I think bullying is really more of an emergent behavior that manifests itself because of natural aggression built in for survival, as well as our complex social-based psychology leading to insecurity when dealing with other:

People who are highly aggressive, and or apathetic to the suffering of others are more likely to control a majority of resources if they don't face significant opposition. This leads to their favored propagation obviously. Then, in their free-time, with all resources under control, they simply continue to do what comes naturally to them: dominating others. It can also work even in those without the ability to actually control resources, due to lack of intelligence for instance. I have met far more non-intelligent bullies than the reverse. The reason for their behavior is still explained by an attempt to control their territory and social status, however ineffective.
Again, due to our complex psychology centered around social interaction, we can develop insecurities about our self-perceived 'fitness', and therefore acceptance by mates and peers. This low self-esteem can lead to bullying others to boost one's ego. Chemically, this can result in a release of endorphins because they feel they have achieved something, which supports bullying behavior as an emergent behavior. Also, those with lower intelligence are likely to have trouble with reasoning skills, and therefore find it difficult to self-analyze and realize their behavior is negative. This leads to bad interactions with others, which can make those individuals feel even more insecure, which in turn fuels their drive to assert themselves through bullying.

Many studies have been conducted on sociopaths/psychopaths. Just like any other evolved trait, whether or not their "personality disorder" is beneficial to the propagation of their genes depends on environmental factors. If they face only opposition from entities that are relatively weak, physically and mentally, then they have an advantage over those peers. But if their peers are sufficiently strong and organized, then the personality disorder becomes a disadvantage if they can't adapt, because they will be attacked by those seeking cooperation from others when they misbehave. Obviously, when our species' numbers were few, high-aggression and a willingness to kill for resources needed for survival aided in survival. In these modern times, its less acceptable for socio/psychopaths to display their innate behavior, due to modern laws, but obviously society can take turns that allow them to express themselves without worry...see the holocaust or any other genocide for an example.

https://link.springer.com/article/10.1007/s40806-017-0097-5

https://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=2&cad=rja&uact=8&ved=2ahUKEwj5vKjk88bjAhUfJTQIHaFDA9wQFjABegQIARAC&url=https%3A%2F%2Fwww.apa.org%2Fpubs%2Fjournals%2Freleases%2Famp-a0038929.pdf&usg=AOvVaw1fUJiPHl8rSKMm6Gc9VEeA


Fluorescent protein tags and colocalisation

"Are protein A and B co-located?" The answer is that it depends. Since your test question included the word "necessarily", this means that the answer to the test question is no. All you have to do is think of at least one plausible counter-example.

Here's a couple:

The flourescently tagged constructs were screwed up somehow, so A, B, and each of their respective tags were actually expressed as 4 separate proteins.
(As per BPinto's comment) the tagged constructs may co-localize even if A and B would not normally do so. This can happen if, for example, the tags bind to each other, or if the tags somehow cause both constructs to get transported to a particular organelle.


The GUG start codon in E. coli: identity of initiating tRNA and efficiency of translation

The NCBI translation table translates all alternative start sites as methionines. To my understanding, all translation is initiated by the fMet-tRNA. I don't know if there are any exceptions to this rule.

Regarding translation efficiency, I only found a 1985 paper in PNAS (Reddy et al, PNAS 82:5656-60), in which they compared the translation efficiency of adenilate cyclase's own UUG start vs GUG or AUG, obtaining a translation ratio 1:2:6 UUG:GUG:AUG, suggesting that AUG is the most efficient one, followed by GUG. Also, Romero and Garcia, FEMS microbiology letters 84:325-330 (1991) compared the efficiency of AUG vs AUC, AUA and AUU, showing a much lower efficiency for those codons, but they did not compare it to GUG.


Can bacteria, viruses, and cancer cells be destroyed by resonance?

Your question included "other forms of waves" so I'm going to assume that the use of ultrasound to destroy cancer cells qualifies.

A paper published in the British Journal of Cancer in 2009: "[High-intensity-focused-ultrasound in the treatment of primary prostate cancer: the first UK series]"1 describes the use of a "Sonablate 500" device used to treat 172 men with prostate cancers at two hospitals in the UK, and its use is described as resulting in "acceptable short-term levels of cancer control."

However, the paper does lament the deficiencies of research in this area, the number of other treatments available, and the lack of longer-term follow-up to this research.

The answer to your question appears to be yes, with the qualification that this is an example using sound waves, rather than electromagnetic waves - isn't radiotherapy, mentioned in the first sentence of the question, electromagnetic waves?


Why do people sleep with their eyes open?

The medical term is "lagophthalmos" if the person is unable to close their eyes at night.

There are several factors involved, and unless it's due to physical obstruction, lid archetecture (such as short lid length (due to surgery etc)), or facial nerve (CN VII) problems, it's not well understood.

I have seen numerous people with varying degrees of this over the years.  For most of those people, it's an intermittent thing.

Tears are essential for eye tissue health, including cleaning and avoiding infection. People complain of dry or irritated eyes mostly.  But in more extensive cases, keratitis and ulcers can occur, which are bad.  If it's frequent, tell the person to make sure they tell their eye doctor (or if they don't have one, get it checked out sometime) so that the health of their eye tissue can be evaluated.

Another possibility is Grave's disease - in that condition, the entire eyeball protrudes and sometimes the eyelids aren't long enough to cover them adequately.  But what you're describing is probably not Grave's disease.

Wikipedia

American Academy of Ophthalmology


So there are no rules per say (although I wish there were). But there are commonalities among plasmid names and they can help people identify them:

Include the empty backbone name in your plasmid name. This simple piece of information can often convey many important details. Once you know the backbone a plasmid is based on, you can usually derive: a) the bacterial antibiotic resistance, b) the promoter that drives the insert, and c) any other selection markers (for use in other cell types, e.g. eukaryotic cells).

Include information about the insert in your plasmid name. This is often a 3-6 letter representation of the gene (or DNA sequence).

Often researchers will add a lower case letter to the beginning of their insert abbreviation to specify what species it is. Example: ‘h’ is for Human (homo sapiens), ‘m’ is for mouse (mus musculus), ‘r’ is for rat (rattus rattus or rattus norvegicus), etc.

Add any tags or fusions that are on your insert. Typically you would list any tag or fusion protein in the order they appear in the plasmid and their relative position to the insert. Example, if you have a Flag tag on the N-terminal of your insert, you would list it first.

e.g.   pBACKBONE-Flag-hGene

If there was also an EGFP fused to the C-terminal of your insert you would list it after the insert.

pBACKBONE-Flag-hGene-EGFP

If your insert contains a mutation or modifcation, this should be included in the plasmid name.  Mutations are generally listed as the amino acid change and not a nucleotide change. The proper way to denote an amino acid mutation is to list the one letter abbreviation of the wild type amino acid immediately followed by its position (number) relative to the start Methionine (Met) followed by the one letter abbreviation of the mutated amino acid currently at that position.

Check for more information at Addgene.com they are the largest plasmid repository in the world.

By collisions I'm guessing you mean naming your plasmid something that is already "taken." This is a benefit of submitting to a repository, they will ensure this doesn't happen.if your planning on filing a patent, your parent attorney will do it.


This is an instar (nymph) of a shield or stink  bug (order Hemiptera, family [Pentatomidae])(https://en.wikipedia.org/wiki/Pentatomidae).

This appears to be similar to the 2nd (or possibly 3rd) instar of Halyomorpha halys.

European and Mediterranean Plant Protection Organization; Credit: Matteo Maspero

UTIA suggests the 2nd instar begins to develop an almost black appearance, where that blackness gradually shifts to browner shades in subsequent instars. According to Medal et al. (2013)1 the 2nd and 3rd instars have median lengths of ~2.75 and ~4.25 mm, respectively. According to WSU Extension, instar nymphs of H. halys are spiny (including on the shoulders) and possess light bands on the antennae.

 Source: WSU Extension

This University of Wisconsin Extension site provides a fairly similar photo to your specimens, which can be found at bugguide.com:

 Source: bugguide.com; Credit: Yurika Alexander

 Citations

1  Medal, J., Smith, T. and Santa Cruz, A., 2013. Biology of the brown marmorated stink bug Halyomorpha halys (Heteroptera: Pentatomidae) in the laboratory. Florida Entomologist, 96(3): 1209-1213. PDF


First I assume many years equals 10 years or more, although the presence of oxygen may drastically speed this up or it may interfere it is hard to say. Nobody was tried to figure out how something will rot in sealed but consciously oxygenated container since is basically does not exist without a custom built chamber.
Your main factor is humidity that is whether the pod has humidity control, if it keeps a human comfortable humidity you will have a skeletal mummy since skin and hair will survive but much of the body will desiccate. If you just treat it like a sealed container the body fluids breaking down will ramp up the humidity and you will just a have a pile of bones and rather disgusting soup. A sealed container is one way to rot down an animal carcass to get bones, it is called maceration and something that has been well studied. I have done it many times and a few years is more than enough to reduce a carcass down to a skeleton.  Note depending on how long you wait even the bone may be damaged or destroyed although the restricted biota may prevent the final stages of this leaving you with extremely fragile skeleton remains.
I must emphasis the smell will be disgusting, as in even seasoned investigators will be tossing their cookies if they smell it. Almost nothing can describe the disgust of the smell of a human body rotting in a sealed container. Our brains have evolved to find human rotting flesh as disgusting as possible.
for additional comparison  a a paper comparing decomposition of several pig carcasses sealed in concrete.
Source link addresses
https://pubmed.ncbi.nlm.nih.gov/2738563/
https://onlinelibrary.wiley.com/doi/10.1002/9781118953358.ch33
https://journals.lww.com/amjforensicmedicine/Abstract/2013/03000/Burial_of_Piglet_Carcasses_in_Cement__A_Study_of.13.aspx


The answer lies in the definition itself of transformation. See from here:

  In molecular biology, transformation is the genetic alteration of a cell resulting from the direct uptake and incorporation of exogenous genetic material from its surroundings through the cell membrane(s). For transformation to take place, the recipient bacteria must be in a state of competence, which might occur in nature as a time-limited response to environmental conditions such as starvation and cell density, and may also be induced in a laboratory.

What is clear from this definition is that host cell needs to be competent for taking up extracellular DNA to call the process transformation. Also, the term direct uptake does not seem to fit here as, you know why, bacteria do not just go on collecting viral DNA from their surroundings.

Obviously, bacteria are not competent to take up viral DNA, nor the virus makes them so. The virus simply injects and joins its own DNA into baterial genome. Now, it would be some common sense to know that the host does not like it, so whether it is competent or not, is just a matter of debate (did anyone ask them?). In short, No, the process of lysogenic cycle would not be considered transformation as the bacteria are not made competent for this process.


