Is it possible to express the cistrons from a polycistronic insertion fragment in a single plasmid?

If I understand correctly, you are seeking option for polycistronic expression. Have you considered using T2A or P2A sequences? These come from virus and essentially break polypeptide into two parts, so-called self-cleaving peptide T2A. Real mechanism of its work is that ribosome stalls on the sequence and unable to create peptide bond, effectively re-starting translation with next after T2A amino acid.

Of course, you lose independent control over expression, both products will be expressed at same level (but degradation might be different).

So, you should consider creating construct that looks something like that:

lac:gene1-T2A-gene2-stop

Thing is that a) it might not work in E.coli and b) it might not be necessary, because primary purpose of T2A is equal expression level of two polypeptides. And, if your 2 genes are big, for bacteria it is easier to handle two separate plasmids, rather than one but much larger.


Providing small molecules to cells on a filter plate

Perhaps you're looking for these hanging inserts, for example: "Millicells"


Doubt in a multiple choice question involving cell organelles

I would say Nucleus is the odd one out. Chloroplast (which have Grana in them) and Mitochondria are involved in the process of creating/breaking down energy, whereas the Nucleus is, so to speak, the blue-prints of the cell.

To summarize:

Chloroplast is involved in Photosynthesis to create energy

Grana are in the Chloroplast, which is involved in Photosynthesis

Mitochondria are "the powerhouse of the cell" and help break down energy (ATP > ADP)

Nucleus is the cell's blue-prints

Therefore, it seems that the Nucleus is the least like the others.


This is, indeed, a nymph (what you called a young stage), but not from a cicada as you suspected: it's a nymph from a leafhopper, which are hemipterans from the Family Cicadellidae (cicadas are also hemipterans, but they belong to the Family Cicadidae). More specifically, this seems to be a sharpshooter, which are leafhoppers from the Tribe Proconiini.

Narrowing down to the Genus is more complicated, but I'd guess it is Oncometopia. Here is an image of Oncometopia orbona for comparison:

This other image (also Oncometopia orbona) is even more similar to yours:


What is the Attributable Risk of birth defects in Zika infected pregnancies?

The article cited in the question (Vital Signs: Update on Zika Virus–Associated Birth Defects and Evaluation of All U.S. Infants with Congenital Zika Virus Exposure — U.S. Zika Pregnancy Registry, 2016) gives the base rate for the definition of "birth defect" that they use:

  The baseline prevalence of defects consistent with those that have been observed with congenital Zika virus infection was approximately 2.9 per 1,000 live births in the pre-Zika years (4). The initial findings from the USZPR represent an approximate twentyfold increase in Zika virus–associated birth defects among pregnant women with laboratory evidence of possible recent Zika virus infection, with an approximate thirtyfold increase in brain abnormalities and/or microcephaly.

The reference for that background is Baseline Prevalence of Birth Defects Associated with Congenital Zika Virus Infection - Massachusetts, North Carolina, and Atlanta, Georgia, 2013-2014.:

  These data, from Massachusetts (2013), North Carolina (2013), and Atlanta, Georgia (2013–2014), included 747 infants and fetuses with one or more of the birth defects meeting the case definition (pre-Zika prevalence = 2.86 per 1,000 live births). Brain abnormalities or microcephaly were the most frequently recorded (1.50 per 1,000), followed by neural tube defects and other early brain malformations† (0.88), eye abnormalities without mention of a brain abnormality (0.31), and other consequences of central nervous system (CNS) dysfunction without mention of brain or eye abnormalities (0.17). During January 15–September 22, 2016, the U.S. Zika Pregnancy Registry (USZPR) reported 26 infants and fetuses with these same defects among 442 completed pregnancies (58.8 per 1,000) born to mothers with laboratory evidence of possible Zika virus infection during pregnancy (2). Although the ascertainment methods differed, this finding was approximately 20 times higher than the proportion of one or more of the same birth defects among pregnancies during the pre-Zika years.

According to Estimating the Number of Pregnant Women Infected With Zika Virus and Expected Infants With Microcephaly Following the Zika Virus Outbreak in Puerto Rico, 2016. the background of microcephaly in Puerto Rico was around 12 cases per year, while they estimated 180 cases would occur in the presence of Zika.

  We estimated an IQR of 5900 to 10 300 pregnant women (median, 7800) might be infected during the initial ZIKV outbreak in Puerto Rico. Of these, an IQR of 100 to 270 infants (median, 180) may be born with microcephaly due to congenital ZIKV infection from mid-2016 to mid-2017. In the absence of a ZIKV outbreak, an IQR of 9 to 16 cases (median, 12) of congenital microcephaly are expected in Puerto Rico per year.

This is modeling, not pure observation, but was based on observed risk. The paper is online full-text (I think) so you can follow through the assumptions if you want.


