Significant presence/absence of plant species

I am not quite sure what you mean by "significant presence". If you observe any non-zero number of plants of a given species in a cluster, then the rate at which this plant occur in this cluster is different from zero. No stats required to infer such thing. You should clarify your post.

Logistic Regression

It sounds like you would like to do a logistic regression with presence / absence as response and the nominal variable cluster as solo explanatory variable. In R you could for example do something like

# Dummy data
d = data.frame(
 presence = sample(0:1, 120, replace=TRUE),
 cluster =  rep(LETTERS[1:4], 30)
)

# Logistic Regression
m = glm(data= d, formula = presence ~ cluster, family = binomial(link="logit"))
summary(m)

You can find here another example of logistic regression in R

Phylogenetic signal and pseudoreplication

You might want to make sure to decorrelate your variable from the phylogeny to avoid pseudoreplication. There, the solution you might end up going with will depend on your genetic data. If you have a genetic PCA, you could go with using the first 2 axes as simple covariates in a type I sum of squares kind of model (which is probably the default of the logistic regression I performed above). If you have a kinship matrix you could use it with lmekin or MCMCglmm (see here for adding a kinship matrix). There would have many different statistical tools for such decorrelation depending on your data.


Which cultivated plants produce most nectar for pollinators?

Lacy phacelia or purple tansy (Phacelia tanacetifolia), which can be
planted any time of year due to its short growing season. After
flowering, it is plowed into the ground to enrich the soil with
humus
All types of clovers: excellent nectar plants that plowed after
flowering and enrich the soil with nitrogen, or scythe them and use
as feed for animals
Sunflowers: after flowering, they greatly enhance the structure of
soil and enrich it with hummus
Rapeseed and poppy
Buckwheat: planted it in summer and when it fades, the seeds and
ground into flour

Scroll to page 13 (Appendix II). Here you will find a list of all significant nectar-producing plants in Europe

Scroll to page 21 for average nectar production (mg sugar/day/flower) of important agricultural crop flowers

Melliferous potential of twenty-seven plant families determined from the N data sets recorded in thirty-eight papers ranked by decreasing median values - scroll to page 5 under Table 1)

The google keywords you are looking for are along the lines of: "melliferous potential of agricultural crops in europe" and variants of this


In closely related species chromosome has only some genetic variations. Therefore there is chance of their chromosomes joins. But if interbreed occurs the species will not be fertile. The ova of female species can take the most compatible from the closest male type .

It's not like that different species can't breed, in many cases they can. For example Donkey and horse , tiger and lion, etc, but the fact is that when different species breed they do not Produce fertile offsprings. Hinney, mules, liger and other animals that are produced by breeding between different species are infertile.


Do males of all sexual species have Y chromosomes?

Very short answer
No, not all males of all sexual species have Y chromosomes. You might want to have a look to the Wikipedia page on sex-determination systems.
Long answer
Diversity among the species that reproduce sexually
Not all species that have sexual reproduction have sexes. Yeasts, for example, have mating types but no sex.
Diversity among the species that have sexes
Sex is determined by both genetic and environmental factors. In some species, genetic factors are more important than environmental factors in other species it is the reverse. Species which sex is mostly determined by the genetics are said to have GSD (Genetic Sex Determination). For example, humans are GSD, as the female is XX and the male is XY. The species where sex is mostly determined by the environment are called ESD (Environmental Sex Determination). For examples, crocodiles are ESD as sex is determined by temperature. It is important to understand however that there is a whole continuum between these two extremes.
Diversity among the species that are GSD
Among the species that are GSD, some have sexual chromosomes some don't. Some have one locus  (locus=position on a chromosome) that determines the sex, some have many loci (loci=plural of locus). Humans, for example, have sexual chromosomes (X and Y) and have only one locus which determines the sex. This locus is called SRY and it codes for a protein called TDF.
Now you can split GSD with sexual chromosomes into two more categories (it is a bit more complex in reality): XY and ZW. XY are those species where the male is heterogametic (XY), while the female is homogametic (XX). In ZW systems, the male is homogametic (ZZ) and the female is heterogametic (ZW). Birds and some plants have ZW systems for example, while mammals (except "basal" mammals) and Drosophila have XY system.
See also the post What determines sex in birds?
Extra Information
Dosage Compensation
In species that have sex chromosomes, there is a difference in the number of copy of genes between the sexes. In eutherian mammals, for example, females have two copies of all the genes on the X chromosomes, while males only have one copy of most of these genes (plus a few Y chromosome genes). The set of methods to deal with this issue is called Dosage Compensation and there is also an impressive diversity dosage compensations.
Comments on this diversity of sexual systems
The diversity in a sex-determination system, dosage compensation and other things related to sex are impressive. It is even more impressive when we look at how many independent origins there are. Below are some other examples.
The Amazon molly (a fish) is a species that have sexual reproduction but there are no males. The females have to seek for sperm in a sister species in order to activate the development of the eggs but the genes of the father from the sister species are not used. (see this article)
There are also hermaphrodites including sequential hermaphrodites (first male, then females or the opposite) in plants and animals. There are also species where populations are made of hermaphrodites and females and others where there are hermaphrodites and males (very uncommon).
In some species, the sex is determined by social factors. In clownfish, the sex is determined by comparing its own size with the size of the other fishers living in the same anemone.
In an ant species (or two species actually), males and females can both reproduce by parthenogenesis (some kind of cloning but with meiosis and cross-over) but they the meet they reproduce together and their offsprings are sterile workers. So males and females are just like two sister species that reproduce sexually to create an army to protect and feed them. See more information in this paper

Here is a nice figure from Bachtrog et al. 2014 that offers an idea of the diversity of sex determination system (thank to @rg225 for pointing out this figure).

Book suggestion
The Evolution of Sex-Determination is a great book that may interest you.


Question summary: is dam building learned or instinctive in beavers?
A blog post from 2011 references an article in the Juneau Empire titled Running water is sound of spring for beavers.  This article is no longer hosted on the Juneau Empire website, but archived versions are available.
Here's an excerpt (emphasis mine) --

Swedish biologist Lars Wilsson spent years studying captive and wild beavers, and he gained remarkable insights into their behavior. He raised beavers in an outdoor enclosure and in a large indoor terrarium ...
Wilsson initially captured four adult beavers and later he raised a number of beavers from infancy, some in small colonies with their parents and some completely isolated from adult beavers. He isolated the young beavers to see what beavers learn from their parents and what behaviors are instinctive.
He found that young beavers - who had never even seen a beaver dam - were able to build almost-perfect dams at the first opportunity.
The foundation of sticks and logs anchored to the stream bottom, the interwoven lattice of trimmed branches, the mud chinking, every aspect of dam building was hard-wired. Beavers do get more skilled at dam building as they gain experience, but the building behavior is instinctive.
Wilsson learned that the sound of running water is the cue for dam building and dam repair. In one experiment, he played a recording of running water, and the young beavers built a dam in a tank of still water in the terrarium. In another peculiar experiment, his captive beavers built a "dam" on a concrete floor against a loudspeaker that played the sound of running water.


Why are childhood cancers less frequent than infant or adult?

There are 2 main causes of cancer: "born defective" (heritable or genetic problems producing a large predisposition to cancer) and "accumulated damage" (random mutations accumulated over life).

Due to how the UK health system rations treatment (and the recent stories about Charlie Gard being prevented from traveling to the U.S. or Vatican for treatment), it's likely that the government there often "deprioritizes" (complete guess, no idea if they actually do that) infants with severe heritable/genetic problems causing near-immediate cancer. Obviously this means that those cases never live to the 05-09 age bracket.

Cancer deaths peak at 65 rather than 90 or 100 on similar statistical grounds, although late-in-life cancers are almost always due to accumulated mutations  rather than being born defective. Cancer deaths drop off after age 79 because of the relatively large die-offs in the previous few age brackets, in addition to deaths from old age and related conditions.

If there was infinite funding for health treatment and enough hospitals to match, the graph might instead match your expectations as the public would do everything to maximize survival. This means that some of the 00-04 bracket would survive to later age brackets, with the largest cause of death in those cancers being failed treatment.


The conservation biology literature has a great deal of information, particularly with reference to developing species survival plans (e.g., Traill et al. [2007] report a minimum effective population size of ~4,000 will give a 99% persistence probability of 40 generations).

Because the question specifically mentions human populations, I'll focus my answer on the genetics of small human populations, though considerably less information is available.

Hamerton et al. (1965; Nature 206:1232-1234) studied chromosome abnormalities in 201 individuals from a total population size of 268 from the small island of Tristan da Cunha. These authors report increasing chromosome abnormalities (aneuploidy; hypo- or hyperdiploidy) with age and suggest that it may result in decreased mitotic efficiency. This population is thought to have developed from a founder population of only 15. According to Mantle and Pepys (2006; Clin Exp Allergy 4:161-170) approximately two or three of the original settlers were asthmatic, which has led to a very high prevalence (32%) in the current population.

Kaessmann et al. (2002; Am J Hum Genet 70:673-685) present a more modern study of linkage disequilibrium in two small human populations (Evenki and Saami; ~58,000 and ~60,000 population sizes, respectively) compared to two large populations (Finns and Swedes; ~5 and ~9 million). The authors find significant LD in 60% of the Evenki population and 48% of Saami, but only 29% in Finns and Swedes.

Lieberman et al. (2007; Nature 445:727-731) discuss the potential for human kin detection to avoid inbreeding. Such mechanisms have been found in other species, "from social amoebas, social insects and shrimp, to birds, aphids, plants, rodents and primates." Lieberman et al. propose mechanisms contributing to sibling detection in humans, including "maternal perinatal association" and "coresidence duration." Beyond these behavioral cues, the authors also suggest physiological cues such as major histocompatability complex as playing a role.


According to the book, Principles of Animal Locomotion by R. McNeil Alexander, oscillatory movements in animals are limited by an organism's nature in general to minimize metabolic energy costs. The energy capacity, inertial, compliant, and dissipative forces involved in the muscles, tendons, skeleton, and non-actuating load all enter into this cost equation.

