insomuch as it can form $\ce{HA}$ by combining with $\ce{H^+}$. This can occur if you add (or, as occurs in the kidney, reabsorb) $\ce{A^-}$ with some counter ion other than a proton. Then you can drive the equilibrium to to the left, towards $\ce{HA}$, decreasing $\ce{[H^+]}$. Otherwise, $\ce{A^-}$ derived from $\ce{HA}$ will not drive the equilibrium one way or the other. $\ce{H^+}$ will still dissociate as determined by the $\ce{K_a}$.


According to https://en.wikipedia.org/wiki/Human_hair_growth:

Scalp hair is known to grow between 0.6cm and 3.36cm per month. The growth rate of scalp hair somewhat depends on age (hair tends to grow more slowly with age), sex, and ethnicity. It was previously thought that Caucasian hair grew more quickly than Asian hair and that the growth rate of women's hair was faster than that of men.
However, more recent research has shown that the growth rate of hair in men and women does not significantly differ and that the hair of Chinese people grew more quickly than the hair of French Caucasians and West and Central Africans.

Depending on your age, follicle-condition, nutrition or possible inhibiting factors it can vary how long it will take until your hair has grown back to the previous length.


What's the real meaning of "brain shrinkage"?

Brain shrinkage = brain atrophy, which means a decrease in volume of the brain tissue, which involves different types of degeneration on the cellular level.

Here is a Wikipedia article about cerebral atrophy with a list of ~30 causes, such as Alzheimer's disease, stroke, cerebral palsy, malnutrition, AIDS, etc. Mechanisms can involve: loss of cytoplasmatic proteins, loss of complete neurons or connections between them, etc.

Alcohol consumption and frontal lobe shrinkage: study of 1432 non-alcoholic subjects (BMJ):

  The brain tends to shrink physiologically with age. Heavy alcohol
  consumption seems to exaggerate this shrinkage in social drinkers.
  Moderate alcohol consumption does not seem to affect brain volume.

Vitamin B12, cognition, and brain MRI measures (Neurology):

  Methylmalonate, a specific marker of B12 deficiency, may affect
  cognition by reducing total brain volume...


There is 'homology' at the pseudo-autosomal region, a recombining region of the X and Y chromosomes.


Based on this picture, I'd say it's a Macrurocampa marthesia. I realize your specimen lacks the split tail, but I note that the "tails" of the larva of this species are longer in earlier instars. I wonder if this one is just an older caterpillar, getting ready to pupate? The image is a very good match otherwise, and this species does occur in the appropriate range.


How does Topoisomerase II inhibition affect cancer cells?

First question:

In general, topoisomerases are enzymes that relieve supercoiling in DNA strands and tangling in chromosomes. Type II topoisomerases is special among eukaryotic topoisomerases, considering they use divalent metal ions and ATP hydrolysis in their active site. The enzyme cuts both strands of the DNA helix simultaneously (double strand break) in order to manage DNA tangles and supercoils. It changes the linking number of circular DNA by ±2. After the ends are cut, the ends of the DNA are separated and a second DNA duplex is passed through the break. The cut DNA is re- ligated. This allows the enzyme to increase or decrease the linking number of a DNA loop by 2 units. Inhibiting enzyme-mediated DNA ligation means that it prevents the enzyme to re-ligate the DNA strand after it is cut. In other words, the prevention of a phosphodeister bond between nucleotides.

Second question:

In normal cells, DNA topoisomerase II plays several vital roles, mainly to relieve DNA tangles and coiling. This is done by generating "transient double strand breaks" in the DNA strand, which can sometimes cause harmful translocations and damage. Damage of this type is linked to certain specific types of leukemia. This intrinsically "harmful" quality of DNA topoisomerase II can be exploited in cancer cells due to their high replication rate . Certain cancer drugs, such as etoposide, act by altering the active site of topoisomerase II, preventing (inhibiting) the enzyme from ligating cleaved DNA molecules, causing permanent DNA breaks (and inhibiting replication). The fast replication rate of cancer cells ensures that there are large amounts of the enzyme present in the cell, increasing the effectiveness of any Topoisomerase II poisons. However, this drug can also act against some other types of tissues with large amounts of Topoisomerase II, such as cardiac tissue. Also, cancer cells are constantly in a growing/replication cycle, so they exhibit large amounts of the isoform Topoisomerase IIa, the type that is most likely to produce permanent and detrimental DNA breaks.

Source:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2647315/


Neuron connectivity- how are they connected physically

Neurons are suspended, as you say, in an extracellular matrix. Brain tissues are a little bit more specific. Here I quote a few summaries from literature to answer and give your a perspective on your basic question. In bold I highlight important statements which differentiate the brain's ECM from the ECM found elsewhere in the body.

  Barros, Franco & Müller, 2011: An astonishing number of extracellular matrix glycoproteins are
  expressed in dynamic patterns in the developing and adult nervous
  system. Neural stem cells, neurons, and glia express receptors that
  mediate interactions with specific extracellular matrix molecules.
  Functional studies in vitro and genetic studies in mice have provided
  evidence that the extracellular matrix affects virtually all aspects
  of nervous system development and function. Here we will summarize
  recent findings that have shed light on the specific functions of
  defined extracellular matrix molecules on such diverse processes as
  neural stem cell differentiation, neuronal migration, the formation of
  axonal tracts, and the maturation and function of synapses in the
  peripheral and central nervous system.

  Ruoslahti, 1996: The extracellular matrix of the adult brain
  tissue has a unique composition. The striking feature of this matrix
  is the prominence of lecticans, proteoglycans that contain a lectin
  domain and a hyaluronic acid-binding domain. Hyaluronic acid and
  tenascin family adhesive/anti-adhesive proteins are also abundant.
  Matrix proteins common in other tissues are nearly absent in adult
  brain. The brain extracellular matrix appears to have trophic effects
  on neuronal cells and affect neurite outgrowth. The unique composition
  of this matrix may be responsible for the resistance of brain tissue
  toward invasion by tumors of non-neuronal origin.

  Dityatev et al. 2010: The extracellular matrix (ECM) of the
  central nervous system is well recognized as a migration and diffusion
  barrier that allows for the trapping and presentation of growth
  factors to their receptors at the cell surface. Recent data highlight
  the importance of ECM molecules as synaptic and perisynaptic scaffolds
  that direct the clustering of neurotransmitter receptors in the
  postsynaptic compartment and that present barriers to reduce the
  lateral diffusion of membrane proteins away from synapses. The ECM
  also contributes to the migration and differentiation of stem cells in
  the neurogenic niche and organizes the polarized localization of ion
  channels and transporters at contacts between astrocytic processes and
  blood vessels. Thus, the ECM contributes to functional
  compartmentalization in the brain.


This is probably Prionus californicus, which is a coleopteran native to the American west.

Look at the serrate antennae:

Also, the abdomen looks like the one in your specimen:


Is there a term for the group of individual organisms whose matrilineally descended female ancestors all share a common ancestor?

I don't think there is a word for that.

However, you can refer to this specific DNA sequence as being exclusively maternally inherited (such as mtDNA for example; see also mtEve). For this sequence, the classical vocabulary from the field of phylogenetics and population genetics apply nicely.


Can anyone remind me of the name for the inter-scapular space on the back?

"Inter-scapular space" is defined as the space between the scapulae.  It was most likely created by doctors who had no name for the space.  Yet another expansion of the English language by those who have need of a word or phrase to describe something that has no word or phrase already.  I found no other definition.