Apparently, cartilagenous fishes are the oldest extant clade that have the true immunoglobulins (antibodies) and the T-cell receptor (Schluter et al., 1997). All extant gnathostomes, incuding cartilagenous fishes, produce antibodies.

However other animals (invertebrates) and even plants have proteins that belong to the immunoglobulin superfamily (to which the classical immunoglobulins/antibodies also belong). Members of this superfamily are structurally related; they are not necessarily involved in immune responses. Hemolin is one immunoglobulin superfamily protein in insects, that is involved in immune function, but not exactly like vertebrate antibodies.


Shortest strings not present in the human genome

The human genome contains less than 416 base pairs, so, even after including a factor of 2 for the two strands and another to allow for some genetic variation, there must certainly exist some 17-base string not found in either strand of the genome.

Now, 417 bits is two gigabytes, which fits easily within the memory of a typical desktop computer these days, so a simple and efficient algorithm for finding such a string would be to set up an array of 417 bits, initialize them all to zero, and then simply iterate over the entire genome (including all known variations), taking each 17-base subsequence (and its complement), mapping them to base-4 integers and setting the bits in the array at the positions given by those integers to one.

Once you're done, any remaining zero bits will correspond to strings not found in the genome.  More to the point, the longest consecutive block of zero bits will give you the shortest base string not present in the genome.


Book Recommendation: Complex Traits and Complex Genetic Architecture

Suggestions:

Evolutionary Genetics : Concepts and Case Studies: Concepts and Case Studies

Edited by Lexington Charles W. Fox Department of Entomology University of Kentucky, Faculty of Life Sciences University of Manchester Jason B. Wolf Lecturer

The mathematical theory of selection, recombination, and mutation

by R Bürger (as suggested by @rg255 in the comments)

Lynch and Walsh's Genetics and Analysis of Quantitative Traits

(as suggested by @kmm in the comments)

PS: Do tell us if you found a better one.


TADs were initially discovered by computing contact probabilities between regions of the genome using HiC (a chromosome conformation capture method, that try to provide an idea on how the genome is organized inside the nucleus by computing the probability of each contact to be located nearby another locus). People have found that instead of being random, some loci were in contact with some regions of the genome rather than the others, implying some form of functional significance.

In short: a TAD is a genomic region of increased contact probability. They are of functional relevance (for instance, Enhance-Promoter gene expression regulation occurs primarily within one TAD rather than between two (adjacent TADs).

You might be interested in the following papers:

A 3D Map of the Human Genome at Kilobase Resolution Reveals Principles of Chromatin Looping (might be behind paywall)
Topological Domains in Mammalian Genomes Identified by Analysis of Chromatin Interactions

Finally, the following picture (extracted from the latter publication) provides an example of two TADS:

The bottom panel shows the contact probability: two regions of the genome appear to be isolated whereas they are nearby. They show significant self-interaction. One interpretation for that (top panel) is to imagine that the genome exhibit some reproducible condensation, explaining the increased contacts.


Identify caterpillars and, if possible, parasitoid (Sabah, north Borneo)

These are wasp larvae, but likely not parasitoids. They are the larvae of predatory Sphecid or Crabronid wasps, both of which build mud nests, generally provisioned with spiders or other arthropods that have been killed (and by some wasp species, dismembered) or paralyzed by the female (mother) wasp. It looks like one or two of them may be pupae (closer to eclosing--"hatching"--as adults) instead of larvae. If kept carefully they can be raised to adulthood for identification (at least by an expert familiar with the aculeate, or stinging, wasp fauna of that part of the world).


The short answer is no.
Here's a review article with some evidence:

B cell receptor editing in tolerance and autoimmunity
Section: Receptor Editing in Mice with Conventional Autoantibody Transgenes
If multiple κ rearrangements fail to yield a suitable L chain, the κ
locus undergoes rearrangement to a non-coding gene called RS in mice
(RS is referred to as the κ deleting element in humans). RS
rearrangement results in either deletion or inversion of Cκ,
consequently inactivating κ L chain expression on that allele. In cell
lines with λ rearrangements, one or usually both κ alleles are
deleted, whereas in κ-expressing B cells the fraction of RS
rearrangements is approximately 15%.

In summary: After a point with (probably multiple) κ rearrangement failures, both κ loci (usually) get deleted, leaving only λ. So if a B cell expressing a BCR with λ is self-reactive, it won't have the chance to rearrange its κ.
However, there's a lot more involved. For one, it's possible to get a functional and non-self-reactive λ chain BCR without repeated κ rearrangement failures.
Since the quoted passage might be confusing out of context, I'd like to mention briefly that your question's description of light chain recombination is very simplified. In reality, there are many additional mechanisms involved and many different paths to get a functional κ rearrangement, a functional λ rearrangement, neither, or even both. Moreover, there's a lot we don't know, since we learn one experiment at a time, and we can't always directly measure what we'd like to.
First, rearrangement has been observed to occur simultaneously in  κ and λ. This fact might explain why it's possible to get a functional λ chain BCR right away as mentioned above. Second, allelic exclusion (between both κs and both λs) doesn't always work as you and I might expect it to, and a developing B cell can express different BCRs simultaneously (even one with κ and the other with λ). Third, due to receptor editing, a B cell has multiple opportunities for a functional κ chain rearrangement on a single chromosome, meaning that neither λ nor the second κ is needed despite an initially nonfunctional κ rearrangement.
I highly recommend reading the review article!


How does the body "know" how to metabolize foreign substances

One strategy for xenobiotic metabolism seems to be making a lot of similar enzymes with different substrate specifities. Lets take the cytochrome p450s as an example. These are a class of enzymes with 57 genes identified for humans, and I don't know how many alternative splicing products are made from those genes. As a class, they are responsible for about 75% of drug metabolism and are predominantly found in the liver. They work by using a heme group with a carbon monoxide to add oxygens to xenobiotics. Here is a diagram of the mechanism:

It's been too long since my drug metabolism class to go into more detail on these enzymes, but there are other classes of enzyme that fit this multiple enzyme strategy such as the 2 monoamine oxidases, 5 flavin containing mono-oxygenases, and 4 epoxide hydrolases. So the body doesn't really know how to break down xenobiotics, but has a wide array of enzymes with broad and overlapping substrate specificities that work on whatever they happen to bind to, whether it's an endogenous hormone or pharmaceutical compound or toxin.


About. Autosomal recessive diseases in genetics

You are talking about an extremely simple system of inheritence that is a single bi-allelic locus with simple dominance relationships. You are talking about a autosomal recessive disease. In other words, let a and A be the two alleles, where A is dominant of a. By definition of your model, the individual expressing the disease is the individual carrying both a alleles (a aa individual). Anyone carrying the dominant allele would not express the disease (by definition of the term dominance and because you define a model where a and not A is causing the disease).

In short aa express the disease, while aA, Aa and AA individuals don't express the disease. aA and Aa are carrying the allele causing the disease though and might have kids expressing the disease if they mate with an individual that carries at least one allele a.


Use of amino-acid sequences versus use of nucleotide sequences in phylogenetic analysis

In general, many sequence alignment programs can use multiple substitution models, distinguishing between nucleotides, amino acids, and codons. A protein sequence has functional information that is not directly visible in the nucleotide sequence.

The papers you link deal with horizontal gene transfer, where a gene is passed to more distant  organism. Different species have different codon usage biases, i.e. the translation efficiency is different for different codons. On one hand, this means that HGT is more likely to occur between species of similar codon usage. On the other hand, "codon usage of horizontally transferred genes approaches the host usage over time." Thus, on the nucleotide level, the phylogenetic signal will get lost due to the evolutionary pressure on translation efficiency, while on the protein level, there will be more conservation.


DNA will be never replaced (unless you are speaking about something, where DNA might be only trash, like in the case of blood transplantation or in the case when "organ" would be slowly replaced itself by host regenerative power and "organ" transplantation would be only something temporary, but then we are probably speaking about wider definition of organs).

For further evidence, you may look at cases of chimerism. That is, when young embryos fuse together and create single one with two different cell-lines, which later differentiate to create different organs.
https://en.wikipedia.org/wiki/Chimera_%28genetics%29

Furthermore, rather more common but with less drastic effect can be somatic chimeras, that is when (usually) early, when embryo is formed only by small amount of cells, one of cell has a mutation, then later in life, this cell again can give rise to organ or several of them. In that case, those organs will carry this mutation while rest of the body will not. This can be potentially more common as this can happen in any single time during development and even after it (in fact, cancer cells are sort of product of that).
More interesting cases here:
https://en.wikipedia.org/wiki/Mosaic_%28genetics%29

So, from simple fact that these cases exists and are well-spread, and basically means that several different cell-lines can live in the same body, the answer on your question, if organ DNA will be replaced after transplantation is no.

edit: In the case of whole cell replacement, they can be from both donor and host. However, there are a few problems:

Most of cells that we have are not totipotent, not even pluripotent or multipotent (see: https://en.wikipedia.org/wiki/Cell_potency), most of our cells are plain and stupid. This means that highly specialized cells of some organ would probably be replaced only by other highly-specialized cells of that organ (or their precursor cells that are kept for this solo reason, keep regenerativ ability of particular organ, as quite a lot of highly-specialized cells can't divide any more). However, there are a few documented cases with regnancy, where a few cells (embryogenic, thus with bigger "healing" power) migrated through placenta to mother's body and healed her diabetes. So theoretically this is possible, as well as host getting cancer from donor's organ. But again, reason why we are transplanting organs is because human body is not particularly great in regenerating itself and those organs won't grow. So theoretically possible, but not great concern (except for cancer).


Do nerve cells cause action potential in cardiac muscle?

The vagus nerve controls heart rate. This is the best example of a direct nerve action potential impacting cardiac muscle, although one could argue the adrenaline system to be an indirect mechanism.

The vagus nerve is part of the parasympathetic system, it acts to decrease heart rate. Resting heart rate is maintained by permanent vagal stimulation/tone by the release of acetylcholine.


Sharks hear from 10-800hz.
Sharks jump out of water for fun, which makes  huge noise pressure next to their ears. Sound weapons aren't very renowned in Darpa or defence tech. i'd say, you play any kind of patterns to a shark at any frequency, you'll have a tough time upsetting it.  you may have a very good effect at attracting them from afar and delaying predatory response as they assess/avoid the prey. LF takes huge batteries compared to HF. curiously, dolpins hear up to 100khz, whales as low as 2-3 hz for booming across the ocean. precise answer here : https://scholar.google.fr/scholar?hl=en&q=shark+sonic+deterrent&btnG=&as_sdt=1%2C5&as_sdtp=


Does adding milk to cereal make it harder for our body to absorb the vitamins and minerals from the cereal?