Strictly speaking these structures are very difficult to model with any degree of fidelity, and so are often approximated by simple mechanical lumped parameter systems of masses, springs and dashpots. From these simple systems, differential equations can be written, and the frequency that minimizes cost turns out to be the natural frequency - since at the natural frequency the system has the greatest ability to trap, store and re-use energy for the movement.

Size and compliance are therefore the two parameters that matter most. Highest oscillatory speeds are able to occur in the smallest, stiffest muscles, assuming dissipative forces are small and input energy is available.


What goes into a vaccine placebo, typically and in the specific case of Pfizer's SARS-CoV-2 vaccine trials?

Simple answer: This vaccine trial compared their trial vaccine against saline.
See the original publication by Biontech and Pfizer in the New England Journal of Medicine linked below. The relevant information can be found in the methods section:

TRIAL PROCEDURES
With the use of an interactive Web-based system, participants in the trial were randomly assigned in a 1:1 ratio to receive 30 μg of BNT162b2 (0.3 ml volume per dose) or saline placebo. Participants received two injections, 21 days apart, of either BNT162b2 or placebo, delivered in the deltoid muscle. Site staff who were responsible for safety evaluation and were unaware of group assignments observed participants for 30 minutes after vaccination for any acute reactions.

As far as I followed up the case of the allergic reactions, two of these have been observed in England. Both people had an epipen injector for such cases by hand, making it possible that they have underlying problems with allergies (as this is not a medical device people usually have at hand), no such cases have been reported from the trial. Allergic reactions are always a small risk with vaccinations which is the reason why this is done in a controlled medical environment.
As for the vaccine reactions in the placebo group, this can be caused by the nocebo effect, where expecting negative effects leads to a more negative reaction. As @BryanKrause mentioned, all possible effects reported in such trials are recorded as possible side effects. This leads to a lot of things being recorded which happened at the same time as the vaccination but have no connection to it.
Safety and Efficacy of the BNT162b2 mRNA Covid-19 Vaccine


ID mapping
This is called ID mapping. It used to be a headache as programmatic access was the only real way, but it is pretty trivial these days.
As mentioned in the comments, by far the most popular and easy method is to use Uniprot's list uploader for mapping. The corresponding publication can be found here. You must convert from Gene name to Uniprot KB ID
Programmatic access
The Uniprot web user interface will work for thousands of IDs, but is like to result in errors for queries exceeding 10,000 IDs. In that case, programmatic queries are probably better. I've slightly modified this from the Uniprot docs so that the IDs are queried 1 at a time to avoid any errors in exceeding query size. The python code would be:
import urllib,urllib2

list_to_convert = ["CHRNB2", "EGR2", "GCK", "KRT14", "LMNA", "FGF3", "TK2", "ABCC8"]
url = 'http://www.uniprot.org/mapping/'

print "From To"
for i in list_to_convert:
    params = {
    'from':'GENENAME',
    'to':'ACC',
    'format':'tab',
    'query':i
    }

    data = urllib.urlencode(params)
    request = urllib2.Request(url, data)
    contact = "" # Please set your email address here.
    request.add_header('User-Agent', 'Python %s' % contact)
    response = urllib2.urlopen(request)
    page = response.read(200000)
    print page.splitlines()[1] #Ignores the header line returned by uniprot

The output from this looks like:
From    To
CHRNB2  A0A096MXS8
EGR2    A0A096P554
GCK     A0A021WXA1
KRT14   A0A024R1X6
LMNA    A0A096MQV4
FGF3    A0A096NXI3
TK2     A0A096NJ58
ABCC8   A0A088S7J5


Does the anterior primary ramus of T6 innvervate the Rectus abdominis?

Because muscle (mesoderm) and peripheral nerves (ectoderm) develop from different embryonic germ layers, the pattern of innervation is somewhat variable. The muscles are condensing from mesenchymal tissues more or less in place, and nerves are growing out into the muscle masses to innervate them. Because of this, the specific spinal segments that innervate muscles can vary somewhat. This is particularly true in the brachial and lumbosacral plexuses. In the brachial plexus for example:

Grayed out text for C5 in the median nerve and C7 in the ulnar nerve suggest variable contributions from those segments.

In this case, rectus abdominis is "always" innervated by at least T7 to T12. But sometimes T6 as well in some, but not all, people.


Erythrocyte metabolism is unique in that the mature erythrocyte
  contains no mitochondria and therefore no Krebs cycle! Instead the
  energy needs of the RBC are met largely (95%) by anaerobic glycolysis
  in the two pathways: Embden-Meyerhof + Hexose-monophosphate.

+

Virginia University source


As pointed out by @bshane it seems your question is answered by the definition. From the relevant wikipedia articles

  "A seral community (or sere) is an intermediate stage found in ecological succession in an ecosystem advancing towards its climax community."

and

  "In ecology, climax community, or climatic climax community, is a historic term that expressed a biological community of plants, animals, and fungi which, through the process of ecological succession the development of vegetation in an area over time, had reached a steady state. This equilibrium was thought to occur because the climax community is composed of species best adapted to average conditions in that area."

It doesn't lead anywhere, it is the climax. It is the state a community reaches when there is little change in the biodiversity as it because the community is composed of species at proportions that suit the ecology well.

However, in reality it seems that climax communities are rarely (if ever obtained) and, with increasing climate change and habitat invasion by humans, few communities will be in equilibrium. The adaptive landscape varies in time and space, thus while a community may be well suited to the current environment, it may well be poorly suited to future incarnations of that environment and will be undergoing constant change. As such, the term "climax community" is somewhat obsolete with it generally referring to old or established communities rather than those at a climax.


Why can't we move our toes and some fingers separately?

A relatively new area of the brain's cerebral cortex evolved to enable humans and other primates the necessary small motor skills to pick up small objects and deftly use tools, scientists now say. https://www.youtube.com/watch?v=zyl6eoU-3Rg

Primates can move their ears too, here's a theory of it. Other motor skills that are not often developed are individual eyebrow movement, pectoral flexing, ability to sneeze with your eyes open.

Hand movement is new and developing compared to chimps.

Toe movement is latent and receding.

The human hand is built up onto a squirrel/clawed paw, If you take a while to rotate your forearm and the flexors of the fingers, you will see that it's a mutated simple flexing mitt thing with with a new fine motor dexterity that you use all day, added on top of the vestigial clawing and grasping hand.

https://www.youtube.com/watch?v=vlwAoKpSI7s

This page says:
Signals generated in the primary motor cortex travel down the corticospinal tract  through the spinal white matter to synapse on interneurons and motor neurons in the spinal cords ventral horn. Ventral horn neurons in turn send their axons  out through the ventral roots to innervate individual muscle fibers.

The motor cortex is subject to plasticity and remapping. To know this question is beyond my field of knowledge, someone else can go on from here :) you'd have to learn about the motor cortex, plasticity, vestigial nerves, nerve mappings, it's a fantastically complex topic.

What's interesting is the variety and quantity of different muscular abilities that are inherited by a population, it reflects an optimized level of evolutionary plasticity and specific types of variety of useful traits like muscle and joint proportions to ensure fast and flexible species development.


Which area of neuroscience\biology deals with the effects of genetics and drug discovery based on brain microcircuits?

Basically you are sketching a situation where:

Brain circuits are modeled (Computational Neuroscience), which often depends on anatomical (Neuroscience, Biology), structural imaging and functional imaging (Neuroimaging) and electrophysiological data (Electrophysiology). Various other disciplines may come into play (Histology, Pathology, Anatomy, etc.).
Genetic (Genetics, Molecular Biology, Cell Physiology) and environmental effects (Behavioral Psychology, Medicine, Psychiatry) also encompass a wide list of expertise, out of which a small handful is mentioned in bold.
The realm of drug discovery harbors Medicine, Toxicology, Organic Chemistry, Pharmacology, perhaps even Physics and likely a host of others.

In short, your question could, perhaps, better be phrased as 'What Biomedical fields of research disciplines are not related to Drug Discovery?


In short; yes. It depends on the breed (not all lay up to 1 egg/day), the age of the bird and on nutrition. High yielding breeds of chicken are e.g. dependent on supplements of calcium to be able to produce new shells rapidly (e.g. in the form of ground-up shells). Some information on the nutrient requirements of chicken can be found at Feeding the Laying Hen. Egg production will also fluctuate over the year, and will generally decrease e.g. during molting, since energy and nutrients are then diverted to the production of feathers (see info at e.g. The Poultry site).


I can't think of any reason that would explicitly prohibit a dendrite from travelling through a space created by another dendrite's branching pattern. In non-EM images of dendritic branching patterns I don't think I have ever observed dendritic loops, but of course, that has nothing to do with whether or not they occur. Nonetheless, I think there are more likely explanations for what you are seeing in these particular images.

As shown, the upper and lower parts of the "dendrite" in the first image do not look like a continuous structure. I would guess that you are looking at a synapse or some other contact between two different processes in the first image. The 3-4'o'clock connection in the loop suggests this interpretation. Can you see vesicles in the images around those connections?

The other dendrite that shows up in your second image might be a glial cell or some other cell's dendrite that participates in the synapse. Alternatively, the other dendrite may just be a chance passing of two dendrites that don't interact functionally.

Of course, it could be that you and the computer have just completely misunderstood the data. My understanding of the Eyewire interface is that the computer guides a lot of the identification and doesn't easily allow you to see the surrounding areas so you can't track structures all the way to their sources. In such a situation, it seems probable that you would end up with ambiguous instances like this that you would have a hard time resolving without more information/expertise. But maybe Seung or one his colleagues can come weigh in on that?


Why do emperor penguins breed during the antarctic winter?

From my experience working on sheep farms in Australia, it could very well be for similar reasons to why farmers breed their sheep at specific times in the year - they breed their sheep, so that by the time winter hits the lambs are large enough and have enough wool to make it through. The penguins lay their eggs in the dead of winter, but they then incubate for 65-75 days, by this time winter will have largely passed, and the chicks will be growing in the spring and then summer. By laying in the winter, the penguins avoid exposing their young to a winter for as long as possible.

Another point to consider: As you said, Antartica is largely devoid of other life during the winter. To me, what I hear is: There will be no predators to feed on the eggs, or attack the vulnerable penguins incubating their eggs.