The focus upon definition of term is a rhetorical strategy often employed to confuse the issue, especially by laity when discussing technical matters. Word meaning and use are easily a source of ambiguity, confusion, contradiction and such that the appeal to the dictionary definition is often an appeal to false authority. At the very least it is worth pointing out that aside from etymology and morphology, empirical disputes are not settled by consulting Merriam-Webster.

"Evolution" is a fairly general concept and it can be useful when discussing technicalities to specify "biological evolution".  For example, "water" might mean specifically "H2O" or generally "clear, odorless, tasteless liquid"  or possibly might be used without qualification in distinguishing "potable water" from ocean water, et cetera.

Consider that the definition of term is not so much the pertinent legacy of biological evolution (pace Darwin, Wallace et. alii). The kind of explanation biological evolution uses is it's hallmark. In particular, biological evolution removed teleology (the study of purpose)) from biology.

For example:

A teleological explanation of biology:
1) This plant is photosynthesizing in order to survive.
2) This plants species is surviving.

A biologically evolutionary explanation of species:
1) This plant is photosynthesizing
2) Plant species which photosynthesize have an increased likelihood of survival.

Note that survival is still at play, but the argument is no longer circular. This is not to say that cause has been cited, however, the logical structure of the argument no longer "begs the question"


Yes sure I tried this and give good result. But you most chose the best protocol and need to be do this manually. I recommend that use CTAB-PVP (which is use 3 buffers EBA EBB SDS %10) extraction method from "Integrated DNA technologies" and if you cant find this I will tell You.


How could humans have interbred with Neanderthals if we're a different species?

Short answer
The concept of species is poorly defined and is often misleading. The concepts of lineage and clade / monophyletic group are much more helpful. IMO, the only usefulness of this poorly defined concept that is the "species" is to have a common vocabulary for naming lineages.
Note that Homo neanderthalis is sometimes (although it is rare) called H. sapiens neanderthalis though highlighting that some would consider neanderthals and modern humans as being part of the same species.
Long answer
Are neanderthals and modern humans really considered different species?
Often, yes they are considered as different species, neanderthals being called Homo neanderthalis and modern humans are being called Homo sapiens. However, some authors prefer to call neanderthals Homo sapiens neanderthalis and modern humans Homo sapiens sapiens, putting both lineages in the same species (but different subspecies).
How common were interbreeding between H. sapiens and H. neanderthalis
Please, have a look at @iayork's answer.
The rest of the post is here to highlight that whether you consider H. sapiens and H. neanderthalis to be the same species or not is mainly a matter of personal preference given that the concept of species is mainly arbitrary.
Short history of the concept of species
To my knowledge, the concept of species has first been used in the antiquity. At this time, most people viewed species as fixed entities, unable to change through time and without within-population variance (see Aristotle and Plato's thoughts). For some reason, we stuck to this concept even though it sometimes appears to not be very useful.
Charles Darwin already understood that as he says in On the Origin of Species (see here)

Certainly no clear line of demarcation has as yet been drawn between species and sub-species- that is, the forms which in the opinion of some naturalists come very near to, but do not quite arrive at the rank of species; or, again, between sub-species and well-marked varieties, or between lesser varieties and individual differences. These differences blend into each other in an insensible series; and a series impresses the mind with the idea of an actual passage.

You might also want to have a look at the post Why are there species instead of a continuum of various animals?
Several definitions of species
There are several definitions of species that yield me once again to argue that we should rather forget about this concept and just use the term lineage and use an accurate description of the reproductive barriers or genetic/functional divergence between lineage rather than using this made-up word that is "species".
I will below discuss the most commonly used definition (the one you cite) that is called the Biological species concept.
Problems with the definition you cite

A species is often defined as the largest group of organisms where two hybrids are capable of reproducing fertile offspring, typically using sexual reproduction.

Only applies to species that reproduce sexually
Of course, this definition only applies to lineages that use sexual reproduction. If we were to use this definition for asexual lineages, then every single individual would be its own species.
In practice
In general, everybody refers to this definition when talking about sexual lineages but IMO few people are correctly applying for practical reasons of communicating effectively.
How low the fitness of the hybrids need to be?
One has to arbitrarily define a limit of the minimal fitness (or maximal outbreeding depression) to get an accurate definition. Such boundary can be defined in absolute terms or in relative terms (relative to the fitness of the "parent lineages"). If, the hybrid has a fitness that is 100 times lower than any of the two parent lineages, then would you consider the two parent lineages to belong to the same species?
Type of reproductive isolation
We generally categorize the types of reproductive isolation into post-zygotic and pre-zygotic reproductive isolation (see wiki). There is a lot to say on this subject but let's just focus on two interesting hypothetical cases:

Let's consider two lineages of birds. One lineage has blue feathers while the other has red feathers. They absolutely never interbreed because the blue birds don't like the red and the red birds don't like the blue. But if you artificially fuse their gametes, then you get a viable and fertile offspring. Are they of the same species?

Let's imagine we have two lineages of mosquitoes living in the same geographic region. One flying between 6 pm and 8 pm while the other is flying between 1 am and 3 am. They never see each other. But if they were to meet while flying they would mate together and have viable and fertile offsprings. Are they of the same species?

Under what condition is the hybrids survival and fertility measured
Modern biology can do great stuff! Does it count if the hybrid can't develop in the mother's uterus (let's assume we are talking about mammals) but can develop in some other environment and then become a healthy adult?
Ring species in space
As you said in your question, ring species is another good example as to why the concept of species is not very helpful (see the post Transitivity of Species Definitions). Ensatina eschscholtzii (a salamander; see DeVitt et al. 2011 and other articles from the same group) is a classic example of ring species.
Species transition through time
Many modern lineages cannot interbreed with their ancestors. So, then people might be asking, when exactly did the species change occurred? What generation of parent where part of species A and offspring where part of species B. Of course, there is no such clearly defined time in which transition occurred. It is more a smooth transition from being clearly reproductively isolated (if they were placed to each other) from being clearly the same species.
Practical issue - Renaming lineages
How boring it would be if every time we discover the two species can in some circumstances interbreed, we had to rename them! That would be a mess.
Time
Of course, when we talk about a species we refer to a group of individuals at a given time. However, we don't want to rename the group of individuals of interest every time a single individual die and get born. This notion yield to the question of how long in time can a single species exist. Consider a lineage that has not split for 60,000 years. Was the population 60,000 years ago the same species as the one today? The two groups may differ a lot phenotypically and may actually be reproductively isolated if they were to exist at the same time.
Special cases
When considering a few special cases, the concept of species become even harder to apply.
The Amazon molly (a fish) is a "species" that have "sexual intercourse" without having "sexual reproduction" and there are no males in the species! How is it possible? The females have to seek for sperm in a sister species in order to activate the development of the eggs but the genes of the father from the sister species are not used (Kokko et al. (2008)).
In an ant "species", males and females can both reproduce by parthenogenesis (some kind of cloning but with meiosis and cross-over) and don't need each other to reproduce. In this respect, males could actually be called females. But they still meet to reproduce together. The offsprings of a male and a female (via sexual reproduction) are sterile workers. So males and females are just like two sister species that reproduce sexually to create a sterile army to protect and feed them (Fournier et al. (2005)).
Bias
It often brings fame to discover a large new species. In consequence, scientists might tend to apply a definition of species that allow them to tell that their species is a new one. A typical example of such eventual bias concern dinosaurs where many new fossils are abusively called a new species while they sometimes are just the same species but at a different stage of development (according to this TED).
So why do we still use the concept of species?
Naming
IMO, its only usefulness is that it allows us to name lineages. And it is very important that we have the appropriate vocabulary to name different lineages even if this brings us to make a few mistakes and use some bad definitions.
The alternative use of the concept of lineage
It is important though that we are aware that the concept of species is poorly defined and that if we need to be accurate that we can talk in terms of lineages. The main issue with the term lineage is not semantic and comes about the fact that gene lineages may well differ considerably from what one would consider being the "species lineage" as defined by the "lineages of most sequences"... but this is a story for another time.
In consequence
In consequence to the above issues, we often call two lineages that can interbreed to some extent by different species names. On the other hand, two lineages that can hardly interbreed are sometimes called by the same species name but I would expect this case to be rarer (as discussed by @DarrelHoffman and @AMR in the comments).
Homo lineages
I hope it makes sense from the above that the question is really not related to the special case of the interbreeding between the Homo sapiens and the Homo neanderthalis lineages. The issue is a matter of the definition of species.
Video and podcast
SciShow made a video on the subject: What Makes a Species a Species?
For the French speakers, you will find an interesting (one hour long) podcast on the consequence of the false belief that the concept of species is an objective concept on conservation science at podcast.unil.ch > La biodiversité - plus qu'une simple question de conservation > Pierre-Henry Gouyon