Overall, no it doesn't. Cereal is made in a way that it's expected consumers will consume it with milk. Here's a list of some important fortifications added to cereal and milk effects on absorption.

Riboflavin: No. Affected most strongly by light.

Iron: Yes. Calcium can affect absorption. Milk causing a deficiency is rare unless it is being used as a breast milk substitute in babies.

Thiamin: No. Unless you are drinking alcohol with your cereal.

Folic acid: Milk is a source of this!


Success of computer simulations in biology, new discoveries

In my opinion, this question is a question of philosophy of science, not Biology but here are my thoughts anyway.

Science by definition is a methodology that requires the creation of a hypothesis under a specific model and testing the prediction of this particular hypothesis.

Such modelling can be done either analytically (math) or numerically (with a computer). Typically, numerical modelling is being used when there the mathematical tools fail to offer a solution for the system analyzed. To me rejecting, numerical modelling is like rejecting modelling and is therefore like rejecting the scientific method altogether.

Computational modelling has brought a lot in pretty much any field of biology (and pretty much any field of science), so much so that it is hard to know where to start to fully address this claim. There are many models that were only verbal as mathematical tools were not sufficient to bring more quantitative predictions. For many of these models, computer modelling could offer quantitative predictions that could then be further tested.


Lateral corticospinal tract and termination

The answer ends up being on the next page when discussing the ventral corticospinal tract.

  Many ventral corticospinal tract axons have branches that decussate in
  the spinal cord, similar to the re-crossed lateral coticospinal tract
  axons described earlier.

In other words, some axons of the lateral corticospinal tract ignore the pyramidal decussation, join the anterior corticospinal tract (which then synapses bilaterally later at the spinal commissure).


Trying to differentiate between the three muscle tissues with small pictures

Without answering the problem for you, because you have not shown work yet to try to figure out which is which, let me tell you that you have three options.

Skeletal Muscle- striated, peripherally located nuclei, same thickness along length, non-branching
Cardiac Muscle- striated, few centrally located nuclei, branches and anastamosis
Smooth Muscle- non-striated, centrally located single nucleus per cell, tapering ends

Now, hopefully, based on your pictures, which are indeed sufficient for you to figure out which is which, you can answer your own question. Good luck!


Does night sleep provide more energy-regain than sleep during the day?

I think the reason is primarily, that it is more quiet (the chance is very low that other people are disturbing your sleep) in the night as well as it is also dark. Keeping in mind, that the brain "gets tired" due to some proteins (melatonin) and in contrast, being more awake during the day, it seems to be just logical that the sleep in the night is healthier, thus providing more energy.


Wikipedia has a remarkably well-cited article on the subject of silks and their various biological isoforms and mechanical properties. With respect to tensile strength, spider's silk is as tough as high-grade steel.

Explcitly, dragline silk was measured by Pérez-Rigueiro at al. to be 600 ± 50 MPa with a comparison to silkworm silk.

Reference:

 Pérez-Rigueiro J, Elices M, Llorca J, Viney C. 2001. Tensile properties ofArgiope trifasciata drag line silk obtained from the spider’s web. Journal of Applied Polymer Science 82: 2245–2251 [pdf]


What's the difference between the spindle assembly checkpoint (SAC) and mitotic checkpoint complex (MCC)?

It can be helpful look into a few technical articles on the subject to clarify these ideas.

For example, this article has an abstract that lays it out quite nicely in the first 2 sentences of the abstract:

  In mitosis, the spindle assembly checkpoint (SAC) ensures genome stability by delaying chromosome segregation until all sister chromatids have achieved bipolar attachment to the mitotic spindle. The SAC is imposed by the mitotic checkpoint complex (MCC), whose assembly is catalysed by unattached chromosomes...

So the SAC is a human conceptual model of how cells prevent the improper onset of anaphase before chromosomes are set up properly for cell division. MCC is the actual protein complex acting as an agent to make the SAC happen in cells.

The SAC could be thought of as containing the MCC and any other agents that prevent improper anaphase until spindle assembly and chromosome bi-orientation is complete, but it is not a protein complex per se in the sense of a bunch of proteins that stick together for a specific molecular function.


That sentence is located in a paragraph titled "Stages 5-7: Endocytosis and recycling": it's talking about recycling exocytosed membrane which is necessary for making vesicles for further exocytosis.

The sentences before the part you quoted are:

  Synapses possess highly efficient mechanisms for retrieving SVs from the plasma membrane of the presynaptic terminal after exocytosis. Fast regeneration of functional SVs is a prerequisite for synapses to function during prolonged activity.

I think the passage is just somewhat confusingly worded, in that "exocytosis" is used as the subject of the sentence which is strange in this context. You could rewrite that sentence:

  There appear to be two alternative pathways to recycle membrane for exocytosis: clathrin-mediated...

The author likely intended the word "exocytosis" in the original sentence to mean "the entire process of releasing synaptic vesicles, including formation of those vesicles" rather than the specific event of vesicle fusion with the membrane. Kind of like if I referred to "planting trees" as part of "logging" - you typically think of "logging" as cutting down trees, but in the right context it can make sense to refer to the process: you need to have a tree there to be able to cut it down. I could say "Trees are necessary for logging. Logging uses two alternative pathways: planting trees directly as saplings, or leaving land to grow new forest naturally over a number of years."


Can I force evolution in a group of cells by removing all the smaller cells?

Short answer

Yes that would work in the condition that the trait you select for (size) is heritable.

Long answer

The kind of selection you would apply is called truncated selection because you fix a limit in size (depends on your filter) under which individuals do not survive and above which individuals survive and reproduce equally.

The response to selection ($R$) is given by the breeder's equation:

$R = h_N S$

, where $S$ is the selection you apply. In your case, $S$ is the difference between the mean size of the parent generations and the mean size of those you allow to reproduce in the parent generations. $h_N$ is the heritability (more info in additional info).

So, if you measure the mean size of your cells, filter them, measure their size again (or infer their size based on previous measurement and the size of you filter) and calculate the difference between the two measurements you get $S$. Then you let your filtered individuals to reproduce and you measure the size of their offspring which is $R$. By dividing $R$ by $S$ you get the heritability $h_N$. If you do not observe any difference in size between your two generations it means that the heritability is 0 ($\space h_N = 0\space$). Of course, you'll need a population that is composed of enough cells in order to have a good estimate.

Additional info

To be a bit more accurate $h_N$ is the heritability in the narrow sense. It represents the part of variance in the population that has to be accounted to additive genetic variance. The word additive genetic variance might seem obscure. In other words

$$h_N = \frac{V_{Ga}}{V_{P}} = \frac{V_{Ga}}{V_{G}+V_{E}} =  \frac{V_{Ga}}{V_{Ga} + V_{Gd}+V_{E}}$$

, where $V_{GA}$ is the additive genetic variance, $V_{GD}$ is the dominance genetic variance, $V_E$ is the variance due to environmental variance and $V_P$ is the total variance (phenotypic variance)

Hope that helps. Do not hesitate to ask further question if something is unclear or if I missed one of your point.

Edit

Filter

The filter you need should allow you to discriminate the cells based on their size. Therefore, it should be relatively accurate. It is common to classify the phytoplankton based on their size, see this. You should try different filters and see what filter allows a good discrimination.

EDIT

I assumed your cells were all of the same species. Is it the case? If you just sampled them from a lake and let them grow in a container then you very probably have various species. Therefore, you would select (based on their size) for species with your filter rather than selecting individuals within a species (based on their size again). It is kind of the same process anyway and the breeder's equation still holds.


Species richness corrected for area -- should area be log-transformed?

Let me offer my answer even though I have not worked in ecology.

You are asking two questions if I understand you correctly:

Should you normalize to the area sampled?

The answer to that depends on whether the area sampled is a nuisance variable or not. Is it the case that you just happened to sample from areas with (largely) different sizes? Or do you rather expect or are interested in whether it may display some interaction with the environmental factors that you study? In the first case, normalize with clear conscience. On the latter, you should probably include the area sampled in your model. The reason for this is that by normalizing, you are assuming that the relationship between the response variable (number of species) and the predictor (area sampled) is fixed and has a slope of 1 irrespective of the variation of the rest of the variables included in your model. If that is not the case, you want to explicitly add the area sampled as a fixed factor in your model.

Should you log-transform the area sampled?

If the answer to the first question is that the area sampled is a nuisance variable then it does not matter whether you log-transform or not as now you are interested in a new measurement, species density. Hence, you may work with the untransformed variable which would simplify the interpretation of the results by a tiny bit. If the answer to the first question is that you want to investigate the interaction of the variable 'area sampled' with your other predictor variables, then you do not need to log-transform your variable as this is rarely needed, even if you use parametric inference. To summarize, you do not need to transform the variable 'area sampled'.


What can I see with a microscope at what magnifications?

You'll be able to see something that is 1 micrometer as a slightly formed (meaning you can decide whether it's more oblong ore more round) dot. So any structure that is bigger than that can be better observed. Unfortunately, viruses are far smaller, and many interesting cel organelles are too.

Also, many things (like parts of cells) are not visible until they are stained. There are many stains that are suitable for beginners (others are quite toxic or teratogenic). I'd recommend buying a book from 1970 or before (no re-issue), because many stains and chemicals are nowadays deemed too dangerous (although they are not that dangerous if used in amateur-microscopy volumes) and normal light microscopy technique has not changed since then.

With a used microscope from a reputable manufacturer (inquire beforehand whether the tubes are of a standard size so you can get replacement oculars etc.) you are on a good way. Schools and universities will sometimes purge their stock, which is where you can make incredible deals.

Get a microscope with mains-fed light, ideally LED. Some 'tricks' like Dunkelfeld are very interesting to use, but require a good light source and non-broken iris.

Also look at the table, it should have a smooth, no-hysteresis (meaning if you go left, and then right, there should be no 'slack' to take up before the picture moves the other way) x/y platform, ideally with a measure attached.

Total magnification is ocular*objective, and many microscopes offer the possibility to attach a camera, either additionally or as replacement ocular. that is a great thing, as you can take pictures and zoom in (real magnification will not change, but still, some things are easier to see that way) or later tweak the colors or contrast.

Depending on whether you mainly want to look at things that can be put between two glass slides (cells, bacteria, small parts of insects, ...) or at 3D things (insects, flowers, minerals) you can either buy a two-ocular microscope or binocular (3D) or a one-ocular microscope.