Reference: http://www.antarctica.gov.au/about-antarctica/wildlife/animals/penguins/emperor-penguins/breeding-cycle


What could explain discrepancies between dates provided by the fossil record vs. the molecular clock?

First, the example you give is unusual in that molecular dating analysis should be calibrated with fossils to set minimum ages. If Ecrobia grimmi exists in the fossil record, then no proper molecular analysis would estimate them to be younger than those fossils. There are two main causes of discrepancies between fossil and molecular dating.
For fossils you never find the oldest example of a species. If a species diverged 100 million years ago, you might not find a fossil of that lineage for millions of years, meaning that fossil estimates are almost always underestimates, but they do form a baseline upon which to calibrate molecular data. The problem with molecular data is that there is no "molecular clock". Lineages, genes and individual nucleotides all change at different rates. The best you can do is plug in fossil and/or geological dates into a model that is based on other lineages. Hopefully you have calibrated dates for closely related species, and the same genes. Even then, you do not know that the lineage you are working with will follow the same rates as the model predicts. At a minimum, you need to set a minimum possible age in BEAST to 5-16 mya.


Does this procedure for extracting DNA from strawberries work?

The extraction protocol described in the first article is a standard DNA extraction protocol. I've used variations on this method in the lab (with some refinements) on other types of cells at least hundreds, if not thousands, of times. The "strawberry" experiment is very popular for classroom demonstrations, especially at the middle-school and high-school levels, because it's visually interesting and uses commonly available reagents. While these reagents aren't laboratory-grade, they're more than sufficient for a basic extraction of DNA.

I can't think of a scientific basis for why the author in the second article would claim that the extracted substance is "little more than pectin". Since he didn't provide data, or a reference to any data, it's hard to know what he's basing his conclusion on.

It's definitely possible that the DNA is pulling down a certain amount of cellular proteins during the alcohol precipitation step (the final step). This is why in a lab setting you typically perform a few more steps to "clean up" the DNA and remove any co-precipitating proteins. This would be essential if you plan to do further analysis of the DNA, because protein contaminants can interfere with subsequent analyses, making the data unreliable. One exception would be if you're studying protein-DNA interactions, but that's a separate type of experiment.

I'm assuming this experiment will be done for/by beginner level students, as opposed to a college or graduate level class? If so, then for the purposes of a classroom demonstration, those extra purification steps aren't warranted. It's time-consuming, and it would be very boring to watch... As is the case with most labwork. :-) Even if you perform those additional steps, the purified DNA is often precipitated with alcohol again, and it's visually similar to what you saw in the first alcohol precipitation, just a bit less opaque. Probably not something most students would notice or find interesting.

Either way, it's entirely acurate to say that the strawberry experiment is extracting DNA. You could always explain that the DNA might have cellular proteins binding (or "sticking") to it, and that a few other steps would have to be performed if you wanted to analyze the DNA in a lab setting, because the proteins would interfere with DNA analysis. This would also give beginner-level students an introduction to the fact that DNA and proteins interact with each other.

Hope that helps!


Why does a cockroach not die even after decapitation?

Based on an article here, unlike humans, cockroaches have an open circulatory system. They don't have a huge network of blood vessels like that of humans, or tiny capillaries that you need a lot of pressure to flow blood through. Hence after you cut their heads off, very often their necks would seal off just by clotting.

According to the article cockroaches breathe through spiracles, or little holes in each body segment. Plus, the roach brain does not control this breathing and blood does not carry oxygen throughout the body. Rather, the spiracles pipe air directly to tissues through a set of tubes called tracheae. In addition cockroaches are poikilotherms, or cold-blooded, meaning they need much less food than humans do. Hence cockroaches can survive decapitation.


What could I call such nucleic-acid-Sequence? A sort of palindromic sequence? is there any term called mirror repeat?

I think the situation you showed should be called mirror-everted repeats: to my knowledge they occur very rarely, and I only found references in this and this articles, even though no graphic explanation is provided.


-/- means both copies of the gene (both alleles) are knocked out


The link that ddiez has mentioned, has a download link for a zip file (fidist2). The zip file contains windows executables and C-codes. Just compile the C-codes in your terminal.

This is from the readme:

  The .exe files are pc binaries, which is only what most people want. I
  include the source file in case anyone wants to play with them. In
  this case compilation is e.g.:

gcc -o fdist2 -O fdist2.c -lm
gcc -o cplot -O cplot.c as100.c as99.c -lm
gcc -o datacal -O datacal.c -lm

Actually in the readme, the first compile command says fdist.c (no such file) instead of fdist2.c. I corrected that here.

Your system should have gcc. I tried compiling in my system (linux) and it works. It should work in Mac too.


Bug Identification: Tiny Bugs in Fairport NY

These bugs are a type of hexapod called springtails (subclass Collembola). Springtails are often very tiny and hard to see without a lens, so I have to say you did a good job grabbing a fairly detailed picture of this one. Specifically, your specimen appears to be some species in the order Entomobryomorpha.

According to Wikipedia:

  They can be best distinguished from the other springtail groups by their body shape...The Entomobryomorpha...contain the slimmest springtails [with]...long bodies. [They also have] well-developed furculae

Specific species:

Usually, IDing springtails is very difficult, but I believe your specimen matches a fairly widespread species called Entomobrya nivalis (aptly named the cosmopolitan springtail).

 Source: Wikipedia; photo credit: James Keith Lindsey

The description of this species matches yours fairly well. From Wikipedia:

  The cosmopolitan springtail measures about 2 mm in length. Its color consists of a yellow or white background with dark pigment forming transversal bands along the third segment of the thorax and the segments 2 to 6 of the abdomen. The fourth segment of the abdomen has a U- or 11-shaped pattern that easily distinguishes this species from others in the genus Entomobrya+

Somewhat true to its name, this somewhat cosmopolitan species is found in temperate and polar regions across North America and Europe+. Adults typically live among lichens and trees (whereas young live in leaf litter), however, according to NC State Extension:

  Rarely springtails may become exceedingly abundant and may congregate in heaps several inches high on driveways, sidewalks and poolsides.

So what exactly is a springtail??

In general, springtails usually feed on decaying matter, and -- you guessed it -- they're known for their ability to jump!

  Springtails are so-called because they have a unique structure, the furcula, that allows them to jump for considerable distance relative to their tiny size. [source].

 Springing mechanism of a generalized springtail. Credit: Marianne Alleyne [Source]

+ Wikipedia cites Katz, A.D.; Giordano, R.; Soto-Adames, F. (2015). "Taxonomic review and phylogenetic analysis of fifteen North American Entomobrya (Collembola, Entomobryidae), including four new species". ZooKeys. 525. doi:10.3897/zookeys.525.6020


Since you're asking about hyperthyroxinemia with normal TSH serum levels, I suppose you're talking about euthyroid hyperthyroxinemia.

In euthyroid hyperthyroxinemia, the serum T4 and T3 concentrations are increased, but the TSH concentration remains normal. Besides that, there are normally no clinical signs.

The cause of that increase, as you explain in your own question, is a mutation in a transporter protein (like TBG), or an increase in their concentrations (which can happen in patients with hepatocarcinoma, for instance).

However, the free T4 concentration remains the same, and that is the important value for the negative feedback mechanism that regulates the concentration of TSH:

  The euthyroid status of subjects with FDH has been
  confirmed by normal TSH response to TRH, normal free T4 concentration
  measured by equilibrium dialysis using appropriate buffer systems, normal T4
  production rate and normal serum sex hormone-binding globulin concentration.

Thus, without an increase in free T4 levels, there will be no drop in the TSH concentration.

Source: Impaired Sensitivity to Thyroid Hormone: Defects of Transport, Metabolism and Action.


Does antidromic conduction occur in the brain under normal conditions?

Under physiological conditions, action potentials are generally assumed to travel one-way. Action potentials are generated in the dendritic region, and travel from the soma to the axon terminal. Because voltage-gated sodium channels are inactivated after having been active during action potential generation, the action potential cannot travel backwards because the tail-end of the action potential is basically temporarily shut down (Fig. 1). The duration of inactivation of sodium channels determines how fast a neuron can fire, i.e., it determines the refractory period of neurons (Purves et al., 2001).

Fig. 1. Action potential conduction and refractoriness. Source: Zoology.

When neural tissue is artificially electrically stimulated, however, action potentials can be generated anywhere along the neuron. When an axon is activated somehwere in the middle with an electrical stimulus, an action potential will travel both ways, i.e. normally to the axon terminal, but also antiodromically to the cell body.

However, it has been noted in vivo that some neurons do show antidromic action potentials under physiological conditions (Jansen et al., 1996). For modeling purposes I would not bother too much about this, though, because antidromic action potentials are generally only observed under artificial conditions.

References
- Jansen et al., J Neurophysiol; 76(6): 4206-9
- Purves et al., ed. Neuroscience. 2nd ed. Sunderland (MA): Sinauer Associates; 2001


Are there any ways to force DNA-origami to create a geometric shape from non-nucleotides (not from DNA)?

I interpret your question to ask this:
Can DNA origami be used as scaffolds for the guided assembly of other non-DNA structures?
Yes.  From what I've read, two- and three-dimensional DNA structures can be used for nanoparticle assembly and as a nucleation factor in the crystallization of proteins and minerals.  You can find these examples and more in a lengthy review from 2017.1  Specifically, read section 6.6, Programming the Structure and Conformation of Non-DNA Materials.

Fan Hong, Fei Zhang, Yan Liu, and Hao Yan. DNA Origami: Scaffolds for Creating Higher Order Structures. Chem. Rev. 2017, 117, 20, 12584–12640.


Conversion and storage of glucose to glycogen

Glycogen storage limitation is due to these additional facts also:

Glycogen is a hydrophilic molecule. This means an increase in glycogen concentration will cause a proportionate increase cell weight due to water accumulation. As cells can contain only limited volume the amount of glycogen stores are limited. Lipids are hydrophobic hence can be accumulated without increasing the volume and weight of cell due to water accumulation.
As a source of energy lipids are approximately 2.5 times more efficient than glucose.


Why do high cholesterol levels result in a buildup of fat in blood vessels?