Here is a related answer


How do migrating birds know where to migrate?

Why do birds migrate?

The primary reasons for why birds migrate are food availability and nesting locations. There are many other factors that can also play a role in why a bird migrates; too name a few, it includes responses to weather patterns, geography, and day length.

Since you use Canadian Geese as an example, I’ll use North America as the example region. There are over 650 migratory birds in North America and many scientists are studying individual species and learning that different factors have a variety of importance when it comes to migration. Generally birds can be classified into residents (non-migratory), short-distances migrants and long-distance migrants.

Residents are able to find food year-round and there is no need to migrate. Short-distance migrants tend to respond to food and weather (1). Long-distance migrants are more complex, but it is thought that response to day length and hormonal changes are important influences in their decision to migrate.

Now how do birds know where to go?

The most important factor is genetic predisposition, which can be composed of many variables such as moult, reproduction, and physiology (2). Just because there is a leading Canada goose, doesn’t mean the others don’t know where they are going. They can all have the same genetic factors affecting their decisions. There also can be cases where a young Canada Goose, doesn’t know where he is going, but he joins the V-formation and learns where to go from others in which he can then pass this knowledge on to future generations (I’m just using Canada Goose as an example for birds in general).

Navigation cues can also play a role such as geography, suitable habitat, landmarks, sun position and earth’s magnetic field. Geography can play a role in migration by acting as a barrier or a funnel, in North America, migratory birds can be limited as to where they travel. For example, they will not cross the Rocky Mountains or Atlantic Ocean. Suitable habitat also plays a role, for example North America has a variety of habitats, but to classify them simply there are: deserts, plains/ prairies, deciduous forests, boreal forests and mixed forests. The bird in question will be looking for these locations to nest or spend its winter. Many birds exhibit a step-wise migration where they stop at sites along their route to feed and regain strength and these areas are frequented annually.

As you can see, there are many answers to why a bird migrates which can create even more questions and led to many different explanations. Here's a website with a nice summary and a good starting point to learning about migratory behaviour that could help you understand further:

https://www.allaboutbirds.org/the-basics-how-why-and-where-of-bird-migration/


Inflamed sinuses are often associated with some kind of illness or irritant such as flu, the common cold, or hay-fever. As an example the cold causes sinus pain and inflammation because the virus is attacking/located in the nasal passages which causes swelling in the mucus membrane (the mucus membrane lines the sinus cavities). The swelling, along with increased mucus production, combines to create clogging and the pressure associated causes pain. Humidity will help loosen the mucus and anti-inflammatory medication should help reduce pain by reducing the mucus build up and swelling - thus relieving pressure.

The increase in mucus production is because of the role it plays in our bodies - it is produced to trap foreign bodies and help keep our system clean. The more mucus we produce the more our bodies are trying to clean up. This can cause an excess which is difficult to clear such that our sinuses become blocked and dried mucus becomes an irritant.

Sinusitis is the painful condition of swelling in the mucus membrane. Sinus comes from the latin for bent or curved surface, and -itis is from greek meaning swelling or inflammation linked to disease.

In summary: Painful sinuses, aka sinusitis, are painful because of infection in the mucus membrane producing swelling and excessive mucus build-up.


Emergence of Micronuclei and Their Effects on the Fate of Cells under Replication Stress (2010) explores how micronuclei behave and determine cell fate. It found that micronuclei is pretty closely related to apoptosis. If the cells with micronuclei didn't go through apoptosis, there were instances where the micronuclei would literally just disappear. They were unable to determine if it was expelled by the cell or reabsorbed into the main nucleus. However, there were also cases where there would be an increase in the number of micronuclei.

They concluded that there is a number of ways for the cell to get rid of the micronuclei and they were unable to determine which is the most likely.

I was unable to find any more recent in-depth studies (that I could understand).

So, according to this paper there are several answers...

Case 1: It is reabsorbed into the nucleus and most likely the information within is saved.
Case 2: It is expelled from the cell and the information within is lost.
Case 3: The cell undergoes apoptosis and all information is lost.


Why does cholesterol need to attach to proteins to travel through the blood?

It is not LDL that does the Job. The target cells "know" which lipoproteins (LDL,HDL,VLDL...) they should take up. They express the specific Membrane receptor that binds the Protein part of e.g. LDL and therefore take up specifically LDL rather than e.g. HDL from the blood. Example: cells that express receptors for apolipoprotein B-100 (one of the Protein parts of LDL) specifically "filter" LDL from the blood. The "filtering" occurs via endocytosis. Hope that helps.


I think this is Ribes americanum or wild black currant.
I'm basing this on page 306 of Newcomb's Wildflower Guide, an excellent source for the Eastern US and some of Canada.  On that page we have two main choices:

Base of flowers prickly or bristly... or

Base of flowers not prickly or bristly...

Your excellent pictures suggest that your specimen is in category 2.
From there, we have:

a. Flowers solitary or 2-3 in a cluster; branches bearing a few thorns. or
b. Flowers 5 or more in racemes.

Your specimen looks to have quite a few flowers, so in category 2b we have a choice of Ribes americanum:

Whitish or yellowish flowers, longer than wide (and fruit black, you can check later I guess),

or Ribes sativum:

Greenish flowers, wider than long (and fruit red).

Color in the white/green/yellow range is a bit subjective, but your flowers look longer than wide, hence Ribes americanum.
Of course, with this in mind you might re-inspect the plant and refine this a bit.


How does a fertilized egg form 23 pairs of chromosomes?

After fertilisation the zygote has two copies of each of the chromosomes (not worrying about sex chromosomes). When each of these is replicated the cells will have chromosome pairs, which will then divide in mitosis.

The classical chromosome image of pairs of X-shaped chromosomes relates to the situation at mitotic metaphase when each of the chromosomes has replicated and consists of two sister chromatids. As anaphase proceeds the splitting of the centromeres means that each of the sister chromatids becomes a chromosome, and each cell ends up with a pair of each chromosome type, just like a zygote.


Non-nucleated cell-like population with RNA

Maybe you are seeing extracellular vesicles1?

At least might be worth checking out since extracellular vesicles containing RNA have been reported within the hemolymph of mosquitos2.