Objectives and oculars are small tubes with many lenses built into them - this means humidity and even rot can slip between those, so be sure to check used material (especially from learning institutions) for clear pictures.


How does one find the corresponding SNPs in the pair of chromonosmes in a FASTA file?

If you are looking for simple one off queries it might be better to load the BAM file and a relevant reference genome into a browser like IGV and simply navigate to that specific position.

For some data I had lying around a heterozygous SNP would look like the picture below, there has been an A to G SNP and a C to T:

For longer lists of queries I would take a look at BEDtools: https://bedtools.readthedocs.org/en/latest/content/bedtools-suite.html

If this does not help you, I recommend you ask your question on https://www.biostars.org/ There you will find help from true bioinformaticians.


How would the result of Hershey and Chase experiment been different if protein was the genetic material?

Hershey and Chase did two experiments to prove that DNA is the carrier of the genetic information.
First, they grew phages (viruses which infect bacteria) in a medium containing radioactive sulphur (35S). This marked all the proteins of the phage (the hull) radioactive. They then used this phage to infect bacteria. To do so, the phage attaches to the surface of the bacteria and injects its genetic material. This looks like in this picture from the Wikipedia page on Bacteriophages:

The bacteria with the attached phages are then blended, so they will loose the attachment to the bacterial surface. The mixture of bacteria and phages is then centrifuged, this makes the heavy bacteria sediment at the bottom of the tube, the lighter phages stay in the supernatant. Hershey and Chase then measured where the radioactivity from the marked phage proteins had gone, since they found it in the supernatant, they knew, that no proteins had entered the bacteria.
If proteins would have been the carrier of the genetic information they would have entered the bacteria and had been found in the sediment inside the bacteria.

In the second experiment (the proof if you want to say so) they marked the DNA of the phages radioactive (with radioactive phosphorus, 32P). They repeated the experiment and found the radioactivity in the sediment with the bacteria, proving, that the DNA had indeed entered the bacteria.
If the DNA wouldn't be the carrier, it wouldn't have entered the bacteria and would have stayed in solution.

The whole experiment is nicely shown in this Wikipedia illustration:


Ashok's Bronzeback (Dendrelaphis ashoki).

This is a relatively small snake (typically 70 cm in length) that feeds on lizards, frogs and small rodents.

More information can be found here or here.

It's range is Southwestern India:

You can differentiate this species from closely related D. girii based on it having a longer "postocular" black line than D. ashoki -- in D. ashoki it stops shortly caudal to the eye (e.g., see here).


Why is free ribose not reduced to deoxyribose rather than the reduction occuring on ribonucleotides

Clarification

I assume that question is posed in the knowledge that ribose is an intermediate in the dark reaction of photosynthesis and can be synthesized in the hexose monophosphate shunt in animals. Hence I assume that the question is not why ribose precedes deoxyribose in the metabolism of mammals and other living things. Rather, the question would seem to be why ribose is not converted directly to dexoyribose, but only after ribonucleotides have been formed (in the ribonucleotide reductase reaction).

Possible Answer

Question as to why a metabolic pathway has one form rather than another can sometimes have a chemical explanation, but in this case I suggest answers can only be speculative.

Thus, one possible answer could be:

  There is no need for free deoxyribose in the cell, and that if free
  deoxyribose were produced there would be potential competitive
  inhibition of enzymes that catalyse reactions involving ribose.

If an ‘RNA world’ preceded the modern ‘DNA world’, then one could argue that:

  The simplest way for the shift from an RNA genome to a DNA genome would by the introduction of a
  specific reaction for the reduction of the ribose in nucleotides. The
  fact that the base that differentiates DNA from RNA — thymine —
  is also synthesized as a nucleotide (see my answer to this
  question)
  is consistent with (but does not, of course, prove) this idea.


What alternatives are there to the amyloid hypothesis?

Alzheimer's disease is a very complex field, and I am going to restrict my answer to two particular areas: the neuritic plaques and the neurofibrillary tangles. This area is also of interest to me, hence the protracted answer.

The two pathological hallmarks of Alzheimer's disease, first described by Alois Alzheimer in about 1906, are the extracellular neuritic plaques and the intracellular neurofibrillary tangles which occur (exclusively) in the brain of humans with this disease.

The Neuritic Plaques (Amyloid Precursor Protein and β-Amyoid)

[References to the information given below may be found in Price & Sisodia (1998) and in Lowery et al. (1991)]

The major component of the extracellular neuritic plaques is a small, appromimately 4 kDa protein known as the β-Amyloid (Aβ),  or A4-protein.

The Aβ, whose tertiary structure is that of a β-pleated sheet, is itself derived by proteolysis (see below) from a much larger protein known as the Amyloid Precursor Protein (APP).

A number of isoforms of Aβ are known which contain between 36 and 43 amino acids, the most common of which are  Aβ40 and Aβ42.
The Amyloid Precursor protein (APP) is a very large protein (≥ 695 amino acids) of unknown function which is a normal component of brain. It is predicted to have a single transmembrane span.

A number of isoforms of this protein are also known, which contain  695, 714, 751 & 770 amino acids.

The AA751 and AA770 isoforms contain a domain (Kunitz domain) homologous to a class of protease inhibitors, strongly suggesting the proteolysis plays a key role in normal function, and perhaps in (abberant?)  Aβ formation.
One of the cleavages which produces the Aβ, that catalyzed by γ-secretase, occurs within the transmembrane-spanning domain of APP.  How the protease has access to its substrate within the lipid bilayer is a major source of interest.

Researchers who believe that neuritic plaques and  Aβ hold the key to Alzheimer's disease are known as baptists. Their counterparts, who believe that the neurofibrillary tangles are key, are known as tauists, for reasons that will become obvious (see also here).

For the past number of years, baptists have been to the forefront. In my view, the tauist story is even more interesting, and must surely be important in any final understanding of Alzheimer's disease.

 Neurofibrillary Tangles, Paired Helical Filaments and Tau Protein

Examination of the neurofibrillary tangles under the electron microscope revealed that they had a twisted ribbon-like structure which was called the paired helical filament (PHF) (Kidd, 1964; Wisniewksi  et al., 1984).

PHFs are practically insoluble and for a long time this impared progress.  However, extraction using the detergent sarkosyl, followed by sequence analysis and immunological investigations, produced a  major surprise:

  A component of the paired helical filament is the
  microtubule-associated protein tau (Goedert et al., 1988;
  Wischik et al., 1988), a most unusual and interesting soluble protein
  which had already been purified to homogeneity and extensively characterized by Kirschner & co-workers
  (Weingarten et al., 1975; Cleveland  et al., 1977a, 1977b).

A perusal of pubmed shows that at this stage interest in tau increased dramatically!

  It is now accepted that microtubule-acssociated protein tau in a
  hyper-phosphorylated state is the major structural component of the
  paired helical filament (Lee et al., 1991; Kosik & Greenberg, 1994).

Some key properties of tau are the following.

Tau was first isolated as  a series of closely related proteins (isoforms) which co-purify with porcine tubulin during successive cycles of polymerization/depolymerization (Weingarten et al., 1975).  On an SDS gel, one sees (with bovine brain tau) 4 bands quite close together from (say) 58 - 64 kDa.
Interaction with tubulin is the only known 'normal' function of tau.  It promotes the polymerization of tubulin into microtubules under polymerization conditions, for example (Cleveland  et al., 1977a, 1977b).
Tau is encoded by a single gene, located on chromosome 17, and differential mRNA splicing gives rise to the brain isoforms (six in humans and four in cow) [Andreadis et al., 1989; Goedert et al., 1989; Himmler, 1989], and a single high molecular weight tau ('big tau') in peripheral tissues (Goedert et al., 1992).
Tau contains a series of imperfect amino-acid repeats, located in the C-terminus of the protein.  These repeats are thought to be responsible for microtubule binding (see, for example, Lee, 1990).
Although tau occurs in a hyper-phosphorylated state in the PHF, and may be phosphorylated in normal brain, phosphorylation is not necessary for formation of paired-helical filaments (Goedert et al., 1996).
The tau gene may be knocked out without any visible alteration of phenotype! (experiments done in mice) (Harada et al., 1994).
Mutations in the tau gene are not known to cause Alzheimer's disease, but are associated with very rare 'taupathies', such as an inherited dementia called frontotemporal dementia and Parkinsonism linked to chromosome 17 (FTDP-17; possibly identical with Pick's disease) [Hutton et al., 1994].
The crystal structure of tau has not been obtained to date.  Current thinking is that the soluble form of tau is mainly a random coil (see von Bergen et al., 2006).

The fact that tau can be knocked  without serious consequence, together with the lack of mutations causing Alzheimer's,  has led to much criticism of the tauist story.

However it still is the major structural component of the paired helical filament (neurofibrillary tangles), and must surely be a key player in the understanding of Alzheimer's disease.

This is not to imply that Aβ and tau are the only shows in town.  As stated above, the field of Alzheimer's disease is very complex

An allele of Apolipoprotein E (ε4 allele) is genetically associated with an increased risk in late-onset Alzheimer's, for example (Corder et al., 1993).

Mutations in the presenilin genes are also associated with the disease (Sherrington et al., 1995).  Presenilins form part of the γ-secretase protease complex involved in Aβ formation (see Takeo et al., 2012).

I do not know enough about these fields to comment any further (although this does not usually stop me).

It should be emphasized, however, that most cases of Alzheimer's disease are sporadic, and only a small subset has a genetic component. It is a disease of the brain, and of aging. There is no known cure, no known cause and no reliable (biochemical) pre-mortem test (although a clinic diagnosis may of course be made).