The phrase "high cholesterol", and the measurement itself is a marker for high levels of a particular lipoprotein, Low density lipoprotein (LDL). Because cholesterol and triglycerides are not soluble in plasma, they are packaged by the liver into soluble particles called lipoproteins. Packaged in lipoproteins, these lipids are transported throughout the body, for use by different organs and tissues. As these lipids are dropped off, the lipoprotein is converted from one form to another, with characteristic biophysical and physiologic properties. The LDL is a late stage of a lipoprotein before reuptake at the liver (and other organs, but mainly the liver) via the LDL receptor. We happen to know that people who have high levels of circulating LDL are at risk for, e.g., cardiovascular disease because of The Framingham Study, and that if you can reduce circulating LDL levels you can decrease the risk for these diseases. The molecular basis of this risk was demonstrated to be, in large part, failure of clearance of LDL particles because of ineffective receptor mediated endocytosis, as described in this wonderful 1986 paper in Science.

From this presentation:

Some LDL cholesterol circulating through the bloodstream tends to deposit in the walls of arteries. This process starts as early as childhood or adolescence.
White blood cells swallow and try to digest the LDL, possibly in to digest the LDL, possibly in an attempt to protect the blood vessels.
In the process, the white blood cells convert the LDL to a toxic (oxidized) form.
More white blood cells and other cells migrate to the area, creating steady low steady low-grade inflammation in the artery wall.
Over time, more LDL cholesterol and cells collect in the area. The ongoing process creates a bump in the artery wall called a plaque. The plaque is made of cholesterol, cells, and debris.
The process tends to continue, growing the plaque and slowly blocking the artery.

There is a good overview of the general physiology here in Robbins The Pathologic Basis of Disease. Chapter 5, Genetic Disorders, reviews the physiology, and the relevance to disease, in the section on Familial Hypercholesterolemia. The review is relevant to hypercholesterolemia in general.


Short answer
Shedding or reabsorbing the endometrial lining is energetically advantageous to the female.The advantage of shedding over re-absorption may be that sperm-born pathogens are removed from the uterus. A more parsimonious explanation, however, is that the endometrium in primates has developed into too large of a structure to be completely reabsorbed by the uterus wall.

Background
Basically you ask why are estrous cycles in mammals accompanied by regression and build up of the endometrial lining? The main reason for either reabsorbing or shedding the endometrial lining is thought to be to save energy. It has been calculated that, when implantation fails, a cyclical regression and renewal of the endometrium is energetically less costly than maintaining it in a metabolically active state required for implantation. In the regressed state, oxygen consumption in human endometria declines nearly sevenfold. Metabolic rate is at least 7% lower, on average, during the follicular phase than during the luteal phase in women, which signifies an estimated energy savings of 53 MJ over four cycles, or nearly six days worth of food (Strassmann, 1996; Crawford, 1998).

In fact, impaired shedding of the endometrial lining may lead to pathologies. If no egg is released and the estrogen/progesterone system becomes imbalanced, the endometrium may continue to thicken, instead of breaking down and being shed normally as a menstrual period. This abnormal thickening is called endometrial hyperplasia. Periodically, the thickened lining is shed incompletely and irregularly, causing irregular and more heavy bleeding. If this cycle of abnormal thickening and irregular shedding continues, precancerous cells may develop, increasing the risk of cancer of the uterine lining (endometrial cancer), even in young women (source: MSD manual).

Now the question of why human females shed the endometrial lining instead of resorbing it? Indeed, shedding the endometrium is mainly limited to primates, as opposed to reabsorbing it (like in most other mammals). Here, I do not have a definitive answer, but I like to share two opposing hypothesis on the matter.

Hypothesis 1:  Profet (1993) hypothesized that shedding the endometrium may be an effective way to get rid of sperm-based pathogens. The accompanying bleeding, Profet hypothesizes, delivers immune cells into the uterine cavity that can combat pathogens.
Hypothesis 2: Strassmann (1996) surmises that the endometrial microvasculature is designed to provide the blood supply to the endometrium and the placenta, and that external bleeding appears to be a side effect of endometrial regression that arises when there is too much blood and other tissue for complete reabsorption. The relatively large blood loss as seen in humans and chimpanzees can be attributed to the large size of the uterus relative to adult female size and to the design of the microvasculature in the uterus wall.

References
- Crawford (ed), Handbook of Evolutionary Psychology: Ideas, Issues, and Applications, Psychology Press (1998)
- Profet,  Quarterly Rev Biol (1993); 68(3): 355-86
- Strassmann, Quarterly Rev Biol (1996);71(2): 181-220


Here are just a few points that might apply:

Urine is used for scent marking by some species, so the ability to store urine could be useful.
At the opposite side, controlling the release of a strong scent would help in stealth for both predators and prey.  (In addition, a single strong scent might temporarily overload a predator's sense of smell making tracking more subtle scents more difficult.)
Flushing an excretion point (single point reduces opportunities for invasion) under some pressure could help avoid blockage and parasitic invasion/accumulation.  (Providing a tube from the extraction organ to the excretion point allows more flexible (and protected) placement of the organ, but also increasing the benefit of a flushing mechanism.)
Flushing could also reduce contact with skin. Urine might act as an irritant and a nutrient source for parasites.
Adding a buffer is a common technique for any pipelined operation to allow smaller resources to handle temporal variation in input and output rate.  Without a such a buffer, all stages have to be sized for the maximum utilization rather than something closer to average utilization.
Avoiding potential contamination of food and water may also be a benefit of controlled urination (or excreting might have a fertilizing or pest-deterrent aspect for plants).

Since terrestrial animals presumably retained urinary bladders developed by their marine ancestors, benefits associated with terrestrial lifestyle would only provide selective pressure to retain such a feature. However, if somehow a line of terrestrial animals abandoned urinary bladders, it is not entirely implausible that even scent marking benefits could increase the selective pressure enough to overcome some peculiar opposing selective pressure.

Initially, the animal might apply scents by scratching at an area of skin irritated by urine release against some surface. Then this scratching might be preferentially located (i.e., a scent marking behavior is developed). Having such a behavior would then obvious bring benefits to storing a significant amount of urine and eventually to being able to squirt the urine (allowing the scratching behavior to fall away).

The above are just somewhat reasonable speculations about what selective pressures might encourage the development (and retention) of a urinary bladder.  Hopefully, someone with actual knowledge will provide a better answer documenting established theory and evidence for how urinary bladders actually developed.


What is the minimum length required for a circular DNA ligation?

I stumbled across this paper demonstrating it is between 150-200 base pairs.

DNA flexibility studied by covalent closure of short fragments into circles
D Shore, J Langowski, and R L Baldwin
PNAS 1981 78 (8) 4833-4837

http://www.pnas.org/content/78/8/4833.full.pdf


Is O4I2 sufficient to reprogram cells (ie induce pluripotency)?

No, the chemical O4I2 (thats a name, not a chemical formula btw) only helps to induce production of the Oct-4 transcription factor. Even if just this chemical is sufficient to express Oct-4 (which it might not be, I'm not really sure about that), you still need to induce transcription of other genes (usually Sox, cMyc & Klf4) to obtain iPS cells.


Do not have too a "panselectionist" view of evolution!

You can survive in a bath of mercury for a little while. You can survive naked in the outer space for a while (see here). Yet none of your ancestors where exposed to such conditions. We can be tolerant to certain conditions without having been selected to tolerate it.

Similarly, you managed to survive in your very specific environment. Yet none of your ancestors ever encountered this specific environment.

In other words, evolution is more than just natural selection. Not every phenotype in every environment you can think of is the result of a direct selective pressure acting on it. A classical and easy to read paper on the subject is Gould and Lewontin (1979).

Why fish not die suddenly outside of the water?

The main reason why fish die outside of water is that they cannot intake oxygen from air (see Breathing under water; not considering lungfish). So once fish are exposed to air only, they stop intaking oxygen, consume the oxygen that they have left in their circulatory system and tissues and slowly die of asphyxie but there is no reason for the death to be direct and sudden.


The phenomenon you are observing is probably Adventitious buds. The plantlets can develop on intact leaves or on injured one.

Back to Begonia, this phenomenon usually occurs on injured leaves, so, probably, the plant was injured during movement/by insect or by other means and because of this started to create plantlets.


Does the complimentary base pairing of rRNA with itself play a role in its transcription?

Summary

The process of the termination of transcription is still not well understood. It differs between eukaryotes and prokaryotes and between mRNA and rRNA. Although it involves stem-loop structures, such structures may be necessary, but are not sufficient for termination. The idea that the termination signal might be part of the mature functional transcript — especially for rRNA comes up against a number of problems, and turns out to be incorrect. Such problems include the extensive nature of the stem loops (which to use?) and the fact that the smaller stem loops emanating from the core conserved hydrogen-bonded skeleton, are not necessarily themselves conserved (reviewed by Brimacombe). In fact the large and small rRNAs are in a single transcription unit with other genes at the end of which are specific termination signals outside the region encoding the mature rRNA.

Prokaryotic rRNA transcription

This has been reviewed by Condon, Squires and Squires (1995). The structure of the well-studied rrnB operon of E.coli is shown below, with the promoters indicated as ‘P1’and P2’ and the terminator sequences as ‘T1’ and ‘T2’. (Adapted from Pfeiffer and Hartmann.)

This transcription unit includes the 5S rRNA as well as a tRNA.

Eukaryotic rRNA transcription

This has been reviewed by Goodfellow and Zoomerdijk(2012), from which the diagram below, of the mammalian rDNA repeat, is taken. The terminator elements are ‘T1–10’.

In eukaryotes the 5S rRNA is not in the same transcription unit as the large and small rRNAs (and the 5.8S rRNA). Indeed it is transcribed by DNA-dependent RNA polymerase III, rather than the DNA-dependent RNA polymerase I, which transcribes the rDNA repeat shown.


Can a single strand of mRNA form different polypeptide chains?

I believe, your book refers to  polycistronic mRNA. This is mRNA where multiple genes are encoded together in one mRNA and are often (but not necessarily) translated one after another. This is mainly found in prokaryotes where the proteins encoded on the same mRNA often form a metabolic pathway together.


Is protein folding symmetric with respect to reversing the sequence order?