References:
1: Van der Pol, E., Böing, A. N., Harrison, P., Sturk, A., & Nieuwland, R. (2012). Classification, functions, and clinical relevance of extracellular vesicles. Pharmacological reviews, 64(3), 676-705.
2: Severo, M. S., Landry, J. J., Lindquist, R. L., Goosmann, C., Brinkmann, V., Collier, P., ... & Levashina, E. A. (2018). Unbiased classification of mosquito blood cells by single-cell genomics and high-content imaging. Proceedings of the National Academy of Sciences, 115(32), E7568-E7577.


Genetic diversity is indeed very important for many reasons, most notably resistance to diseases.

The Gros Michel banana used to be the most cultivated banana, until it was almost completely wiped out by a fungal disease due to lack of resistance in the genetically homogenous cultivars grown in plantations. As a result, it had to be replaced by the Cavendish banana across most of its former range by banana growers.

Furthermore, the answer is a definite "yes" to people with genetically transmitted diseases helping the gene pool.

For example, the case of sickle cell anemia clearly shows why even people with genetic diseases can help the gene pool by providing useful alleles. Heterozygotes for the sickle cell allele are resistant to malaria. This has led to the allele having a high propensity in subsaharan Africa, where malaria is endemic.

  The first example of genetically controlled innate resistance to human malaria was the demonstration in 1954 that sickle-cell heterozygotes have less severe Plasmodium falciparum infections than do children with normal adult hemoglobin. This observation has been repeatedly confirmed, most recently by independent studies of genome-wide associations in severe falciparum malaria, which have identified the HBB locus as the major signal of association.

Additional examples are the cystic fibrosis gene, which confers resistance to cholera, and thalassemia, which confers resistance to heart attacks.


Converting fmri data to association matrix

You can get raw FMRI data from https://openfmri.org/ on that website you'll also download your conditions files for the experimental design (you'll need this in creating your matrix). This is a link to an experiment(it's data) with "healthy" participants and participants diagnosed with schizophrenia: https://openfmri.org/dataset/ds000115

Raw image files from a scanner will be in .dcm format. You can use http://www.mccauslandcenter.sc.edu/mricro/mricron/dcm2nii.html to convert the multiple ".dcm" images of a scan into a 3 single 4D images for anatomicals, also known as T1 images. That converter will also convert the BOLD images into a single 4D image.

After conversion, the images you will want and need to load into whichever fmri data analysis software you're using will be in ".nii.gz".

Your question suggest that you don't need data analysis software but if you do,  I'm only familiar with FSL, you can find information on FSL from here http://fsl.fmrib.ox.ac.uk/fsl/fslwiki/

Hope this helps.


Identification of beetle: black with orange stripe and 2 orange dots

Looks very much like Nicrophorus investigator https://www.pinterest.com/pin/815362707508687290/


The following papers are a good starting point:

René Thomas, Boolean formalization of genetic control circuits, Journal of Theoretical Biology, Volume 42, Issue 3, December 1973, Pages 563-585 <= A classic paper in the field.
Thieffry D. Dynamical roles of biological regulatory circuits. Brief
Bioinform. 2007 Jul;8(4):220-5.
Remy E, Ruet P. From minimal signed circuits to the dynamics of Boolean
regulatory networks. Bioinformatics. 2008 Aug 15;24(16):i220-6

You can also have a look at Computational Methods in Systems Biology, International Conference CMSB 2007, Edinburgh, Scotland, September 20-21, 2007. Proceedings, specifically the chapter "Decision diagrams for the representation and analysis of logical models of genetic networks" by A. Naldi, D. Thieffry and C. Chaouiya,


How do anaerobic bacteria produce ATP for their own cellular activities?

The product is 4 ATP not 2, 2 is the net product because two are used to start the reaction.

Looking at the complete glycolysis reaction helps.

ATP can be used to start another round of glycolysis which yields 4 ATP which can then start 2 rounds of glycolysis which yields 8 ATP, rinse, repeat. It is an exponential process, ATP can be taken from this for other processes since as long as you still have 2ATP around to can restart the exponential cascade. For example from the yielded 8 if you take half for other uses, you still get 8 ATP from the next round of glycolysis reactions.


Why don't restriction endonucleases digest transformed plasmids?

Laboratory strains used for the purposes of cloning have been genetically engineered to address this issue, typically by deleting genes of the various restriction-modification systems. There are four broad classes of restriction modification systems, which I will discuss individually. Unless individually referenced, most information below is based on the following supplier technical notes:

Promega: What are the effects of the bacterial DNA restriction-modification systems on cloning?

New England Biolabs: Restriction of Foreign DNA by E. coli K-12

Type I

In Escherichia coli, this system consists of the hsdR, hsdM and hsdS genes and is capable of both restricting (digesting) unmethylated DNA and methylating hemimethylated DNA. Knockout of hsdR and/or hsdM prevents restriction and methylation, respectively. This allows engineering of strains for specific purposes. For example, a common E. coli strain used for cloning, DH5α, has the genotype hsdR17 (rK–, mK+) which abrogates restriction activity but maintains methylation activity. This means that exogenous DNA will not be restricted, but will be methylated and therefore able to be subsequently transformed to r+ strains without worry of degradation, if the need may arise.

Type II

This is the class of restriction enzyme commonly used in the lab to cut DNA because they generally recognize short, palindromic sequences and cut within or near the recognition site. The E. coli background strains K and B, from which most lab strains are derived, do not contain Type II enzymes. The Type II enzyme EcoRI, for example, was isolated from the E. coli RY13 strain (Yoshimori, 1971; PhD thesis).

Type III

Similarly to Type II, the K and B strains do not possess this restriction-modification system, which was first characterized in E. coli 15T-.

Type IV

This system differs from the others in that it cleaves methylated and hemimethylated DNA, though it does not recognize methylation by Type I or Type II modification systems, nor Dam or Dcm methylation. In E. coli, this system consists of the mcrA, mcrBC and mrr genes and is most problematic when attempting transformation of DNA from organisms with ubiquitous cytosine or adenine methylation (eg plants and mammals). For example, the lab strain T7 Express, which is derived from the common strain BL21, has the genotype Δ(mcrC-mrr)114::IS10 which deletes mcrBC, hsdRMS and mrr.

Note on Dam and Dcm Methylases

These bacterial enzymes methylate adenine and cytosine residues, respectively, but are not directly involved in the restriction-modification systems discussed above. However, some Type II enzymes used for cloning are sensitive to this methylation and so lab strains are available with these enzymes deleted.


My guess (as your question need heavy editing!!) would be MiRdup.

  MiRdup Goals:

  Validation of pre-miRNAs predictions
  Prediction of mature miRNA

  Abstract: MicroRNAs (miRNAs) are short RNA species derived from hairpin-forming miRNA precursors (pre-miRNA)
  and acting as key post-transcriptional regulators. Most computational
  tools labeled as miRNA predictors are in fact pre-miRNA predictors and
  provide no information about the putative miRNA location within the
  pre-miRNA. Sequence and structural features that determine the
  location of the miRNA, and the extent to which these properties vary
  from species to species, are poorly understood. We have developed
  miRdup, a computational predictor for the identification of the most
  likely miRNA location within a given pre-miRNA or the validation of a
  candidate miRNA. MiRdup is based on a random forest classifier trained
  with experimentally validated miRNAs from miRbase, with features that
  characterize the miRNA-miRNA* duplex


Was HindII the first restriction endonuclease to be extracted?