References

Andreadis, A., Brown, W. M. & Kosik, K. S. (1992) Structure and novel exons of the human tau gene. Biochemistry, 31,  10626-10633.
von Bergen, M, Barghorn, S, Jeganathan, S, Mandelkow, E.M., Mandelkow, E.  (2006) Spectroscopic approaches to the conformation of tau protein in solution and in paired helical filaments.  Neurodegener. Dis. 3, 197-206.
Cleveland, D. W., Hwo, S.-Y. & Kirschner, M. W. (1977a)  Purification of tau, a microtubule associated protein that induces assembly of microtubules from purified tubulin. J. Mol. Biol. 116, 207-225
Cleveland, D. W., Hwo, S.-Y. & Kirschner, M. W. (1977b)  Physical and chemical properties of purified tau factor and the role of tau in microtubule assembly. J. Mol. Biol. 116,  227-247.
Corder, E.H., Saunders, A.M., Strittmatter, W.J., Schmechel, D.E., Gaskell, P.C. Small, G.W. Roses, A.D., Haines, J. L. & Pericak-Vance, M.A. (1993) Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families. Science 261, 921-923.
Goedert, M., Wischik, C. M., Crowther, R. A., Walker, J. E. & Klug, A. (1988)  Cloning and sequencing of the cDNA encoding a core protein of the paired helical filament of alzheimer disease:  Identification as the microtubule associated protein tau. Proc. Natl. Acad. Sci. USA  85, 4051-4055. [pdf]
Goedert, M., Spillantini, M. G., Jakes, R., Rutherford, D. & Crowther, R. A. (1989) Multiple isoforms of human microtubule associated protein tau:  sequences and localization in neurofibrillary tangles of alzheimer's disease  Neuron 3, 519-526.
Goedert, M., Spillantini, M. G. & Crowther, R. A. (1992) Cloning of a big tau microtubule associated protein characteristic of the peripheral nervous system. Proc. Natl. Acad. Sci. USA 89, 1983-1987. [pdf]
Goedert, M., Jakes, R., Spillantini, M. G, Hasegawa, M., Smith, M.J. & Crowther, R. A. (1996) Assembly of microtubule-associated protein tau into Alzheimer-like filaments induced by sulphated glycosaminoglycans. Nature, 83, 550-553.
Harada, A., Oguchi, K., Okabe, S., Kuno, J., Terada, S.,  Ohshima, T., Sato-Yoshitake, R., Takei, Y., Noda, T. & Hirokawa, N. (1994). Altered microtubule organization in small-calibre axons of mice lacking tau protein. Nature 369,  488-491
Himmler, A. (1989)  Structure of the bovine tau gene:  alternatively spliced transcripts generate a protein family. Molec. Cell. Biol.  9,  1389-1396.[pdf]
Hutton, M., Lendon, C. L., Rizzu, P., Baker, M., Froelich, S., et al. (1998) Association of missense and 5'-splice-site mutations in tau with the inherited dementia FTDP-17. Nature  393, 702-705.
Kidd, M. (1964) Alzheimer's disease - an electron microscopical study. Brain 87,  307-320.
Kosik, K. S. & Greenberg, S. M. (1994)  Tau protein and alzheimer disease. In Alzheimer Disease.  Terry, R. D., Katzmann, R. & Bick, K. L., eds.  pp 335-344.  Raven k. Press, New York.
Lee, G. (1990) Tau protein:  an update on structure and function. Cell Motil. Cytoskel. 15, 199-203
Lee, V. M.-Y., Balin, B. J., Otvos, L. & Trojanowski, J. Q. (1991) A68:  A major subunit of paired helical filaments and derivatized forms of normal tau. Science 251,  675-678.
Lowery, D.E., Pasternackj, J.M., Gonzalez-DeWhitt, P.A., Zurcher-Neely, H.
Tomich, C-S. C., Altman, R.A., Fairbanks, M. B., Heinrikson, R. L.
Younkin, S. G.  & Greenberg, B. D. (1991) Alzheimer’s Amyloid Precursor Protein Produced by Recombinant Baculovirus Expression. Proteolytic Processing And Protease Inhibitory Properties.  J. Biol. Chem. 266, 19842-19850.  pdf
Price, D. L. & Sisodia, S. S. (1998) Mutant genes in familial alzhiemer's disease and transgenic models. Annu. Rev. Neurosci. 21, 479-505.
Sherrington, R, Rogaev, E.I, Liang, Y, Rogaeva, E.A, Levesque, G, Ikeda, M, Chi, H, Lin, C, Li, G, Holman, K, Tsuda T, Mar, L, Foncin, J.F, Bruni, AC, Montes,  M.P, Sorbi, S, Rainero, I, Pinessi, L, Nee, L, Chumakov, I, Pollen, D, Brookes, A, Sanseau, P, Polinsky, RJ, Wasco, W, Da Silva,  H.A, Haines, J.L, Perkicak-Vance, M.A, Tanzi, RE, Roses, A.D, Fraser, PE, Rommens, J.M, St George-Hyslop, P.H. (1995)  Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease. Nature, 375, 754-760.
Takeo, K, Watanabe, N, Tomita, T, Iwatsubo, T.  (2012)  Contribution of the γ-Secretase Subunits to the Formation of Catalytic Pore of Presenilin 1 Protein.  J. Biol. Chem. 287, 25834-25843
Weingarten, M. D., Lockwood, A. H., Hwo, S.-Y. & Kirschner, M. W. (1975)  A protein factor essential for microtubule assembly. Proc. Natl. Acad. Sci. USA  72, 1858-1862. [pdf]
Wischik, C. M., Novak, M., Edwards, P. C., Klug, A., Tichelaar, W. & Crowther, R. A. (1988)  Structural characterization of the core of the paired helical filament of alzheimer disease. Proc. Natl. Acad. Sci. USA,   85, 4884-32768. [pdf]
Wisniewski, H. M., Merz, P. A. & Iqbal, K. (1984) Ultrastructure of paired helical filaments of Alzheimer's neurofibrillary tangle. J. Neuropathol. Exper. Neurol.,  43,  643-656.


Immunotherapy for tumours which do not have TSA

Yes, in some circumstances.

In some cases the antigen being targeted, even if it leads to loss of normal cells, can be targeted. This is most evident in the targeting of CD19 to treat various forms of B-cell derived tumours. Example of such an application and response biomarkers are described here
https://www.ncbi.nlm.nih.gov/pubmed/28291388

Secondly, opportunities may be created by the generation of epigenetic states. Cancer-germline antigens are usually only expressed in gonad tissues (which enjoy immune privilege) but are often aberrantly reactivated in tumours, but not in other somatic tissues. This too can create specificity to immunotherapy even if the antigen is not truly tumour-specific, and is rather striking as a phenomenon in testicular cancer.

https://www.ncbi.nlm.nih.gov/pubmed/28555838


Effect of nerve pills and relationship to Shingles

I gather you are talking about anti-axiety drugs (anxiolytics). Benzodiazepines is one of the major groups of anxiolytics, and includes Xanax. Benzodiazepines are central nervous depressants, meaning that they reduce the activity of neurotransmitters in the brain. They do this by binding to the GABA-A receptor and enhancing the effect of the inhibitory neurotransmitter GABA when it binds to the same receptor. The binding of GABA to a GABA receptor on a neuron causes hyperpolarization of the neuron by ion flow through the cellular membrane and decreases the chance of an action potential. So yes, nerve pills act by supressing the nervous system.

As for your question about interaction with Shingles, I think that's considered off-topic under the personal medical questions policy.


What kind of caterpillar type bug is this?

Likely to be a black carpet beetle larvae

http://www.ipm.ucdavis.edu/PMG/PESTNOTES/pn7436.html

For more facts try: http://www.ipm.ucdavis.edu/PMG/PESTNOTES/pn7436.html
Don't worry though, they live everywhere!

Wikipedia has some info on the family of beetles that they belong to (http://en.wikipedia.org/wiki/Dermestidae). I don't think they really cause any harm, except in natural history museums where they tend to munch the collections of animals...although this can also be a good thing:

'They are used in taxidermy and by natural history museums to clean animal skeletons' 1

1 VanClay, Mary. "Bitten By the Bug". www.johnsonstring.com. Retrieved November 10, 2012.


What is the active site (not metal binding site) of tyrosinase and other monooxygenase/oxidoreductases?

Tyrosinase uses two copper ions as cofactors. The copper binding site is the enzyme active site.

The active site of the crystal structure of tyrosinase from Streptomyces sp. (PDB code: 3AWT) is shown below. Note the two copper ions (coordinated by active site histidine amino acid residues) and an oxygen atom (of a water molecule) bound to the copper ions:

Matoba et al. (2011) J Biol Chem 34: 30219-30231.

  The Cu(II)-soaked crystal structure of tyrosinase ... possesses two
  copper ions at its catalytic center.


DNA polymerase in PCR (polymerase chain reaction)

No, this does not happen, as the DNA polymerases used for PCR are DNA dependent. This means that they only synthesize DNA when it is bound to DNA. Even if your primers bind to the RNA, the polymerase will not starting new strands here. To use RNA as a template for PCR you first need to reverse transcribe it.


Why do some people have cold hands and some have warm?

Though I haven't heard of people having warm hands in cold temperatures (unless your using a hot pack or something), there are biological explanations for cold hands.

  Having cold hands even when you're not in a cold environment is
  common. Often, having cold hands is a part of your body's natural
  response to regulate your body temperature and shouldn't be cause for
  concern.

  But if you have persistently cold hands, particularly if accompanied
  by color changes, it could be a warning sign. For example, having cold
  hands could mean you have a problem with the nerves or blood
  circulation or a problem with tissue damage in your hands or fingers.
  If you are outside in extreme cold weather and you have cold hands,
  you should watch for warning signs of frostbite.
  - MayoClinic

Other than frostbite, there are also reports of the Reynaud's disease.

Sources:
Clinic
CNN


Simulating DNA sequences in R with a given value of $\theta = 4N_{e}\mu$

There are a number of tools but I don't know any that comes with an R library. They are usually all called from the command line. I don't either of any that produce FASTA file. SimBit (my own software) can produce vcf files which can easily be converted into FASTA with PGDspider.

However, if your simulations are so easy, you might not need these individual-based softwares. Just write the code yourself. It might only be take a few tens of lines. Here is a simple example

freq = 0.1 # initial frequency
N = 1000   # Constant population size
mu = 1e-7  # mutation rate

for (generation in 1:nbGenerations)
{
   # Drift
   freq = rbinom(1,N,freq) / N

   # Mutations
   oneWayMutations   = rbinom(1,N*freq,mu) / N
   otherWayMutations = rbinom(1,N*(1-freq),mu) / N
   freq = freq - oneWayMutations + otherWayMutations
}

If you need something more complex (such as several loci), then you should probably use one of the existing individual-based software. See the post Sequence evolution simulation tool


In fact, there are two T2 hormones, depending on the position of iodine atoms on the thyronine backbone molecule [5].
One of them, 3,5-diiodothyronine (3,5-T2) is the most active of all thyroid hormones with a relative T4 potency of 8 to 15. Thereby, it is 2 to 5 times as potent as T3. Its plasma concentration is rather low, however, being 0.2 to 0.37 nmol/l [1–3]. It is weakly bound to plasma proteins and has a short half-life [7, 8]. 3,5-T2 seems to be a risk factor for atrial fibrillation [3], and it is able to suppress pituitary thyrotropin (TSH) secretion [4]. It is upregulated in critical illness (NTIS/TACITUS) [1, 3, 6].
The second isomer, 3’,5’-T2 is an inhibiting thyroid agent that is able to block the activity of deiodinases and receptors for thyroid hormones, similar to reverse-T3 (rT3) [5].