No! Although there is a relationship, the protein would not fold properly since the C and N terminals are reversed consider the following:

H(NH)-A-C(=O)(NH)-B-C(=O)(NH)-C-C(=O)(NH)-D-C(=O)(NH)-E-(C=O)OH

as appose to :

HO(C=O)-A-(NH)(C=O)-B-(NH)(C=O)-C-(NH)(C=O)-D-(NH)(C=O)-E-(NH)H

These are completely different molecules!

http://www.ncbi.nlm.nih.gov/pubmed/1604320 http://www.pnas.org/content/95/13/7287.long http://www.pnas.org/content/111/32/11679


Introductory literature for synthetic / systems biology

Systems Biology

Wingreen & Botstein who run the graduate systems biology course at Princeton wrote a paper about how to teach the subject (Wingreen & Botstein, 2006). In the paper they highlight the key concepts they think are crucial to understanding modern systems biology, and they teach the course through discussion of seminal papers in the field.

Here's the reference...
Wingreen, N. & Botstein, D. (2006) Back to the future: education for systems-level biologists. Nature Reviews Molecular Cell Biology. 7 (11), 829–832.

The paper is unfortunately not open access, so for those who can't access the paper  edit: @uvesten found a free PDF copy! I have listed their choices below, along with the key concept they think each provides...

Robustness (i.e. retaining function despite fluctuations)
Barkai, N. & Leibler, S. (1997) Robustness in simple biochemical networks. Nature. 387913–917.

Evolutionary perspective
Eisen, J.A. (1998) A phylogenomic study of the MutS family of proteins. Nucleic Acids Res. 264291–4300.

Microarray analysis (and more generally, the importance of data visualisation)
Eisen, M.B., Spellman, P.T., Brown, P.O. & Botstein, D. (1998) Cluster analysis and display of genome-wide expression patterns. Proc. Natl Acad. Sci. USA. 9514863–14868.

Individuality of elements in a system:
Elowitz, M.B., Levine, A.J., Siggia, E.D. & Swain, P.S. (2002) Stochastic gene expression in a single cell. Science. 2971183–1186.

Maximum likelihood
Felsenstein, J. (1981) Evolutionary trees from DNA sequences: a maximum likelihood approach. J. Mol. Evol. 17368–376.

Ultrasensitvity
Goldbeter, A. & Koshland, D.E. (1981) An amplified sensitivity arising from covalent modification in biological systems. Proc. Natl Acad. Sci. USA. 786840–6844.

Biophysical modelling
Hodgkin, A.L. (1958) Croonian Lecture, ionic movements and electrical activity in giant nerve fibres. Proc. R. Soc. Lond. B. Biol. Sci. 1481–37.

Specificity
Hopfield, J.J. (1974) Kinetic proofreading: a new mechanism for reducing errors in biosynthetic processes requiring high specificity. Proc. Natl Acad. Sci. USA. 714135–4139.

Random processes and distributions:
Luria, S.E. & Delbruck, M. (1943) Mutations of bacteria from virus sensitivity to virus resistance. Genetics. 28491–511.

Stable switching between states:
Novick, A. & Wiener, M. (1957) Enzyme Induction as an all-or-none phenomenon. Proc. Natl Acad. Sci. USA. 43553–566.

Sequence similarity
Smith, T.F. & Waterman, M.S. (1981) Identification of common molecular subsequences. J. Mol. Biol. 147195–197.

Synthetic Biology

A good place to start in this subject is the Synthetic Biology network:

Syntheticbiology.org
iGEM.org
BioBricks.org


Variation of length of circadian rhythm in humans in absense of time reference

This might be the study to which you refer in your answer, the people tested averaged a daily cycle of 24 hours and 11 minutes with a surprisingly small variation in their rhythms:

  The variation between our subjects, with a 95 percent level of confidence, was no more than plus or minus 16 minutes, a remarkably small range.

Worth noting they were all healthy and so it doesn't tell us much about insomnia.

This study about insomnia in adults with ADHD shows that circadian rhythms of insomnia sufferers aren't so much longer as delayed (for sleep-onset insomnia anyway). Figure 2 might be of interest, showing that insomnia sufferers have significantly delayed melatonin production.


Using BLAST for molecular replacement in structural biology

Identity, Similarity, E-value are the key numbers, for the prediction of the 3D structure of proteins. The Length of the query and selected results should also be close to each other.
E-value:
The first value to look at is indeed the E-value.
For the most accurate predictions, E-values less than $10^{-100}$ are of extreme importance While E-values ranging between $10^{-50}$ to $10^{-100}$ come as the second priority. E-values less than $10^{-20}$ or so, should not be trusted. (As you know the larger amount of E-value accounts for random hits which may not have any evolutionary background with your query)
Similarity and Identity:
The ranges for these amounts differ for each survey and should be assessed with other statistics. Needless to say, Identities below 5% for amino acid blasts and below 25% for nucleotide blasts are useless. For proteins identity above 25% is acceptable and 35-50% (and more) are of greater importance. Similarity plays a more important role in the overall shape and structure of the protein. "Total score" in Blast NCBI should suffice for these evaluations.
Length:
The sequence length of your results should be reasonably near to one another. For example, having a sequence of 600 amino acids as your query, the acceptable range for the selected results (to eventually predict 3D structure with) should be 600 $\pm$ 30. Five percent difference is usually enough. Deviation from this would result in extra 3rd and 4th structures induced by other subunits.
Other considerations: In the case that your organism is known, pick the sequences which share a common evolutionary history with your organism of interest See Tree of life. The number of subunits and Symmetry types might be useful in some cases. Avoid selecting ab-initio based 3D structures in your results all the time and focus mainly on X-ray diffraction-based structures. If you're using the PDB website for data retrieval, Refinement Resolution is also extremely important. Try both CIF and PDB formats as input, as the results may sometimes improve.
At last but not least, try blasting using curated databases. In blastp, refseq_protein , swissprot , pdb , refseq_select are ideal.
This is just a rule of thumb and should not be generalized as the exact numbers differ substantially from one query to another.


If you click through to some of the samples in the study, eg. GSM194397, GSM194398, etc. it mentions under the "Data processing" section that "The data were analyzed with dchip with default normalization settings".

You can learn more about dChip over at the dChip website.


Since frogs are ectotherms and supposed to have low metabolic rate, why do they grow so fast and eat so much?

Rather than saying ectotherms can't grow fast (which is obviously false), it's probably better to think about it as a two-part argument:

Ectotherms and endotherms can grow rapidly at an optimum temperature
Ectotherms can't maintain themselves at their optimum growth temperature

If you keep ectotherms at their optimum temperature, then they can reach optimum growth. In the wild, they might not find that optimum temperature for more than a few hours per day, though in your aquarium they might be at it all day long.

There are several publications supporting this such as

Effects of temperature and volume of water on the growth and development of tadpoles of Pleurodema diplolister and Rhinella granulosa (Amphibia: Anura)
Effects of Temperature on Growth, Development and Survival in Larvae of Pelophylax ridibundus (Pallas, 1771) (Amphibia: Anura): Linking Global Warming to Amphibian Development
Thermal tolerance limits and effects of temperature on the growth and development of the green toad, Bufotes viridis

I don't see a specific reference for this but will add that ectotherm probably have greater growth potential than endotherms if they're at their optimum temperature, because endotherms have to waste energy on a whole suite of molecular machinery that's designed to maintain their body temperature.  All that extra energy can be diverted into growth by ectotherms.


What are the trade-offs between polymerase chain reaction (PCR) vs Loop-mediated isothermal amplification (LAMP)?

Having to use more primers is definitely one of the big reasons. Primer design is difficult and time-consuming, and even more so if you're dealing with similar targets. For instance, if you're trying to differentiate closely related bacterial strains, having to design primers for 6 or 8 regions instead of just two is going to lower your ability to differentiate the strains. It's even worse if you're working with viruses - these mutate quickly and therefore your LAMP primers will fail to amplify the virus sooner than normal PCR primers.

LAMP is good because it's cheap and portable, but there are portable PCR thermocyclers starting to be produced (eg. miniPCR, Biomeme) and so diagnostically speaking, it's a lot easier to just use existing PCR primers that have been validated and are widely used, instead of creating new primers that you'll have to validate all over again.

The primers again are important if you're trying to amplify multiple targets - it's a lot easier to create degenerate or consensus primers for a standard PCR than it is for LAMP, and also easier to distinguish multiple target bands on a gel, which isn't possible for LAMP.

It can vary, but in my personal experience, I have always found Taqman-based PCR to be more sensitive than LAMP. You can't use Taqman probes with LAMP. You also can't use LAMP for cloning, and melt-curve analysis isn't possible with LAMP, which is useful for detecting primer dimers and diagnostically for distinguishing between targets.

So, LAMP is good because it's cheap, requires less equipment, can be done in the field with minimal reagents, and tends to be more robust than PCR as it is less prone to be affected by inhibitors. This means it is great for in-field diagnostics in developing regions. But there is a range of things PCR can do that LAMP can't, and the complex primer design alone will prevent it from overtaking PCR.


How is a stem-cell induced to assimilate a knock-in DNA construct?

There are two ways to introduce genetic material past a cell membrane. Infection and generation of a porous cytoplasm. Viruses and bacteria generally are used. Retroviruses tend to cause leukemia so they are avoided however they are the only way to get past the nucleus in vivo of multicellular life. Electroporation and needles generate a porous cytoplasm allowing genetic material to seap or be inserted into the cell.

Once the genetic material is in the cell it has to have contained site specific oligonucleotides to hybridize with the strand of interest.

  Procedure

  The procedure for making mixed-genotype blastocyst.

  Breeding scheme for producing knockout mice. Blastocysts containing cells, that are both wildtype and knockout cells, are injected into the uterus of a foster mother. This produces offspring that are either wildtype and coloured the same colour as the blastocyst donor (grey) or chimera (mixed) and partially knocked out. The chimera mice are crossed with a normal wildtype mouse (grey). This produces offspring that are either white and heterozygous for the knocked out gene or grey and wildtype. White heterozygous mice can subsequently be crossed to produce mice that are homozygous for the knocked out gene.
  There are several variations to the procedure of producing knockout mice; the following is a typical example.