The explanation here is quite simple: HindI, despite having been isolated/discovered before HindII, is a type I Restriction Enzyme, not a type II:

  A type I restriction enzyme from Haemophilus influenzae, Hind I, which requires adenosine 5'-triphosphate and 5-adenosyl methionine, was studied for its activity on transfecting and transforming deoxyribonucleic acid (DNA) [...] Most of the restriction enzymes from Haemophilus belong to type II restriction enzymes according to the classification system proposed by Boyer. These enzymes require only Mg2+ for their action in contrast to type I enzymes that require Mg2+, adenosine 5'-triphosphate (ATP), and S-adenosyl methionine (SAM).

(Source: Biological Properties of a Haemophilus influenzae Restriction
Enzyme, Hind I)

Thus, in fact, HindII was the first type II Restriction Enzyme isolated/discovered, as it's well documented.

PS: As a bonus, here is a table with the main differences among RE types I, II, III and IV (Source: Thermo Fisher Scientific):

Type I:

Multi-subunit protein with both restriction and methylation activities
ATP requirement
Cleavage site a variable distance from recognition site

Type II:

Specific recognition sequence
Cleavage site within or close to recognition sequence
Generates 5′ phosphate and 3′ hydroxyl termini at cleavage site
Mg2+ requirement for most

Type III:

Two-part recognition sequence in inverse orientation
Cleavage site a specific distance away from one of the recognition sequences
ATP requirement

Type IV:

Cleavage of only methylated DNA
Cleavage site approximately 30 base pairs away from recognition site


How can the melting temperature of PCR primers be so far below the extension temperature?

Note that 'melting temperature' is actually about POPULATIONS--it's generally the temperature at which 1/2 of all of the millions of copies of 2 things will be stuck together and 1/2 apart. Once stuck, not all primers will leap off the template simultaneously even at much higher temperature... As you indicate, there's nothing to stop the polymerase from starting its work (extending the primer) before the extension temperature.

And, as in another answer, polymerase can add stability to the pairing.


Is there a free alternative to Gelcompar for comparing banding patterns across multiple gels?

Try this one

Pavel, A. B. & Vasile, C. I. PyElph - a software tool for gel images analysis and phylogenetics. BMC Bioinformatics 13, 9+ (2012).

You can download here
http://sourceforge.net/projects/pyelph/


It is a moth and all moths and butterflies belong to the order of Lepidoptera. Based on the shape of the forewing and the orange color of the hindwings I think this moth belongs to the genus Catocala https://en.m.wikipedia.org/wiki/Catocala, see also here for some pictures.

EDIT:
theforestecologist did a excellent suggestion that this might be Catocala streckeri based on the wing pattern. This species does occur in Korea, see this website for a distribution map. So it may indeed be Catocala streckeri. However, Asia is very rich in Catacola species, and I know that this family often has species looking very alike, so I can't say with 100% certainty.

Most, but not all, moths are nocturnal. Some Catocala species are known to fly on sunny afternoons (Waring&Townsend 2006).


Transcript(omics) terminology: cDNAs, ESTs, RNA-seq, etc

The quick answer is that you are misinterpreting ESTs. EST stands for Expressed Sequence Tag. They are obtained by collecting and sequencing any mature (i.e. poly-A) mRNAs found in a living cell. Well, it was living until the experiment was performed at any rate :).

The term EST is not applicable to sequences derived from genomic data. It only applies to expressed sequences. You do have ESTs that are derived from cDNA libraries but these are expressed cDNAs. Short reads are not ESTs because we have no information on whether that sequence is actually expressed in a living cell.

You could apply the term to RNAseq reads (depending on the experimental procedure involved) but that is not what most people would understand by the term.

In summary, the operative term of EST is "expressed". You cannot call anything an EST if you do not have evidence that it is actively expressed in a living cell.


How do plants store energy by potassium battery?

I'll give it a layman's attempt in sort of an "ELI5" approach. I hope the analogy isn't too simplistic, and please don't take it too literally.

How do plants use K+?

Plants control K+ concentrations and do work within the plant by pumping K+ between different compartments. Because water tends to follow solute concentrations (osmosis), plants can do things like suck in water simply by moving potassium around.

(note: animal cells do something similar: this is how your nervous system, kidneys, digestive tract, and other cells/organs perform their functions, but using different ions or combinations of ions)

Analogy to some human activities

Moving all this K+ around takes a lot of energy. Creating a concentration gradient is a lot like pumping water uphill: you put some energy in, but you are storing that energy as potential energy for the water flowing back downhill, or the ions flowing back against their concentration gradient (or water flowing the other way). But normally, plants use this as a way to spend energy to do useful things, rather than a way to store it. It's like they are pumping the water up the hill and then floating useful ores or lumber on a boat as it flows back down the hill.

What is actually happening that Wikipedia describes as a plant "K+ battery"

The article cited on Wikipedia, though, Gajdanowicz et al 2011, shows that sometimes plants take advantage of the mobility of potassium ions to assist the H+ ATPase that is another form of energy storage. Plants use H+ (proton) concentration gradients similarly to how they use K+ concentration gradients, but they are used to power different processes in the plant. Sort of like two different types of batteries.

Return to the analogy, and why this is useful to the plant

Normally both H+ gradients and K+ gradients are powered by ATP, which is indirectly produced via photosynthesis: think of it like the plant's coal-fired power plant. Converting K+ concentration gradients to H+ concentration gradients would be like using the water you pumped up the hill to power a hydroelectric plant that is charging a car battery. The benefit for the plant is that, because K+ can be easily moved around, the plant is able to power those hydroelectric plants anywhere around the hill, and that can be advantageous if a particular part of the plant is low on other sources of energy.


Are different eye colors indicative of chimerism?

You will find this wiki entry [1] informative.

While chimerism is one possible explanation, it is certainly not the only one.

[1] https://en.wikipedia.org/wiki/Heterochromia_iridum


Why do plants create enough energy for the entire ecosystem?

Plants collect energy for themselves via photosynthesis, not for others.
It is used for it's own growth and survival.

It's energy is then redistributed to other organisms when either the plant dies and decomposes or when it is consumed. Many organism cannot collect their energy like plants do, and thus must feed on organisms (like plants) that are able to collect and store energy. This is in many cases detrimental to the plant (it should be intuitive why being eaten might be bad), and many, many plants do have traits to discourage other organisms from eating them (plants with toxins, thorns, etc.).


Identify this plant from the Netherlands with big white flower

Like @skymningen thought, this is a Clematis. However, the only wild Clematis in the Netherlands is Clematis vitalba, that has much smaller flowers (about 2 cm diameter) see "Heukels' Flora van Nederland" (the official Dutch flora) and here.

So you have photographed a plant that "escaped" from a garden. Most garden Clematis are hybrids from Chinese or Japanese origen. As there are about 300 species and new hybrids constantly being produced, the likelyhood of finding it's name is low. https://en.wikipedia.org/wiki/Clematis


Which kind of tick is this and what is that thing around its back?

As your link suggests, it looks like a female tick of the genus Ixodus. It is likely female because the scutum or shield only covers part of the dorsal surface. E.g.,

which comes from Bristol University Tick ID. The translucent posterior portion may just be from light passing through.

If you are able to zoom in closer on different parts, you can key out what species it is.


Please give information about this insects

It looks like an insect belonging to the family Cicadidae. Further information is needed to identify this cicada species.