References

Pinna G, Meinhold H, Hiedra L, Thoma R, Hoell T, Gräf KJ, Stoltenburg-Didinger G, Eravci M, Prengel H, Brödel O, Finke R, Baumgartner A. Elevated 3,5-diiodothyronine concentrations in the sera of patients with nonthyroidal illnesses and brain tumors. J Clin Endocrinol Metab. 1997 May;82(5):1535-42. PMID 9141546. https://pubmed.ncbi.nlm.nih.gov/9141546/
Lehmphul I, Brabant G, Wallaschofski H, Ruchala M, Strasburger CJ, Köhrle J, Wu Z. Detection of 3,5-diiodothyronine in sera of patients with altered thyroid status using a new monoclonal antibody-based chemiluminescence immunoassay. Thyroid. 2014 Sep;24(9):1350-60. doi: 10.1089/thy.2013.0688. Epub 2014 Aug 1. PMID: 24967815. https://pubmed.ncbi.nlm.nih.gov/24967815/
Dietrich JW, Müller P, Schiedat F, Schlömicher M, Strauch J, Chatzitomaris A, Klein HH, Mügge A, Köhrle J, Rijntjes E, Lehmphul I. Nonthyroidal Illness Syndrome in Cardiac Illness Involves Elevated Concentrations of 3,5-Diiodothyronine and Correlates with Atrial Remodeling. Eur Thyroid J. 2015 Jun;4(2):129-37. doi: 10.1159/000381543. PMID 26279999. https://pubmed.ncbi.nlm.nih.gov/26279999/
Pietzner M, Lehmphul I, Friedrich N, Schurmann C, Ittermann T, Dörr M, Nauck M, Laqua R, Völker U, Brabant G, Völzke H, Köhrle J, Homuth G, Wallaschofski H. Translating pharmacological findings from hypothyroid rodents to euthyroid humans: is there a functional role of endogenous 3,5-T2? Thyroid. 2015 Feb;25(2):188-97. doi: 10.1089/thy.2014.0262. PMID 25343227. https://pubmed.ncbi.nlm.nih.gov/25343227/
Hoermann R, Midgley JE, Larisch R, Dietrich JW. Homeostatic Control of the Thyroid-Pituitary Axis: Perspectives for Diagnosis and Treatment. Front Endocrinol (Lausanne). 2015 Nov 20;6:177. doi: 10.3389/fendo.2015.00177. PMID: 26635726; PMCID: PMC4653296. https://pubmed.ncbi.nlm.nih.gov/26635726/
Langouche L, Lehmphul I, Perre SV, Köhrle J, Van den Berghe G. Circulating 3-T1AM and 3,5-T2 in Critically Ill Patients: A Cross-Sectional Observational Study. Thyroid. 2016 Dec;26(12):1674-1680. PMID 27676423. https://pubmed.ncbi.nlm.nih.gov/27676423/
Louzada RA, Carvalho DP. Similarities and Differences in the Peripheral Actions of Thyroid Hormones and Their Metabolites. Front Endocrinol (Lausanne). 2018 Jul 19;9:394. doi: 10.3389/fendo.2018.00394. PMID: 30072951. https://pubmed.ncbi.nlm.nih.gov/30072951/
Köhrle J, Lehmphul I, Pietzner M, Renko K, Rijntjes E, Richards K, Anselmo J, Danielsen M, Jonklaas J. 3,5-T2-A Janus-Faced Thyroid Hormone Metabolite Exerts Both Canonical T3-Mimetic Endocrine and Intracrine Hepatic Action. Front Endocrinol (Lausanne). 2020 Jan 8;10:787. doi: 10.3389/fendo.2019.00787. PMID: 31969860; PMCID: PMC6960127. https://pubmed.ncbi.nlm.nih.gov/31969860/


How is haemophilia dominant in human females?

X-linked Hemophilia is caused by the lack of production of the clotting factors VIII or IX. It is not inherited dominantly, but instead inherited in an X-linked recessive manner.
These proteins are produced in multiple regions around the body. In a female heterozygous for the gene coding for Factor VIII or IX, X-inactivation would randomly prevent one of the chromosomes from expressing its allele. Therefore, the production of active Factor VIII or IX would only occur in half the cells which have the faulty allele inactivated.
However, half the production of the relevant factor results in a close to normal phenotype, as the hemophilic phenotype would not manifest unless the clotting factor activity levels are very low.
This Medscape article on hemophilia states that:

Normal values for FVIII assays are 50-150%. Values in hemophilia are as follows:
Mild: >5%
Moderate: 1-5%
Severe: < 1%

Therefore, despite X-inactivation reducing the production of clotting factors by 50%, the heterozygous female still displays the healthy, non-hemophilic phenotype.
While the clotting factor concentration can only be reduced to approximately 50% of normal, it is still possible for heterozygotes to suffer from mild hemophilia. This is because other genetic factors may also affect the hemophilia phenotype.
For example, the gene encoding FVIII may have point mutations which reduce the effectiveness of the protease, therefore reducing activity levels below the expected 50%. Mutations in regulatory elements or interacting proteins may also result in hemophilia due to the regulatory elements downregulating the expression or activity of the protein.

Approximately 40% of cases of severe FVIII deficiency arise from a large inversion that disrupts the FVIII gene. Deletions, insertions, and point mutations account for the remaining 50-60% of the F8C defects that cause hemophilia A.
Low FVIII levels may arise from defects outside the FVIII gene, as in type IIN von Willebrand disease, in which the molecular defect resides in the FVIII-binding domain of von Willebrand factor.


See here. Bacto is a brand which used to be marketed by Difco. It is a casein (milk protein) hydrolysate.


Relationship between our microbiome and personalized nutrition

does the microbiome affect food metabolism?

Most definitely (and not surprisingly). The Arumugam paper [1] notes that

The drivers of [enterotype 1] seem to derive energy primarily from carbohydrates and proteins through fermentation, … because genes encoding enzymes involved in the degradation of these substrates (galactosidases, hexosaminidases, proteases) along with glycolysis and pentose phosphate pathways are enriched in this enterotype […]
Enterotype 2 … is enriched in Prevotella … and the co-occurring Desulfovibrio, which can act in synergy to degrade mucin glycoproteins present in the mucosal layer of the gut […]
Enterotype 3 is […] enriched in membrane transporters, mostly of sugars, indicating the efficient binding of mucin and its subsequent hydrolysis as well as uptake of the resulting simple sugars by these genera. […]
The enriched genera indicate that enterotypes use different routes to generate energy from fermentable substrates available in the colon, reminiscent of a potential specialization in ecological niches or guilds. In addition to the conversion of complex carbohydrates into absorbable substrates, the gut microbiota is also beneficial to the human host by producing vitamins. Although all the vitamin metabolism pathways are represented in all samples, enterotypes 1 and 2 were enriched in biosynthesis of different vitamins […]

[All emphasis mine.]

is the food that we eat affecting the microbiome?

Yes, just as certainly. I don’t have a publication handy but it should be obvious that our food influences our gut microbiome – in the extreme case, it can kill it (consider antibiotics side effects).
[1] Manimozhiyan Arumuga, Jeroen Raes & al., Enterotypes of the human gut microbiome, Nature 473, 174–180, May 2011.


According to this Psychology Today blogpost, it is quite likely that animals can dream.  Particularly mammals that according to the blogpost:

  All mammals share the same neural structures that are important in sleeping and dreaming.

However, for your second question, I do not think it is at all possible to know what they are dreaming about (if they indeed do dream).


Can HIV be transmitted via breastfeeding?

Yes, it is possible and the chances are pretty high. According to the WHO paper linked below, the rate of partially or completely breastfed children which get infected by this route is about 20-35%, while the rate of children which are not infected and doesn't get breatfed is zero (no surprise here).

The mechanism by which this infection occurs is currently unknown, but it is hypothesized that the virus enters via the mucosa. See these two articles below for more information:

A review of HIV transmission through breastfeeding.
HIV transmission through breastfeeding : a review.


Can a chicken really be hatched outside of the egg?

Yes it is real, in the sense that this protocol has been through a peer reviewed journal.

Note that the embryo is developing outside the shell, not outside the egg. It is the fertilized egg that develops into the embryo. The shell only provides protection and allows exchange of gases. You can replace the shell with any other material that does the same job. Embryos of non-placental animals can grow in a petridish as well. Someone seems to have done this back in the 1980s (Scadding, 1981).

You can see a video along with the detailed protocol of this process in this article published in the Journal of Visual Experimentation.

  Why do I never see an embryo in my frying pan?

Because it has probably become an omelette.

  how warm do the eggs have to be?

37-39oC is the ideal temperature and usually hen eggs hatch in 21 days (common poultry facts). However, the incubation time can depend on other factors (including temperature) such as humidity and air composition.


Why spider's web don't burn when electricity touches it?

Spider silk can conduct electricity. Some spiders use this material property of conductivity to capture prey. https://www.ncbi.nlm.nih.gov/pubmed/24323174

So I'm going on the assumption that both electrical lines spanning the web are bare and that they are live, i.e. carrying current. I will also assume that these lines are carrying the same current.

With electricity, it might help to think of the analogy of a waterfall. Water at the top of a waterfall has potential energy, which is converted to kinetic energy when it goes over the waterfall. The water accelerates towards the earth as it falls. There is a height or "gradient" between the top of the waterfall and its bottom, which allows water to accelerate from the top towards the bottom of the fall.

Electrons in electricity work in much the same way. Between two points along a conductor, you need a voltage gradient to establish an electric field, which moves electrons in a particular direction — just as the waterfall creates a gradient of high ground to low ground that enables water to flow.

If you have two wires (both conductors) running at the same voltage, and if you connect them with another conductor, like a spider's web, electrons will not run through the web because there is no voltage differential that creates an electric field that drives the flow of electrons between that connection. https://en.wikipedia.org/wiki/Electric_potential

Here, the web and spider are likely unhurt, because the two lines do not provide a voltage difference needed to have electrons move across the silk, like water would flow over a waterfall.

If the spider web was grounded — if its web were instead connected from one of the electrical wires to the earth — electricity would likely run through the web and, potentially, burn the web (and the spider). But from your photograph, it looks like the web is connected to both wires that ℗r assumption) are at the same voltage.