  The gene to be knocked out is isolated from a mouse gene library. Then a new DNA sequence is engineered which is very similar to the original gene and its immediate neighbour sequence, except that it is changed sufficiently to make the gene inoperable. Usually, the new sequence is also given a marker gene, a gene that normal mice don't have and that confers resistance to a certain toxic agent or that produces an observable change (e.g. colour or fluorescence).

  Stem cells are isolated from a mouse blastocyst (a very young embryo) and grown in vitro. For this example, we will take stem cells from a white mouse.
  The new sequence from step 1 is introduced into the stem cells from step 2 by electroporation. By the natural process of homologous recombination some of the electroporated stem cells will incorporate the new sequence with the knocked-out gene into their chromosomes in place of the original gene. The chances of a successful recombination event are relatively low, so the majority of altered cells will have the new sequence in only one of the two relevant chromosomes - they are said to be heterozygous.
  The stem cells that incorporated the knocked-out gene are isolated from the unaltered cells using the marker gene from step 1. For example, the unaltered cells can be killed using a toxic agent to which the altered cells are resistant.

  The knocked-out stem cells from step 4 are inserted into a mouse blastocyst. For this example, we use blastocysts from a grey mouse. The blastocysts now contain two types of stem cells: the original ones (from the grey mouse), and the knocked-out cells (from the white mouse). These blastocysts are then implanted into the uterus of female mice, where they develop. The newborn mice will therefore be chimeras: some parts of their bodies result from the original stem cells, other parts from the knocked-out stem cells. Their fur will show patches of white and grey, with white patches derived from the knocked-out stem cells and grey patches from the recipient blastocyst.

  Some of the newborn chimera mice will have gonads derived from knocked-out stem cells, and will therefore produce eggs or sperm containing the knocked-out gene. When these chimera mice are crossbred with others of the wild type, some of their offspring will have one copy of the knocked-out gene in all their cells. These mice will be entirely white and are not chimeras, however they are still heterozygous.

  When these heterozygous offspring are interbred, some of their offspring will inherit the knocked-out gene from both parents; they carry no functional copy of the original unaltered gene (i.e. they are homozygous for that allele).
  A detailed explanation of how knockout (KO) mice are created is located at the website of the Nobel Prize in Physiology or Medicine 2007.

-wikipedia


Is human mtDNA unique in its single origin?

You can trace back any piece of DNA (from any life form) to a single ancestor called LUCA (Last Universal Common Ancestor), so the short answer is 'yes'. But be careful in your interpretation.

If you look backward in time, you can see that lineages merge (siblings merge first, then cousins merge, etc...) and you necessarily end up with a single individual. In absence of recombination (which is the case for mtDNA), you can always trace back a piece of DNA this way and always find a single ancestor. The age of this common ancestor depends mainly on the population size and demographic history of the lineage. Typically, in a panmictic diploid population of constant size $N$, the expected time to the MRCA (Most Recent Common Ancestor) of the population is $2N$ generations.

So yes, you can find an "original Eve mtDNA" in any species. But please by "original" don't think this ancestor must have represented any novelty or anything of interest and do not make the mistake to think that before this ancestor no one had mtDNA.

The second paragraph is an extremely vulgarized explanation of coalescent theory. You should have a look at an intro to coalescent theory (wikipedia article here) but you might well need an intro to evolutionary biology first. Understanding Evolution might be a good way to go.


Does DNA analysis allow determining amount of chromosomes?

This depends completely on the quality of the DNA. Since each chromosome is essentially a very long strand of DNA, breakages and missing sections are very common in extinct species due to degradation over time.

If a full DNA read is absent, no determination of chromosomal number can be performed.

Assuming a full read (covering all breakages) of the DNA is present, the telomeres of each chromosome can be found, and since chromosomes usually only have one set of telomeres each, this may be useful for chromosomal number determination.

Caveat 1: Chromosome 2 (human) is an example of how this method may fail, since a recently fused chromosome will still possess the tandem repeats characteristic of telomeres.

Caveat 2: Telomeres may vary in length due to the age of the cell, as well as be broken in multiple regions. Due to the tandem repeat nature of telomeres, it is nearly impossible to tell these different states apart experimentally.


Botany related question: liverwort sporophyte

I think it should be a part of the gametophyte because it is formed from the fusion of leaves (which are haploid) and protects the archegonium and the developing capsule.

It also can be logically thought out. Since it develops before the sporophyte forms , it should be part of the gametophyte.


What are the main mechanisms of interaction between the nervous and immune systems?

It is not only the immune system that prevents us from getting ill. Worrying much in my opinion won't make you catch a cold; rather, you can get problems with your cardiovascular system (arrhythmias, hypertension, angina pectoris) or limbic system (panic attacks, sweating attacks etc.).

The connections are many; here are some possible ones:

There are many glands in our body that are either densely innervated (like the thyroid gland) or are a part of nervous system (like pituitary gland, epiphysis). They can release hormones directly to our blood and make our hormone profile unstable, hence also impacting the immune system.
Sympathetic/parasympathetic nervous system is under direct control of the CNS (N.vagus, carotide sinus sinus etc.) and can dramatically change the peripheral resistance of our vascular system by constricting (=> angina pectoris, hypertension) or dilating (swellings, bowel movements problems -> constipations etc.) the small vessel. This alone can start so many different mechanisms resulting not only in being ill, but also being dead.

Speaking about connection between the nervous and immune system we must consider that:

Many neuromediators, like adrenaline, for example, have clear effects on immune cells.
The mediators and humoral factors released by nerve endings can easily diffuse outside of the synaptic cleft and act locally, attenuating immune response.


Erm. Sort of. Kind of depends on your definition. It hasn't been done for multicellular organisms though.

Craig Venter et al did this exact experiment a few years ago with a completely synthetic Mycoplasma genome.

http://www.jcvi.org/cms/press/press-releases/full-text/article/first-minimal-synthetic-bacterial-cell-designed-and-constructed-by-scientists-at-venter-institute-an/

If you just want to change small segments of DNA that's where cloning and gene therapy come in, and we do that A LOT.


Allow me to start off with a nice picture showing the differences - note female gametes are on the left while male gametes are on the right in my examples:

Isogametes

For a gamete to be considered an isogamete the other gamete that it meets up with to produce is exactly the same in both size, structure and movement. [2] It is literally trying to find itself. The "male" and "female" are literally no different and it is impossible to tell which is which.

When you look at the picture the two gametes are exactly the same in every way except that they are facing each other in this picture.

The next two are forms of anisogamy:

(source: ulsfmovie.org)

Heterogametes

These gametes differ in at least one of the following:

size
structure
sex

Although it can also be a combination of these three things. [3] As you can see here the female can be structurally the same as the male. (Bottom and top examples of the second picture). From my understanding (although someone can come and prove me wrong) Oogametes are a specific from of heterogamous.

Oogametes

Oogametes differ in size, sex AND function. Females are stationary while males move. [4] Females are also much larger than males. (For instance in humans the cell that divides to make sperm divides equally while the cell that divides in the female divides to make one egg and three polar bodies.)


What kind of insect eggs are these (found in Malaysia)?

This eggs belong to Mictis profana which is a species of insect in the family Coreidae known by the common names crusader bug and holy cross bug. It is distributed in Australia, Indonesia, and the Indo-Pacific.


How does Hemocytoblast constantly get formed into so many blood cells and yet remains there in the bone marrow throughout the lifetime?

The trick for the stem cells lies in the way the proliferate and differentiate. See the image (from the reference 1):

Stem cells have the problem that they need to differentiate and maintain their population at the same time (subfigure a). This can either be done by asymmetric cell division which leads to one daughter which is still a stem cell and one which has been differentiated (subfigure b). Then it is possible that the cells divide only symmetrical (as shown in subfigure c) so they will either deliver two stem cells or two differentiated cells. And then it is possible (shown in subfigure d) that both possibilities are mixed and that symmetrical and assymetrical division occurs. Either way you get both: Differentiated cells and you still manage to maintain the stem cell pool.

References:

Asymmetric and symmetric stem-cell divisions in development and
cancer
Asymmetric cell division of stem and progenitor cells during
homeostasis and cancer
Asymmetric cell division


Can beavers control the direction a tree falls?

It is difficult to find a scientific answer to this question, but let me insert this citation from a specialist site:

  Contrary to popular belief, beaver cannot plan the direction in which trees will fall. Many trees become hung up in the branches of surrounding trees and are lost to the colony. In heavily forested areas, this loss may amount to one-half of the trees felled.

Another source says the same.

But scientists think beavers may actually plan the direction of falling:

  By measuring the falling angle of 888 trees of a variety of sizes cut
  near 8 different dams in southwestern Saskatchewan, we tested the
  hypothesis that beavers (Castor canadensis) fell trees in a non-random
  direction. We predicted that trees would be preferentially felled
  towards the dam to minimize the costs of transporting materials to the
  dam and to minimize the amount of time beavers spend on land. We
  established a 150 m wide × 250 m long transect at each dam and
  determined the felling angle of at least 100 aspen trees cut in each
  transect. We found that trees were felled by beavers with a mean
  felling angle of 357.9°, a direction not significantly different from
  that of the dam. In all, 62% of trees were felled within 45° of the
  direction of the dam. While our data are consistent with the
  hypothesis, an experimental test is required to establish the
  reason(s) for the pattern we found.

Their picture is better than thousands of words:

And another paper:

  We studied patterns in the orientation of cutting when beavers (Castor canadensis) cut trees around Alum Creek Lake in central Ohio. For 462 trees, we measured the slope at the base of the tree, the orientation of the cut relative to this slope, the distance of the tree from the water, the radius of the tree, and the symmetry of the cut. The land around Alum Creek Lake generally slopes toward the water, so to direct the fall of a tree towards the water a beaver should cut a symmetrical tree from the downhill side. Cutting from the downhill side occurred for trees >9.0 m from the water. Near the shore, trees tended to lean toward the water and would fall toward the water regardless of the side from which the beaver cut. At distances <9-0 m from shore, beavers cut predominantly from the uphill side where it should be easy to sit and there is little danger of the tree falling on them. At all distances, beavers showed random orientation when cutting trees on shallow slopes (<20°), whereas on steep slopes (especially slopes >30°) they cut predominantly from the uphill side. Beavers cut small trees (<5.0 cm diameter) mostly from the downhill side, but tended to cut trees >5.0 cm in diameter from the uphill side. Overall, enough factors interacted that no single pattern of cutting existed for all trees.