I think Wallace (1968) developed the ideas of hard and soft selection, as they relate to genetic load. He further explains the concept in Wallace (1975). As the idea was his, I'd go with Wallace's definition over Whitlock's.  I haven't had time to watch the Whitlock video to see if they are saying more or less the same thing overall.

Consider a hypothetical population of individuals, each with 1000 loci (I'm basing example and ideas on an example given by Ridley 2004, pgs. 162-167). Heterozygotes at each locus has the greatest fitness (heterozygote advantage). Homozygotes at any locus will have reduced fitness. Therefore, the fitness of each genotype is given as:

AA: $1-s_{AA}$

Aa: $1$

aa: $1-s_{aa}$

Even if every individual in the population at time zero was heterozygous at each locus, Mendelian inheritance ensures that no individuals will be heterozygous at all loci after the second generation.  Assume that fitness reduction at each homozygous locus is just 1%. Given that well over half of the loci will be homozygous, fitness of those individuals will be reduced to 0. They will die before reproducing.  This is hard selection.  If hard selection of this magnitude occurred in a population, then extinction would occur. This is what Wallace (in your link) is saying.  This mortality due to the genetic load is added to the normal background mortality.

Soft selection compares the fitness of an individual to the genotype with the greatest fitness in the population, even if that genotype does not the theoretical optimum fitness. Soft selection replaces some of the background mortality with selective mortality, so the population size is not decreased overall.

Literature Cited

Ridley, M. 2004. Evolution. 3rd ed. Blackwell Publishing, Malden, Massachusetts, USA.

Wallace, B. 1968. Polymorphism, population size, and genetic load. pp. 87-108 in R.C. Lewontin, ed. Population biology and evolution. Syracuse University Press, Syracuse, New York, USA.

Wallace, B. 1975. Hard and soft selection revisited. Evolution 29: 465-473.


What pH ranges are used in industrial scale fermentation?

Fermentation pH will differ a great deal depending on the bacteria or fungi being used and the process. But it is not uncommon to have a relatively narrow range of pH as a target. Remember pH is the -log[H+] so the pH scale is not linear. Also some fermentation reaction involve very expensive pharmaceuticals or intermediates, a single fermentation batch may have a value in the hundreds of thousands of dollars so keeping +/- 0.3 range in pH is trivial.


What is the Edward O. Wilson fuss about?

After reading the article, the fuss is about this:

In currently accepted theory Eusociality or "kin selection" explains altruistic behavior (the sacrifice of yourself or resources you control for the betterment of something else besides you) by relating the act to the amount of genetic information passed on.

The relevant equation is Hamilton's rule:

                                                                $rB > C$

C is the cost to the actor (the person giving up resources). B is the number of others involved, and r is the relationship value to the actor in terms of genetic similarity.

So if you and two full-siblings (who each share on-average 50% of your genome) and a bus comes straight at the group, and you have the capability to push them out of the way while dying yourself, kin selection suggests you shouldn't because the genetic cost is equivalent. You eliminate yourself from the gene pool, and save the equivalent of yourself for future generations (2 x 1/2 = 1).

However, if you and three siblings were in the situation, then it's evolutionarily advantageous to be altruistic. You would die (a cost of 1), but you would save the equivalent of 1.5x your genome (3 x 1/2 = 1.5) to pass on to future generations.

Thus, communal and social behaviors like those of ants basically boil down to: Everybody is so closely related that spending resources to help your kin is essentially spending resources to ensure the majority of your genome survives (which is the big point of evolution, after all).

Wilson's argument, what I can glean from the small brief of the study and the article, is that you don't need the relatedness equation to explain altruistic behavior in social situations (basically the row is he's saying the currently accepted theory is wrong). All you need to start with is a genetic mutation somewhere along the line that causes the offspring to stick close to home. Once you have a few generations that don't leave the nest, you start to develop social behavior that results in altruism because you've gone from selfish individuals to a group setting.

The article and Wilson don't give any more insight other than altruism apparently develops spontaneously from the formation of groups. Simply being social is the explanation for why some individuals will give resources to others to ensure the success of the others.

Whether or not Wilson is correct isn't really discussed. He openly admits to needing a lot of research, some of which is being performed.


Why does deamination in the lagging strand lead to an increase in the relative number of guanine and thymine to cytosine and adenine?

I think you are referring to this sentence from your wikipedia link:

  There is a richness of guanine over cytosine and thymine over adenine in the leading strand and vice versa for the lagging strand.

Note that this is not saying (G+T) > (C+A). It is instead saying (G)>(C) and (T)>(A). I think that those are not the same as saying (G+T) > (C+A), though that is also true, probably?

So I think that there is no contradiction there- it is just, as you say, more Ts (relative to expected equality with As) and fewer Cs (relative to expected equality with Gs).

If I understand correctly, the importance of the GC skew, and the reason that it is interesting, is that it acts as a deviation from Chargaff's parity rules (as explained in the article). These rules state that for any given hunk of DNA, (G)~(C) and (T)~(A), which is the expected composition for (for example) double-stranded DNA, because of base-pairing.

Edit: for more information on Chargaff's rules, see this other question which I have (through pure coincidence) answered here. Note that the second parity "rule" is a statistical phenomenon, rather than a logically required rule. The wikipedia page on Chargaff's rules is also informative.

Hope that helps.


How spinal cord play its roles in human beings sex?

One of the major functions of the spinal cord is to serve as a "highway" for signals to travel between the brain and the sensory (and motor) organs. Thus, sensory the signals that are generated on the body during sex must travel up through the spinal cord in order to get to the brain, where it will be processed into a pleasurable sensation. If the spinal cord is damaged, the signals will not be able to reach the brain and thus there will be no generation of pleasurable sensations.

Here's an image that shows the general sensory pathways. You can see they travel from the sensory organ to the spinal cord, and up it to the brain.


This sort of thing absolutely happens; useful search terms are "sex ratio distortion", "segregation distortion" (i.e. modifying the ratios with which different chromosomes segregate), and "meiotic drive" (a specific form of segregation distortion).
Your scenario (Y-chromosome genes forcing all offspring to be male) is much less common than the reverse (X-chromosome genes, or other genomic elements, forcing all offspring to be female), because it's easy for an all-female lineage to maintain itself by parthenogenesis. Lyttle (1991) says:

Strong Y drive is of necessity transitory, since drive
suppression must either evolve very quickly or the population will be pushed
to extinction. This may explain why few Y drive systems have been observed
in nature.

However, Lyttle goes on to describe

W-chromosome drive in butterflies (in butterflies, females are the heterogametic sex — the sex chromosomes are Z and W, ZZ individuals are male and ZW individuals are female). So this is a little bit like your Y-chromosome example, except that the populations end up all-female rather than all-male
male drive in mosquitoes

Jaenike (2001) says

Although several species exhibit Y drive, X drive is far more common.

Table 1 in that paper lists Y-drive examples in houseflies, mosquitoes, medflies, lemmings, and field mice. (I would include an image, but the table extends over 4 pages ...)

As for your final question,

I would therefore expect that such a mutation would spread, skewing the sex ratios away from 1:1 ... Have scenarios like the one I outlined above actually occurred in species? If not, why not?

I haven't dug through all the original literature that Jaenike (2001) cites, to see if there are populations in nature that are male-skewed due to selfish Y chromosomes. The point that Lyttle makes is that, even if you can find evidence of the existence of selfish Y chromosomes hiding in the population, it's very unlikely  that these will persist in natural populations for very long, because of the strong selection against them at the population level (and from the rest of the genome); either the population will go extinct, or moderators will evolve that suppress the driving effect of the Y chromosome.