This is the same principle that allows electricians to work on maintaining electrical pylons without shutting down the power grid. https://en.wikipedia.org/wiki/Live-line_working

They work in such a way as to maintain the same voltage as the lines they are working on. If they were grounded — if they held a copper wire, say, that was plugged into the earth — or if there was anything conductive that the electrician was connected to that established a dangerous voltage gradient, and if they started working on live electrical lines, they would get fried. Same with the spider, if the web was grounded in a similar way.

Further, if the two wires were running at different voltages, then electricity could conduct through the spider web and cause some damage.

This answer relies on a lot of assumptions from the photograph. Feel free to clarify if those assumptions would change the parameters of the question and my answer.


Those are the break points of the inversion. So chromosome 4 was cut at p13 and q22 and the fragment was reinserted in the reverse direction, giving a pericentric inversion.


What is Mendelian Randomization, and how is it used to infer causality in epidemiology?

Epidemiological studies analyze human observational cohort data to try to statistically link disease risk and biomarkers. For instance, it is know a well know fact that smoking increases the risk of lung cancer, yet before the 1950s it was widely considered otherwise until observational evidence proved irrefutable (Levin, 1950).

Confounding

However, inferring causality using observational data can be tricky. For instance, there is a very strong statistical association between ice-cream sales and risk of drowning in the UK. In this example it is quite clear that the association is confounded - that is, there is a 'hidden' variable we have not accounted for that links the 2. It is easy to infer that ice-cream sales don't increase your risk of drowning, but the 2 are correlated because both ice-cream sales and risk of drowning increase at the same time of year; both are positively correlated with 'nice weather' traits.

In the above example it is easy to say that the relationship is confounded. However, in a hypothetical study on type-2 diabetes that finds higher blood hematocrit (% volume of blood made up of red blood cells) is associated with increased odds of being diabetic, it is less clear whether higher hematocrit increases susceptibility/risk of becoming diabetic, or whether diabetes increases hematocrit. Longitudinal studies that follow the same individuals for many years help determine which came first - this is based on the assumption that if raised hematocrit is associated with increased risk of diabetes 5 years later, it is more likely that hematocrit is causal, and you have a biomarker for diabetes risk (although you still cannot say it is causal, it may just be a proxy for another 'hidden' trait, or the effect may be mediated by another unmeasured marker).

Causality

Genome-wide association (GWA) studies have become increasingly popular since the completion of the human genome project, and there are currently (15th August 2012) 7039 genetic variants (SNPs, single-nucleotide polymorphisms) documented in the catalogue of published GWA studies (www.genome.gov/gwastudies). These SNPs have been robustly associated with traits such as 'risk of type-2 diabetes', or 'blood adiponectin levels', by large genetic epidemiological studies, usually with many thousands of participants sampled.

The key point about SNP associations is that the direction of effect is always known; a particular SNP may affect your adiponectin levels, but adiponectin does not affect the SNPs you inherit.

Mendelian Randomization

In an observational study that finds an association between (for example) circulating triglyceride levels and type-2 diabetes (using fasting glucose and insulin as 'proxies') it is not possible to determine the causal direction; do triglycerides increase risk of diabetes or vice versa? (This is an actual case study by De Silva, et al. 2011).

Using the assumption that the inheritance of SNPs is essentially random (i.e. not affected by the trait you are measuring - in this example triglycerides) it is possible to determine the causal effect of triglycerides on the risk of diabetes. Note: this is only possible for traits (such as serum triglyceride levels) that have SNPs identified by GWA studies.

First of all, you have already calculated the association between triglyceride levels (in this study a 1 standard-deviation (SD) increase in triglycerides was associated, with an Odds Ratio (OR) of 2.68, with type-2 diabetes in almost 10,000 human participants). Because it is a cross-sectional study, only an association is reported, with no causal implications... yet!

Enter the SNPs

Having identified the SNPs that increase triglyceride levels (at the time of the study, 10 were reported in the literature), each participants genotype for these SNPs needs to be measured or inferred (generally this is performed in large cohort studies, which are then used for many different individual projects).

A combined 'score' is then derived for each individual. This is conceptually very simple; if an individual has 4 of the 10 triglyceride raising alleles, they are given a score or 4, and so on. This is complicated by the fact that the SNPs have different effects on the triglycerides, so a 'weighted allele score' is derived instead (simply put, the coefficient of the SNP~triglyceride association is taken into account when adding risk allele scores). By using this kind of score, a 'per allele' estimation of the effects can be estimated;

The association between the triglyceride levels and the allele score is then determined (by linear regression analysis - adjusted for age and sex, as these are known to affect triglycerides). There are actually 2 ways of performing the next analysis, the first of which is conceptually simpler, but the second of which is more robust.

Method 1: the 'triangulation' approach

The two observed associations calculated so far (per-SD trig. levels are associated with diabetes, and the per-allele SNP score are associated with per-SD trig. levels) can then be used to calculate an expected association. This is simply derived by multiplying the 2 coefficients together. Below is the 'triangulation' representation of this;

This expected association between the triglyceride-raising SNPs and risk of diabetes is only true if raised triglycerides increase the risk of diabetes. The observed association between the SNP-score and diabetes can then be calculated. If the expected and observed estimates are similar, then triglycerides raise diabetes risk, and are a causal biomarker. If the observed association is null (or, at least, much smaller), then triglycerides are likely to be secondary.

Method 2: the instrumental variable analysis

This method is for the more hardy statisticians. Instrumental variables are derived variables, and represent an intermediate between a proposed 'cause' and the 'effect', or outcome (in this case the triglyceride raising alleles are proposed to 'cause' diabetes, and this is mediated by the triglyceride levels themselves).

Using a linear regression, the "fitted values" from a model with triglyceride levels as the outcome, and the weighted SNP score as the only independent variable, are extracted. These fitted values represent the variance in the triglycerides that is predicted by the SNP score. We are using the SNPs as the instrument here, as they directly influence the biomarker (exposure, i.e. triglycerides), and are not affected by either the exposure or the outcome (diabetes). The important assumption here is that the effect of the SNPs on the outcome is not confounded, and can only be mediated by the exposure - this is true for genotypes (Lawlor, et al. 2008).

By then determining the association between the derived variable and diabetes, you will know whether the proportion of the triglyceride variance predicted by the SNPs is associated with diabetes - if so, then triglycerides increase the risk of diabetes.

Results

The study performed both types of Mendelian Randomization analysis and found no evidence to suggest a causal association between triglycerides and diabetes phenotypes.

So Mendelian Randomization is a useful tool for inferring causality with biomarkers. It is not necessarily conclusive evidence, but it can help distinguish biomarkers of particular importance and interest (with regard to interventions) from those that are just markers of the disease.


As electrons are moving through the ETC, how is ATP produced for the active transport to even happen?

ATP formation is done using the Complex V called as ATPsynthase (also called as F0/F1 particle) and the theory explaining this process is called as the Chemiosmotic Theory2.

During cellular respirationKreb’s cycle (in the mitochondria) and Light dependent Photophosphorylation photosynthesis (in the chloroplast thylakoids) a set of reactions establish a proton gradient across the inter-membrane space ( hereby referred to as IMS) of the mitochondria/chloroplast( if you remember mitochondria/chloroplast are double membrane bound organelles).

Just as in a battery/cell we have EMF(electron motive force) we have, in the IMS of the mitochondrion/chloroplasts, a proton motive force.

Since substances always flow from higher potential to lower potential, the IMS of mitochondrion/chloroplast having a high amount of protons is a region of high potential and lumen of mitochondrion/chloroplast is a region of low potential since there are less number of protons.

The only way protons can move from the IMS  of the mitochondrion/chloroplast to the lumen of the mitochondrion/chloroplast is via the complex V (also known as ATPsynthase).

The ATPsynthase is a lollipop shaped protein structure that is freely rotatable and it brings ADP & phosphate molecules close together so that a covalent bond can be formed in between them.

How does it exactly do this you ask?
So let’s summarise what all we have here:

ATPsynthase that can rotate about its rotor.
Proton gradient across the IMS ( high potential) and the lumen ( low potential).
The only way out for the protons is via the ATPsynthase.

Now we can see a link here.

So what happens is, there’s the F0 subunit of the ATPsynthase through which the protons are able to move across the membrane and during that movement the rotate the F1 subunit.
During this rotation shown in animation here  the ADP & the phosphate group which are present in the active site of the F1 subunit are brought near each other and due to atomic interactions a bond is formed.
The mechanical energy ( movement of protons across the membrane) is converted into chemical energy ( covalent bond) between the two molecules.
This is the process via which the currency of the cell, ATP, is produced.
Hope that answers the question.


As Karl mentioned in his comment, this is a jumping spider in the family Salticidae.

Based on your location and the coloration, I would suppose this might be Phidippus adumbratus.

 Source: Wikimedia

You can see more pictures here and here.

I don't think the angle nor zoom quality of your photo can be used to definitively ID your specimen to species. However, as you can see in the photo above, P. adumbratus is not a bad candidate.

According to Edwards (2004) this genus is sometimes difficult to tell apart, but P. adumbratus can be distinguished from other Phidippus species as follows:

  Males can be distinguished from the closely related P. boei (and all other species of Phidippus in California except P. aureus) by the orange scales dorsally on both carapace and abdomen (P. boei is black with a red abdomen dorsally), although island populations have the OQ scales darker and reduced in number. P. adumbratus has a much longer, narrower embolus apical portion than P. aureus. Females can be distinguished from P. kastoni by the shape of the internal ducts of the epigynum; the duct heads are narrow in P. adumbratus (broad in P. kastoni) and the gland is visible as a rounded projection on the anterodorsal surface of the duct head (not visible in P. kastoni). Females are covered dorsally with orange or gray scales (usually with white abdominal spots), unlike the females of P. boei, which have a similar epigynum but are black in color without markings, or with red dorsal scales only on the abdomen (without spots).

If you'd like a much more detailed of description of P. adumbratus (or others in this genus), you can find whole-page detailed descriptions in Edwards's publication quoted and linked above.

A map of geo-referenced records from GBIF shows the occurrence of this species in southern California:

Edwards, G.B., 2004. Revision of the jumping spiders of the genus Phidippus. Occasional Papers of the Florida State Collection of Arthropods, 11.


What could the etymology of Phallodriline be?

-o- linking vowel indicates Greek. -i- is Latin, unless the second word starts with a vowel (many -ectomy words for example). This is irrespective of declension or gender. Weird I know.

In fact, Latin phallus is from φαλλός.

The second part is worm δρῖλος (drilos). Actually it can also mean penis, but let's gloss over that...


Does prolonged exposure to low pitch but low volume noise affect hearing or stress?