H3K36me3 role in RNA polymerase II elongation

We have a more recent study, Histone H3 trimethylation at lysine 36 is associated with constitutive and facultative heterochromatin and they seem to suggest that in accordance with your '05 paper, H3K36me3 in part contributes to the formation of tightly packed, inaccessible chromatin. You'll see there's a lot of crosstalk, but you would also think that transcription in heterochromatin might be poor.

Looking at yeast studies, though, it would seem that RNA Pol II is capable of transcribing through heterochromatin anyways so long as specific cofactors are present (Acetylation of H3 K56 Is Required for RNA Polymerase II Transcript Elongation through Heterochromatin in Yeast)


With help of canadianer (thank you) I think I found the right article, so just want to share.

This study not talking specifically about telomerase, but about the same approach of using promoters that are upregulated in tumors - exactly what I looked for. Published in 2014.

http://symbiosisonlinepublishing.com/genetic-science/genetic-science03.pdf

  However, the therapeutic approach in humans is limited by
  low efficiency of delivering the suicide genes and concerns regarding
  safety. Thus the number of clinical trials in human patients has been
  limited and treatment benefits observed modest. An intensive research
  effort is necessary to overcome these obstacles and turn suicide gene
  therapy into real benefit for our patients.


This is a pretty old old-wives tale, taking many forms: don't go out into the cold while it's raining, or without a hat, with wet hair, without a warm coat or scarf, without boots, etc., "or you'll catch your death of cold."

The old wive's tale was immortalized by Jane Austin in her book, Pride and Prejudice, when the heroine's sister Jane falls ill after getting a soaking in the rain.

This has been studied extensively. A New York Times article describes one such uncomfortable-sounding study:

  In the 1950's, Chicago researchers repeated the experiment on a larger scale with several hundred volunteers sitting in their socks and underwear in a 60-degree room before being inoculated with infectious mucus. Others, in coats, hats and gloves, spent two hours in a large freezer. The conclusion: all 253 chilled volunteers caught cold at exactly the same rate as 175 members of a warm control group.

In other words, being cold had no effect on catching a cold.

  A survey of the medical literature shows that for more than a century, scientists have invested an extraordinary amount of time and energy in debunking this old saw, with the aid of a small army of shivering, sneezing volunteers. But despite their efforts, the link between colds and the weather still lingers and continues to inspire yet more research.

A 1968 experiment studied the effect of (among other methods of chilling) a cold water bath at several stages during and after inoculation with rhinovirus (one of the many viruses responsible for the common cold). No effect.

Yet the studies continue, because anything shown to decrease the incidence of the common cold would be beneficial to the sufferers, as in the US alone, 75 to 100 million physician visits are due to the common cold, and millions of days are lost from school and work.

But what has never been proven is that getting chilled in any way causes one to come down with a cold.

There are a lot of studies that fail to show a corellation. However...
there are a handful of small studies that show that having cold and dry nasal mucosae increases the susceptibility of infection when inoculated with rhinovirus, though. So, if these studies are accurate, then being in the cold when exposed does increase the chance of becoming symptomatic.

'You'll Catch Your Death!' An Old Wives' Tale? Well...
Exposure to Cold Environment and Rhinovirus Common Cold — Failure to Demonstrate Effect
Acute cooling of the body surface and the common cold


Binding of Multivalent Antibody to mutiple epitopes?

Non-engineered IgM (such as is produced in vivo) has the same binding domain on all "arms" of the pentamer. They don't bind to more than one antigen, instead they can bind to multiple copies of the same epitope. Due to steric hindrance, a single IgM molecule generally will not bind at all 10 binding sites.


How to validate the use of an anti-virus monoclonal antibody in IHC by spiking a fresh organ with infected cultured cells?

Injecting into a fresh organ seems like a needless complication if you're just validating your antibody and not interested in gathering data about the interaction between the cells and the organ. (In fact, if you're using anything more complex than a flatworm I'd hope your IRB would have problems with needlessly sacrificing animals to get those organs.)

It seems like your purpose would be better fulfilled by making an FFPE cell plug and doing your IHC on that. Here's a protocol for making cell plugs:
Johns Hopkins Tissue Microarray Lab Cell Plug Protocol


Do people grow shorter as they age, how common is it, and what triggers it?

Short answer: Yes, we do shrink with age.

The most important reason is that the cartilage in the joints between our bones gets worn out and thinner, as well as disks between the vertebrae of the spine. This results in a compression of the spine and also to a loss in height. Shrinking bones due to osteoporosis can also play a role, as well as muscular atrophy due to ageing.

According to "The Baltimore Longitudinal Study of Aging" (reference 1) adults start shrinking by the age of 30 by 5-8mm per decade. This is relatively short after you completely stop growing. This process gets faster with increasing age, the study says it goes faster after 70.

Men and women do not shrink equally, men loose around 3cm between 30-70 and a total of 5cm by the age of 80. Women loose about 5cm between 30 and 70 and a total of 4.5cm by the age of 80 (these are average numbers from reference 1). Reference 2 also has a nice summary of this original article.

This effect can be attenuated by regulary excercising as the study listed in reference 3 shows.

References:

Longitudinal Change in Height of Men and Women: Implications for
Interpretation of the Body Mass Index: The Baltimore Longitudinal
Study of Aging
Yes, You Are Getting Shorter
Role of physical activity training in attenuation of height loss
through aging.


What is the blood ejection speed outward from human body vein?

Ah, I'm afraid there are a near infinite number of variables that will make a general answer impossible.  Factors such as: age, sex, weight, which vein, additional damage, heart condition, cholesterol level, body position, body temperature, and how the vein was cut and exposed will all lead to different answers.

A general answer from someone with lots of trauma experience, not very far.  Rarely if ever greater than 10cm.  Veins just don't have the pressure that arteries do.


Is recognizing one's own mirror reflection a valid test of animal intelligence/self awareness?

I think it is a necessary test of self-awareness. In order to make the connection that "I am the being in the mirror" and that every action I do will be reflected in the mirror (or, vice versa, every action I see the being in the mirror take is a reflection of my own action), one must first have a concept of self. One requires a constant present-tense (at least) story of oneself: "I am doing this. Now I am doing that. Oh look, I am doing this and that guy is doing the exact same thing." And then there's the ultimate realization, "Ah ha! That's me!". That realization would make no sense if the individual has no sense of "me"!

[speculation] On the other hand, perhaps it is too strict. It seems that it would unfairly favor social species, since it requires not only recognizing another member of the species (and being able to associate the anatomy of another member of the species with one's own anatomy), but it may also require the recognition of intent. That latter requirement is complicated by differentiating between intent and compulsion: at some point, one must realize that the being in the mirror isn't trying to copy but rather it always, inevitibly reflects one's motions. So, perhaps a cat is self-aware, in a sense that it has a constant story in its head of what it is doing and what it intends to do, but it cannot easily ascribe intent to other members of the species and thus cannot figure out that the cat in the mirror is automatically mirroring all of its movements. [/speculation]

Herein lies the rub: there is no perfect test for self-awareness; we can cast doubt on any outcome. The best would be if these animals could communicate with us by language. In lieu of that, we have to think of such tests that demonstrate with reasonable confidence that the species carries all of the characteristics that we attribute to self-awareness. I think another good test would be determining whether the species can plan individual actions in the future; in order to say, "first I will do this, then that; finally, that will allow me to do that", it seems like it would reasonably require an understanding of self and the consequences of one's actions. An example would be birds solving sequential puzzles.


Would two species of yeast with similar genome sizes have the same number of genes or chromosomes?

This question appears to start from the premise that different species of yeast are closely related, but they aren't. Saccharomyces cerevisae and Schizosaccharomyces pombe, both Ascomycetes, are thought to have diverged at least 300 million years ago (c.f. the mammalian divergence from other vertebrates was about 200 million years ago).

S. cerevisiae has a genome size of 12.1 Mb, with 5821 protein coding genes (plus another 786 dubious ORFs) spread over 16 chromosomes.

S. pombe has a genome size of 12.6 Mb with 5124 protein coding genes on just 3 chromosomes.

Filamentous fungi have larger genomes and gene numbers. From memory, Aspergillus nidulans has 8 chromosomes and over 9,000 protein coding genes. So, the similarity in gene numbers in the two yeasts probably reflects their broadly similar lifestyles.


Why are dietary recommendations for methionine consumption combined with cysteine?

In humans, cysteine can be synthesized from methionine and tyrosine from phenylalanine (note that the reverse pathways do not occur). Because their synthesis requires essential amino acids and the biosynthetic capacity of the organism does not always meet its need, they have been labelled conditionally essential. Under normal circumstances, an adult human can live with no dietary source of cysteine so long as dietary methionine is adequately supplied since the dietary deficiency can be compensated for by biosynthesis. Because of this, though, less dietary methionine is required when the diet is also supplemented with cysteine since less methionine is required to synthesize cysteine. This effect is known as cysteine sparing and a similar effect is observed with tyrosine/phenylalanine.
The data you cite are the reference values for PDCAAS, which is an indicative tool to evaluate the essential amino acid composition of protein sources. This system was introduced in 1991 by the WHO, and in this report they give the following rationale for their combined scoring of methionine and cysteine as sulfur amino acids:

The total of methionine and cystine [is] used for scoring purposes... Cystine is not an essential amino acid but can be synthesized from methionine. Cystine in a diet can thus "spare" methionine, and the total of the two has been found more satisfactory for scoring purposes than methionine alone.

They also recognize and somewhat address the weakness in this methodology that inspired your question:

While it is known that cystine can spare part of the requirement for methionine, FAO/WHO/UNU 1985 does not give any indication of the proportion of total sulphur amino acids which can be met by cystine. For the rat, chick and pig, the proportion is about 50%. Most animal proteins are low in cystine; in contrast, many vegetable proteins, especially the legumes, contain substantially more cystine than methionine. Thus, for animal protein diets or mixed diets containing animal protein, cystine is unlikely to contribute more than 50% of the total sulphur amino acids and scores calculated using cystine plus methionine will be appropriate. However, in certain all vegetable combinations, e.g. wheat and legumes, part of the cystine value may not be realized. Because of insufficient data on human requirements, however, the total of the two sulphur amino acids should, for the present, remain the recommended approach for computing amino acid scores.
...
A further complication arises from our lack of knowledge of the proportion of the total sulphur amino acid requirement which can be met by cystine. Without that knowledge, expression of protein values in terms of the sum total of methionine and cystine has both theoretical and practical limitations.