Jaenike, John. “Sex Chromosome Meiotic Drive.” Annual Review of Ecology and Systematics 32, no. 1 (2001): 25–49. https://doi.org/10.1146/annurev.ecolsys.32.081501.113958.
Lyttle, Terrence W. “Segregation Distorters.” Annual Review of Genetics 25, no. 1 (1991): 511–81. https://doi.org/10.1146/annurev.ge.25.120191.002455.


Why is dopamine or a dopamine-receptor agonist not pumped into the brain of Parkinson patients?

Levo-Dopa is used as a first-line treatment of Parkinson's disease. Unlike dopamine, L-Dopa is able to cross the blood-brain barrier. There it is converted into dopamine. To prevent premature breakdown in the gastro-intestinal and circulatory system after oral intake, carbidopa can be co-administered. Also MAO-B inhibitors and COMT inhibitors can be applied to prevent breakdown of L-Dopa in the brain. Oral medication is preferable over invasive intracranial infusion of medication.

Conversion of L-Dopa into dopamine. Source: ADHD treatments.

Dopamine agonists are also in use. Unlike L-Dopa, dopamine agonists are not converted into dopamine. Instead, they mimic dopamine effects in your brain. They aren't as effective as L-Dopa, but they last longer and may be used alongside L-Dopa to smooth the sometimes off-and-on effect.

Parkinson's disease is not fatal, but it can reduce longevity. The disease progresses more quickly in older patients, and may lead to severe incapacity within 10 - 20 years. Older patients also tend to have muscle freezing and greater declines in mental function and daily functioning than younger people. L-Dopa treatment in the long run causes adverse effects, such as dyskinesias, toxicity, or loss of efficacy (Marsden, 1994).

Reference
- Marsden, Clin Neuropharmacol (1994); 17: S2:S32-44


VPg priming of the replication of RNA viruses

Nucleic acid synthesys can occur two ways, with a template or without. In most biological systems the template synthesis is the one that occurs since it is the only way to replicate genomic information. For template based nucleic acid synthesis in biological systems (being of DNA or RNA) the enzymes performing the reactions can use single stranded material (in the case of virus ssDNA or ssRNA virus) however they still need a small region of double stranded nucleic acid to bind and start polymerizing, otherwise synthesis could start anywhere in the template strand which wouldn't be particulartly useful, hence the primers, the polymerases bind to the double stranded region and start polymerizing always adding new nucleotides to the 3' end of the primer strand that are complementary to the nucleotide in the template strand. Usually in living cells the synthesis of new RNA molecules won't occur with an RNA template (there is usually no RNA dependent RNA polymerase, there are exceptions but they are usually result of previous viral infections), but only with a DNA template to procuce messenger/transfer/ribossomal RNAs. In the case of COVID and othe + strand RNA virus, the virus has to encode the RNA polymerase and also produce a primer that will create a double stranded region that will allow RNA synthesis to occur.


What does the empty space in the bamboo stem do?

No, its not xylem. Bamboo is a grass, and the stem (culm) of many grasses are hollow in the middle (see e.g. Grass Structures from Oregon state for some more info).

The exact reason for why Bamboo have hollow stems is most likely due to evolutionary contingencies. However, from a mechanical stability point of view, a hollow stem is much more rigid and stable than a solid (but much thinner) stem composed of the same amount of biomass (Niklas & Spatz, 2012, p. 191ff). So from the perspective of efficiency, the hollow stems of grasses are very useful. The solid node discs found in grass stems (and in other plants with hollow stems) are however really important for increasing overall stability and ability of stems to resist deformations, while only contributing to a very small amount of the total biomass.


How do parents give their offspring a chromosome?

Are the laws of physics deterministic? I think no one knows, currently.

In any event, yes, the segregation of homologous chromosomes during meiosis I is random: there is an equal probability for each chromosome of a homologous pair to segregate into a given gamete, and this is independent of other homologous pairs. This idea dates back to Mendel, who observed that the heritable “factors” (what we now know as genes) responsible for macroscopic phenotypes are inherited independently of one another (this is his Law of Independent Assortment). This isn’t actually true when considering linked genes, but is certainly true of chromosomes, as was described by Sutton in 1903:

  ...many points were discovered which strongly indicate that the position of the bivalent chromosomes in the equatorial plate of the reducing division is purely a matter of chance - that is, that any chromosome pair may lie with maternal or paternal chromatid indifferently toward either pole irrespective of the positions of other pairs...


Coffee does have an effect on the peristaltic movement in the bowel.

  Coffee increases rectosigmoid motor activity within 4 min after ingestion in some people. Its effects on the colon are found to be comparable to those of a 1000 kCal meal. Since coffee contains no calories, and its effects on the gastrointestinal tract cannot be ascribed to its volume load, acidity or osmolality, it must have pharmacological effects. Caffeine cannot solely account for these gastrointestinal effects.

Effectively, decaf and regular coffee stimulate peristaltic movement in the colon as effectively as a meal does. Caffeine is not the active agent then, but some other compound in coffee.

Source: Boekema PJ, Samsom M, et al. Coffee and gastrointestinal function: facts and fiction. A review. Scand J Gastroenterol Suppl. 1999;230:35-9. PMID 10499460.


DNA is about 20 angstroms wide, so each of the two strand is about 10 angstroms wide. That width is the average between a larger purine unit and smaller pyrimidine unit, so let's round up to 12 or 13 angstroms for the larger unit.


What fish (and/or shellfish) species with a multi-year life-cycle, besides salmon, die after spawning?

Many species of Eel (order Anguilliformes) have a semelparous life history (most species? all?), i.e. they only reproduce once and then die (as opposed to an iteroparous life history). Many species are now threatened by extinction (e.g. American eel and European eel), since they have been heavily exploited by fisheries and they are also vulnerable to habitat modifications (e.g. hydroelectric dams) and pollution. The nature of their life history was also unknown for a long time, since they migrate and spawn in the Sargasso Sea after living many years in fresh water (so the opposite migration path compared to Salmon), which is called a catadromous life history. However, there are also many species of eel that are strictly marine, for instance the very large Conger conger, but many of these species still migrate long distances before mating.

(American eel, Anguilla rostrata, picture from Wikipedia in public domain)

As a fun sidenote, captive eel can become very old, and earlier this year a more than 155-year-old European eel that was kept in a well died (see newsstory) - the oldest known eel from what I know. Eels were often put in wells because they were believed to keep the well water clean.

Semelpary is also found in other fish species, for instance in the Smelt (Osmeridae) family, where many species are fished commercially. Some (most?) species in the family have multiyear life histories, but some, e.g. the Delta smelt (Hypomesus transpacificus) only live for a single year. Similarly to Salmon, Smelt also migrate from sea to freshwater to spawn, i.e. an anadromous life history.

Overall, less than 1% of teleost fish are semelparous according to Finch (1994) - see link for more examples of semelparous fish species and background. However, this figure is most likely uncertain, given that we know very little about the life history of many marine species. In some cases, you can also find a range of life-history strategies from semelparous to partially or totally iteroparous within the same species, depending on ecological context. Nevertheless, the low overall proportion of semelparous fish means that semelpary is generally a rare life history strategy in human exploited fish species.

(Delta smelt, Hypomesus transpacificus, picture from Wikipedia in public domain)


How do nuclear receptors locate each other to form a DNA loop?

This probably isn't the complete answer as I don't know so much about eukaryotic transcription, but maybe I can start the answer.