Basically you are asking: (1) does the low-pitch noise affect my hearing sensitivity; (2) has the noise aggravated hearing loss acquired earlier in life; (3) if the noise can induce stress and (4) if the noise may cause tinnitus (kind of a hidden question).

(1) Is the ventilator noise damaging?: Noise-induced hearing loss typically occurs at high sound levels. Occupational safe noise levels are set at around 85 dB SPL (Nat. Stand. Occupational Noise). This is comparable to listening to traffic on a busy road from 10 meters away for 8 hours/day for 5 days/week (see wiki on sound levels), or a diesel truck at 15 meters going 64 km/h. If you can still talk normally, the noise cannot be much more than 60 dB SPL, which is normal conversational level (see sound chart). So the ventilation noise is not bad for your ears as it is well below 85 dB SPL.

(2) Does the noise aggravates present damage?: Similarly to the answer under (1), the noise is not loud enough to be regarded damaging even with existing hearing loss.

(3) Does it cause stress? As @anongoodnurse suggested: yes it causes stress, apparently. Every unpleasant sensation will do so to a certain level.

(4) Effects of the noise on tinnitus: Typically, tinnitus is caused by hearing loss (see cause of tinnitus) and the pitch of tinnitus often coincides with the lost frequencies (see cause and effect of tinnitus). So if your "bad behaviors" at youth refer to loud music, then it is probably noise-induced hearing loss that has resulted in a dip at your hearing acuity at 4 kHz (the 4-kHz notch). In effect, the tinnitus you are experiencing will be around this frequency and therefore high-pitched. As the loudness of the ventilator is too low to cause damage, it is probably unrelated to your tinnitus.


Is the variance of a trait related to its rate of evolution?

The question can be understood in different ways
Causality
I think the question is a bit unclear in using the term associated in terms of what is being causal. Is the interest to understand how do processes that affect speed of evolution also affect phenotypic variance or is the question `how does a change in phenotypic variance affect the speed of evolution.
What is meant by speed of evolution
Speed of evolution has no strict definition. Or rather it has two standard definitions and it can be measured in Haldanes or in Darwins (which are units).
Quite often by "speed of evolution" authors mean "response to selection over medium to long term" as for example in the wiki article for rate of evolution.
Below I am answering to two different questions.
How does processes that affect "speed of evolution" at neutral sequences also affect phenotypic variance
At neutral sequences, the rate at which mutations fixes is equal to the mutation rate (see this answer for explanation). And all else being equal (typically without changing the mutational effect), high mutation rate leads to high phenotypic variance.
How does a sudden change in the phenotypic variance affect the response to selection in regard to this trait?
I think you pretty much said it all. I will just rephrase what you just said with a few simple equations.
Breeder's equation and heritability
The response $R$ to selection $S$ is given by
$$R=S h_N^2$$
, where $h_N^2$ is the heritability in the narrow sense. This above equation is known as the breeder's equation and is a fundamental result from quantitative genetics. The heritability in the narrow sense is defined as
$$h_N^2 = \frac{V_A}{V_P}$$
, where $V_A$ is the additive genetic variance and $V_P$ is the phenotypic variance.
Partitioning phenotypic variance
So it feels like increasing $V_P$ would decrease $h_N^2$ and therefore the response to selection $R$, but that would be very naive as $V_P$ is not independent of $V_A$. It is quite standard to decompose the phenotypic variance into genetic ($V_G$) and environment variances ($V_E$) $\left(V_P = V_G + V_E\right)$. Of course in reality, we should take into account variance due to other factors such as epistasis or developmental noise for example and all of their covariances. The genetic variance can further be decomposed into additive genetic variance $V_A$ and dominance genetic variance $V_D$ $\left(V_G = V_A + V_D\right)$.
Interdependence between $V_P$ and $V_A$
$V_P$ is a function of $V_A$. So as currently stated, it is impossible to answer the question by a simple yes or no. The shortest correct answer would probably be "The response to selection will decrease if the increased variance is not (not mainly) related to increase in additive genetic variance".
To be perfectly accurate, let $\Delta_P$ be the increase phenotypic variance and $\Delta_A$ be the increased genetic additive variance such that $\Delta_P > \Delta_A$. All else being equal the increase in $V_P$ will cause faster response to selection if and only if $\frac{Va+\Delta_A}{V_P+\Delta_P} > \frac{Va}{V_P}$. Isolating the term of interest $\Delta_P$, we got
$$\Delta_P < \frac{\Delta_A V_P}{V_A} = \frac{\Delta_A}{h_N^2} $$
In other words, all else being equal, an increase of phenotypic variance of $\Delta_P$ above the original variance $V_P$ increases the response to selection if and only if this increase is lower than the increase in additive genetic variance $\Delta_A$ multiplied by the inverse of the original heritability (heritability before a change in phenotypic variance occured)."


What physics knowledge can be applied to biology of organisms and ecosystems?

This question is really asking for examples, and the list of ways that knowledge of physics can be used in biology could be very long. However, here are a couple of examples:

Systems ecology, especially with regard to energy and nutrient flow.
This type of ecology can be strongly influenced by physics. For one example see the book Theoretical Ecosystem Ecology: Understanding Element Cycles by Ågren & Bosatta (Ågren was originally a physicist)
Physical limitations to growth and transport
This can include for instance mechanical contraints on plant growth (see e.g. the book Plant Physics by Nicklas & Spatz), water transport in trees (see e.g. this BioSE question) or the biomechanics of movement (see e.g. Hudson et al (2012) on the speed and movement of cheetahs or Wikipedia: Biomechanics).
Allometric relationships between organisms, e.g. with regard to metabolism
To explain these types of relationships knowledge in physics is useful. See e.g. Kleiber's law for more.
MAXENT as a general approach to ecological patterns or to model species distributions
This is basically a tool lifted from physics that can be applied to ecological problems. There are many papers to look at, but Harte & Newman (2014) (Harte is another previous physicist) and Elith et al (2010) are two good starting points.
Dynamical modelling of populations and communities
This field use many of the same tools for analysis as physics, e.g. systems of differential equations. One of the pioneers in this field (among many) were Robert May (also started with a PhD in physics), and his classical book Theoretical Ecology: Principles and Applications is still a good starting point.
Energy harnessing and conversion by organisms
This can refer both to how organsims convert prey to energy (e.g. conversion efficiencies) and the physics of photosynthesis (which is an interesting intersection between physics and molecular biology). See Jang et al (2004) and O'Reilly & Olaya-Castro (2013) for examples of the how quantum mechanics can inform us about photosynthesis.

Hopefully this will give you a sense of some different ways that knowledge in physics can be useful for biology.


No one knows if a uterus is capable of producing so-called "Y-eggs", because in persons affected by sex chromosome abnormalities (XXX and more, XXY, X, XYY, etc.), the presence of a functional Y generally produces a male phenotype, whether or not they are sterile or have natural levels of testosterone, because the Y contains the sex-determining gene SRY and other male developmental and fertility factors. In contrast, people with only X chromosomes (regardless of the number) are generally female-appearing, with at least some development of the associated organs and structures.

A second question is whether a male-derived stem cell could be coaxed, hormonally and otherwise, to become a uterus in the first place. An X is already present, so all the purely genetic (though not necessarily epigenetic) instructions are there, but, as far as I know, the question of whether a Y would interfere with the development process has not been answered in humans.


What is the name of this bush with red fruits?

It is Arbutus unedo, called "strawberry tree" in English, "arbousier" in French and "medronheiro" in Portuguese. The fruits are ripe around October or November. They are full of little seeds, but if you bear the annoyance, they can be quite tasty. They are used to distill an alcohol in Portugal.


They do that because a bacterium contains all the molecules required for life, that is they are a source of amino acids, lipids, glucids and nucleic acids. This is the same reason why we eat in the first place: we need a source of these molecules to survive or, in other words, to allow our cells to carry out their tasks such as replicating the DNA or producing proteins.

Bacteria can kill other bacteria by a kind of infection: the predator bacterium enters a bigger prey and then start consuming the prey's molecules. By the same token, Mycobacterium tuberculosis enters the macrophages and used them for its own biochemistry, for instance.

Interestingly, this process of bacterial predation is under scrutiny for the development of a new breed of antiseptics in the age of antibiotic resistance (see https://phys.org/news/2017-03-predatory-bacteria-antibiotic.html).


What happens to the red blood cell in CaCl₂ solution?

The reason why the cell would shrink more in CaCl2 solution is because it has a higher van't Hoff factor i.e. total number of dissociated ionic species per solute molecule (it is 2 for NaCl whereas it is 3 for CaCl2).

(Nonionic solutes do not dissociate and will therefore have a van't Hoff factor of 1)

Osmotic pressure (and other colligative properties) are proportional to van't Hoff factor. Therefore osmotic pressure in CaCl2 solution will be 3/2 times of that in an equimolar NaCl solution.

Note that the ionic chemical potential is not what drives osmosis; it is the differential concentration of water (or any other solvent) that drives it.


I would try to use the audio features of dictionaries on the internet.

Ideally you would buy a good scientific dictionary app with audio pronunciation for your iPhone, just as I have for foreign language dictionaries on mine. However, the scientific offerings I found on the app store did not fit the bill (there may be something hiding there that I missed), so I looked on the web, and what I found was:

The Science Dictionary

Now this appears not to be an actual dictionary itself, but an aggregating site. So when I searched for Chordae I got several options, mainly from Wikipedia, which did not provide audio pronunciation, but also from

Dictionary.com

which did — for both the singular (which is what is the listing) and the plural.

Dictionary.com doesn’t always provide audio pronunciations. When I tried squamous suture there was only a definition — but there were individual pronunciations for squamous and suture.

(Loop of Henle was also there with pronunciation. Perhaps going directly to dictionary.com is your best bet.)

Rider and caveat

As @JM97 mentioned in a comment, some entries in the free dictionary have audio pronunciation, although others do not. There may be other on-line facilities that do likewise. However with any on-line dictionary one should ask oneself how reliable is the pronunciation; and it is difficult to tell because one doesn’t know how it is done in the way one does with a primary dictionary with a print reputation.

For example, take the pronunciation of the word "caeca". The open dictionary pronounces this in a classical Latin style with a hard C, whereas dictionary.com. pronounces it in a mediaeval Latin style with a soft C, the way it is pronounced by scientists I know who dissect it.


To answer the question in you title, the leaves appear both on new and old growth. In addition to vegetative and floral buds, there are also dormant buds that activate themselves on old growth after leaves or branches are cut. You can read here a list of buds.

For the following questions in the text I think the answer is different for every species.