What is the normal duration of human sexual intercourse?

First, "premature ejaculation" is a matter of definition. Here is an authoritative source. From the American Urological Association's news site, a 2008 notice:

'The ISSM [Int'l Soc. for Sexual Med.] has defined premature ejaculation as “a male sexual dysfunction characterized by ejaculation which always or nearly always occurs prior to or within about one minute of vaginal penetration; and, inability to delay ejaculation on all or nearly all vaginal penetrations; and, negative personal consequences, such as distress, bother, frustration and/or the avoidance of sexual intimacy.”'

The main author of the ISSM paper was Sharlip. Sharlip ID, Hellstrom WJG, Broderick GA: The ISSM definition of premature ejaculation: a contemporary, evidence-based definition. J Urol, suppl., 2008; 179: 340, abstract 988.

If this is the threshold for PE then it is not a stretch to say that almost anything else is within normal limits. If "typical latency is 4-8 minutes" then 1.5 minutes would be near the low extreme of normal.

I think the issue of stress is at least as important as duration. If something isn't bothersome it never becomes a medical issue.

A nice study involving 491 men is reviewed here. The mean IELT (intravaginal ejaculatory latency time) is 5.4 minutes. As you can see from the graph on the site, most of the results are contained in the first few minutes with a tail of longer times to the right.

The original source for that information is MC Waldinger et al. A multinational population survey on intravaginal ejaculation latency time. Journal of Sexual Medicine 2005 2: 492-497. This also addresses your question about the timing of measurement--it's post-entry.

An expert in this area could update my information but it's a recent average so I don't think things have changed much.


What is the fluid clearance rate inside the retina?

As I mentioned in a comment, the RPE (retinal pigment epithelium) is in charge of absorbing the "water" from the retina and beneath it.

  Water is eliminated from subretinal space by active transport by the
  RPE. The transportation rate was estimated to range from 1.4 to 11 µl
  x cm-2 x h-1.


How are new staining protocols designed for microscopy?

This answer addresses the question of how stains were developed historically, which may bring into perspective your overly modern assumptions.

Most of these older (but stil very usefull!) staining techniques, such as haematoxylin (or rather haematein), cochenial/carmine etc. were inspired by the work of textile dyers of that era, starting somewhere in the middle of the 19th century.

It was more a question of trial and error, coïncidence and luck, rather than it being a case of systematic, structured research, starting from the well known molecular structure of the dye and the sample to be stained... Most of the time those were still -at least partial- mysteries.

You should keep in mind, that many of the protocols still in use, were developed in an era when the dye industry as well was still in its infancy, so to speak. Standardization of dyes, Biological Stain Commission and all that, came later. Biologists, histologists etc. used what worked for them. At that time, at that place, with that lot of dry dye powder. Much inspiration, the right idea at the right time and a fair amount of luck. Up to well into the 20th century.

As an illustration: in 1917-1918 there was a shortage on haematoxylin in the German histopathological labs, due to the allied blockade. A lab worker, Fraulein Wilhelmina Schmidt, inspired by the impossibillity to remove elderberry stains from her hands, wondered if it would be possible to use elderbery juice as a substitute for haematoxylin. As there wasn't really an alternative, it was tried. Elderbery juice was concentrated by boiling, diluted with an alum solution and tried. It turned out to work very well.

The story went unnoticed until 1949, when an article on it was published in the German “Zeitschrift für die Wissenshaftliche Mikroskopie”. In the article, the author, Grüber, pointed out that, even after more than 20 years of storage, the slides were still vividly stained, not showing any trace of fading.


How much smaller is the diffusivity of a molecule in the retina as opposed to the vitreous of the eye?

Unfortunately, I don't have a good, simple answer for you. The reason is that the answer may depend significantly on details of the macromolecule more than its size - like how strongly it binds to the environment.

In addition, within an environment that is more elastic than viscous, and with a very complex shape, you might expect to get various sorts of anomalous diffusion, rather than a single diffusion coefficient.

Transport in tightly confined biological spaces is complex, and still pretty controversial. A paper I found useful as a simple introduction to some of this:
Morphogen Transport - http://dev.biologists.org/content/140/8/1621


Can jellyfish improve the Black Sea ecosystem?

To quote the PI from the BBC article:

But, Dr Dabiri explained, the jellyfish were unlikely to be the "primary ocean mixers".  "Crustaceans - like copepods and krill - are likely the primary biogenic mixers, because there are so many of them," he explained.
"But much of the open ocean is like desert," he added, "and the density of these animals is unlikely to be sufficient (to cause mixing)."

My guess therefore is no, jellyfish would not be sufficient to dramatically change the current structure of ocean layers.  Animals in general, as the paper and its references suggest, do contribute significantly, on-par with tides and wind.


There are some recipes available on the web, my answer is based on this webpage and this information:
The process itself is rather easy and you can either use ready bought apple juice, homemade juice or apple cider (basically unfiltered apple juice). You will need some specially cultivated yeast, baker's yeast is generally not recommended since it might produce a lot of unwanted (and probably bad tasting) side products.
For the fermentation itself you need some (very) clean vessels in which the process can take place. These should be from a material which is not corrosive, as the vinegar would otherwise react with the vessel. Food-grade plastic, glass or stainless steel should be ok.
To have the reaction take place, the process need oxygen, otherwise the reaction will stop at the step of ethanol. This is also why acoholic fermentation is always sealed against the air, to avoid the oxidation of the alcohol the acetic acid. A cheese cloth will leave oxygen in, but keep insects and other contaminations out. If you need to filter the vinegar at the end of the process, a standard coffeefilter is good enough.
The following step by step directions come from this website:

Step 1 - Make or buy your apple cider or apple juice
Apple juice or apple cider is the starting point for making apple
cider vinegar. You can make your own, or buy it ready made, fresh,
bottled or frozen.  You can use a mechanical or steam juicer to
produce the juice / cider. To make your own juice (which is the same
as plain unfermented apple cider), see this page. Keep in mind that
you want to select sweet apples, like Fuji, Delicious, Mutsu, Gala,
etc. Green, unripe and unsweet apples (like Granny Smith) do not have
enough sugar to make good cider vinegar. Tips about selecting apples:
Apples used for cider don't have to be flawless. They do, however,
have to be free from spoilage. You can use blemished apples and small
sized apples. You can mix apple varieties together or use all one
variety. The only rule is to cut out any spoilage areas on otherwise
good apples. Spoiled areas will cause the juice to ferment too rapidly
and will ruin the cider. Don't use apples that appear brown, decayed
or moldy. Apples should be firm and ripe. Green, undermature apples
cause a flat flavor when juiced. The best cider comes from a blend of
sweet, tart and aromatic apple varieties. A bushel of apples yields
about 3 gallons of juice.
Step 2 - Make your starter yeast
Adding yeast to activate fermentation is not essential, but will speed
up the process and can produce a higher quality. Special cultivated
yeasts are available for this purpose at wine-making shops and
biological labs but bread yeasts are not recommended. To make a
starter, crumble one cake of yeast into one quart of cider and mix.
This makes enough starter for 5 gallons of cider; double the recipe
proportionately when making more.
Steps 3 - Making Alcohol and Acetic Acid
Pour all of the juice or cider into one or more containers to about
three-quarters capacity; do not close the lids on the containers.
Instead, cover the openings with cheesecloth secured with a rubber
band or string.
Step 4 - Store out of direct light, but some place with constant temperature
Stir the mixtures daily, making sure the cheesecloth is put back in
place. Keep the containers away from direct sunlight and maintain the
temperature at 60 to 80 degrees F.
Step 5 - Keep stirring daily, monitoring and tasting for the next 3 to 4 weeks
Full fermentation will take about 3 to 4 weeks. Near the end of this
period, you should notice a vinegar-like smell. Taste samples daily
until the desired strength is reached.
Step 4 - Filter Mother of vinegar
When the vinegar is fully fermented, filter the liquid through several
layers of fine cheesecloth or filter paper—a coffee filter works well
for this. This removes the mother of vinegar, shown at right,
preventing further fermentation or spoilage of the product. Mother of
vinegar is completely harmless and the surrounding vinegar does not
have to be discarded because of it. It can be filtered out using a
coffee filter, used to start a bottle of vinegar, or simply left in
and ignored.
Step 6 - Done! Storing Your Vinegar
The vinegar is now ready for storage in separate, capped containers.
Stored vinegar will stay in excellent condition almost indefinitely if
it is pasteurized. To pasteurize, heat the vinegar before pouring it
into sterilized bottles, or bottle, then place in a hot water bath. In
both cases, the temperature of the vinegar must reach at least 140
degrees F to pasteurize the product, and should not exceed 160 degrees
F. Use a cooking thermometer to ensure the correct temperature is met.
Cool the containers and store at room temperature out of direct
sunlight.


Differences Between Protein Motifs and Protein Domains?

These are completely different concepts, which sometimes may be connected.

A motif in biology is a mathematical model, typically of a sequence, that predicts which sequences belong to some defined group. For example, a DNA sequence motif can characterize the binding site of a transcription factor, i.e. which sequences tend to be bound by this factor. For proteins, sequence motifs can characterize which proteins (protein sequences) belong to a given protein family. A simple motif could be, for example, some pattern which is strictly shared by all members of the group, e.g. WTRXEKXXY (where X stands for any amino acid). There are also more complex motif models.

Protein domains, on the other hand, are a structural entity, usually meaning a part of the protein structure which folds and functions independently. So, proteins are often constructed from different combinations of these domains.

So how are motifs and domains related? Well, when you think about protein families, it makes sense not only to look at the whole sequence but also to focus on individual domains. Since they are a elementary functional-structural units, it makes sense to find sequence motifs for individual domains. So, you often find that a protein contains multiple domains, each domain characterized by having a sequence that matches the motif of its family.