First of all DNA bending can be sequence dependent - the double helix is not intrinsically straight.  DNA is also pretty easy to bend - it spends most of its time coiled pretty easily around histones, and eukaryotes, supercoiled into chromatin.

In transcription though, there are proteins that come along and effect bends in the DNA or even tight loops, so that the transcription initiation complex (TIC) can be activated by transcription factors (TFs) upstream as the DNA flops over.

see this happening in this video at about :40:
http://www.youtube.com/watch?v=5MfSYnItYvg&feature=related

I think in some cases there might be other proteins bound upstream of the TIC to make the influence of various TFs greater.   I know in highly regulated genes (such as developmental genes in animals) transcription regulation can be impossibly complicated with lots if internal logic.  The classic example is ENDO16 from sea urchin (see second image) which has scores of protein binding sites in front of it.

I was told that DNA binding proteins find their binding sites at a rate faster than diffusion.  The prof told me that she thought that there might be a tendency to diffuse along the length of the DNA because of its charge.  I have no reference for this, but it might help answer your question as to how the NRs pair up so quickly.


Applying drugs to brain via scalp (transdermal)

The short answer is no, it will take forever for a drug to pass through skull bones.

The usual reason to apply drugs on skin is if you want them to act right there, on the skin. Acne creams fit here. You need less drugs, you get where it is needed sooner, and you have fewer off-target effects, when compared to taking them by mouth. The brain is not "right there", so this scenario does not apply.

The second reason is convenience. Some drugs cannot by taken by mouth, because they would be degraded by the stomach or guts. In most cases, the drug has to be given through painful, expensive injections. But if such a drug does pass through skin (usually when it is a fat-loving small molecule), you may get away with applying it on skin. Testosterone is one such drug. However, it usually doesn't matter whether the skin you are applying on is close of far from the target organ. The drug will be taken from the skin by blood, get to the heart through veins, and then spread to the whole body, eventually reaching the target. There is no reason to shave your head, since it will go through the same detour before reaching the desired destination.


The "histone code" is not like the genetic code where one codon in an ORF always is translated to a single amino acid. It's closer to something like GC content or CpG islands: a single instance doesn't tell you anything, but enrichment over some finite window may be biologically significant.

You may want to review the basics, starting with the Wikipedia page on the histone code. In particular read the paragraphs at the end:

  Every nucleosome in a cell can therefore have a different set of
  modifications, raising the question of whether common patterns of
  histone modifications exist. A recent study of about 40 histone
  modifications across human gene promoters found over 4000 different
  combinations used, over 3000 occurring at only a single promoter.
  However, patterns were discovered including a set of 17 histone
  modifications that are present together at over 3000 genes.[13]
  Therefore, patterns of histone modifications do occur but they are
  very intricate, and we currently have detailed biochemical
  understanding of the importance of a relatively small number of
  modifications.


What happens to the molecules of the pathogens after phagocytosis?

The ingestion of a bacterium by a macrophage involves phagosome lysosome fusion, which you can read about in Abbas Basic Immunology, Ch 2. As you suspected, in addition to bacterial killing and antigen processing, the phagolysosome breaks down bacterial macromolecules, as any lysosome does, using a variety of lysosomal hydrolases. There are export pathways for the end products, including lipids, carbohydrates, and amino acids, as discussed in this review, which does allow for re-use by anabolic pathways. As discussed in the linked review, the process of digestion and catabolite export is regulated, as should be expected. In culture models, nutrient availability appears to be important.


What would be the fate of protein made from D-amino acids after ingestion by humans?

One aspect of the basic biochemistry needed to approach this question is the fact that the enzymes that catalyse cellular reactions show various levels of specificity towards their substrates (reactants), including stereo-specificity. This is illustrated below (an ill-favoured thing, but mine own). The first example shows that the specificity of proteases may depend on the general chemical or physical nature of the substrate. The second shows the how stereospecificity works.

The enzymes that are relevant here are proteases, which are responsible for breaking down proteins to their constituent amino acids, which are then absorbed by the gut, and then the enzymes that would normally catabolize (break down) or metabolize (convert to other compounds) those amino acids. It is well known that the specificity of the enzymes is such that, even if the proteins were broken down to D-amino acids, these could not be used for protein synthesis.

I am not an expert in this area (‘for’ loops are more my sort of thing) but I found some pertinent references in a recent paper on D-amino acid analogues of peptides. To quote from the introduction to that paper:

  A useful consequence of this is that (D)-proteins are highly resistant to degradation and have low immunogenicity (7). The fundamental change in backbone–side-chain connectivity and geometry means they are not recognized as proteins by many (L)-proteins—including proteases. Consequently, (D)-proteins are reported to have greatly increased gut, blood plasma, and intracellular half-lives (8). Better cell penetration has also been reported in some cases (9, 10).

The references are:

Uppalapati M, et al. (2016) A potent D-protein antagonist of VEGF-A is nonimmunogenic, metabolically stable, and longer-circulating in vivo. ACS Chem Biol 11:1058–1065.
Rabideau AE, Pentelute BL (2015) A D-amino acid at the N-terminus of a protein abrogates its degradation by the N-end rule pathway. ACS Cent Sci 1:423–430.
Nickl CK, et al. (2010) (D)-Amino acid analogues of DT-2 as highly selective and superior inhibitors of cGMP-dependent protein kinase Ialpha. Biochim Biophys Acta 1804:524–532.
Brugidou J, Legrand C, Méry J, Rabié A (1995) The retro-inverso form of a homeobox-derived short peptide is rapidly internalised by cultured neurones: A new basis for an efficient intracellular delivery system. Biochem Biophys Res Commun 214:685–693.

So it would appear that the D-amino acid proteins are less likely to be metabolized and thus would be less likely to be useful as food. I do not understand why they would have low immunogenicity, but if this is the case it seems unlikely that they would cause allergic reactions.


How does RNA polymerase achieve higher processivity?

The structure in the presence of s (holoenzyme) is on the right; note the open channel for DNA binding. The structure in the absence of s (the core enzyme) is on the left.  Note that the channel is now closed, as if the fingers and thumbs of a hand now closed to make a circle. This striking conformational change that occurs when s dissociates is thought to confer high processivity on the RNA polymerase.

SOURCE: http://biowiki.ucdavis.edu/Genetics/Unit_III%3A_The_Pathway_of_Gene_Expression/10%3A_Transcription%3A_RNA_polymerases


Are there dichotomous keys for identifying medical conditions?

For histopathology they use them all the time to describe cells and tissues, very much as they are used to describe biological entities.  Characteristics like size, cytoplasm to nucleus ratio, grouping, staining characteristics, immunohistochemistry and now molecular attributes are all used to categorize a cell of interest.  For cancer, the identity of the malignant cell is crucial to diagnosis and subsequent effective treatment - based on successful treatments used in the past for people with that type of cancer.

Here is a histopathology dichotomous key I found at Noelways.com


If you have water on you, does it *actually* cool or down, or do you just *feel* cold?

When your wet skin experiences air flow over it, water will evaporate. Evaporation causes cooling, as energy is transferred from the remaining water molecules to the ones that evaporate - energy in water molecules is being experienced as heat. Less energy -> less heat -> sensation of cooling.

This is why you feel cold, as opposed to when you stay submerged in the pool, or your skin is dry and it is just air movement - no evaporation is taking place.


I think this is a Canistel (Pouteria campechiana):

The fruit are yellow when when ripe, but the form and also the leaves look very similar. The fruit are edible raw, you can find some more information here.