After some general research there are specifically 3 arguments that I came across that people give for supporting this particular theory.

1) somebody seriously injured might be given an anesthesia shot by the doctor or whoever that treats him first up for relief from the pain and distress. This would lead to relaxation of the stomach muscles and the contents of your stomach can travel up to your throat and into your lungs which would be fatal. Read about pulmonary aspiration.

2) the second case is if there is an injury to the gut or the GI tract, then providing water would be counter productive. A layman might not be able to assess the level of injury to someone just by sight.

3) the third is that giving water would increase blood pressure and (sometimes) apparently dilute the scars. This could also lead to chances where sutured wounds might reopen.

There are no real guidelines as to how much water can be given to an injured person. Depends on the situation or how much time he has been bleeding for and the kind of environment that he is subjected to like you pointed out. Some medics have recommended sucking on citrus fruits to prevent dehydration. Also, swabbing the patient all over the body with a cold compress can provide some relief and delay dehydration.

Guidelines for bleeding victims are here.


Legality of doing private or scholastic virology with human pathogens?

tl;dr I think that doing this unofficially, at home, might be no big deal, but doing it in an institutionally supported lab (or any kind of institutional setting, e.g. if you wanted to publish a paper from the results) could involve lots of hassle and red tape.

I'm not a microbiologist, but ... technically I think this would fall under the category of BSL-2 - via Wikipedia:

  Biosafety level 2 is suitable for work involving agents of moderate potential hazard to personnel and the environment.[9] This includes various microbes that cause mild disease to humans, or are difficult to contract via aerosol in a lab setting.[11] Examples include Hepatitis A, B, and C viruses, human immunodeficiency virus (HIV), pathogenic Escherichia coli, Staphylococcus aureus, Salmonella, Plasmodium falciparum, and Toxoplasma gondii.

BSL-2 requires (among others) access control for labs; special safety training for all lab personnel; use of containment equipment for procedures that may cause infectious aerosols or splashes ...

It may seem a little crazy to lump a common-cold-causing rhinovirus with HIV, but BSL-1 (the mildest level of infectious agent control) is restricted to

  well-characterized agents which do not cause disease in healthy humans

(emphasis added). Note that even BSL-1 requires lab safety protocols beyond those for non-infectious agents.

A bit more internet searching on BSL classification for rhinoviruses (the typical cause of the common cold) suggests some variation: e.g.

Google search for "rhinovirus BSL" brings up a bunch of hits from the American Type Culture Collection (ATCC) for a variety of rhinovirus isolates that range from BSL-1 to BSL-2
the Public Health Agency of Canada classes rhinoviruses as BSL-2


Recycling and storage of nitrogen from breakdown of macromolecules?

Short answer: This is because the most common form of nitrogen found in multicellular organisms (not incorporated into any other compound) i.e. ammonia is too toxic to be stored or recycled.

Background: Ammonia, the product of deamination of amino acids, is basic in nature ($NH_3~+~H_2O \rightarrow NH_4OH \rightleftharpoons NH_4^+ + OH^-$) and thus disturbs intracellular pH (Ohmori et al, 1986). Though the mechanisms through which ammonia exerts its toxic effects are not known, hyperammonemia is known to alter several amino acid pathways and neurotransmitter systems, cerebral energy metabolism, nitric oxide synthesis, oxidative stress and signal transduction pathways, leading to irreversible damage to the developing central nervous system: cortical atrophy, ventricular enlargement and demyelination; causing cognitive impairment, seizures and cerebral palsy (Braissant et al, 2013).

Talking about how it is produced (just for information, skip this part if you are aware of urea cycle): Amino acids are deaminated for storage since the carbon skeleton of these amino acids can be easily converted to glucose or fatty acids for storage. This reaction yields ammonia which, in liver, is converted to urea (via urea cycle) which is not only less toxic, but also requires lesser water for excretion. See this page for more information and the diagram below.

Talking about why it is not recycled, there has always been a constant supply of amino acids to organisms (through nitrogen fixation or food). Indeed, amino acids are deaminated for storage i.e. we already have more than enough of it. Also, storing urea is also not easy since it is toxic too (it is just less toxic than ammonia). And since these products are so much harmful, it seems difficult for an organism to evolve itself so that it can store toxins rather than just throwing it away so that it can later be ingested in a useful form (amino acids from plants or herbivores). Finally, evolution works as decent with modification, meaning if something is a better alternative of current situation, it is not necessary that organisms will evolve towards that (unless there is strong selection pressure for it). In short, evolving to recycle nitrogen is (most likely) just not worth it.

P.S. you might be interested in this question to know more about evolution. Another answer here talks about storing excess nitrogen by adding ammonia into amino acids, yielding glutamate and glutamine. However, this process can be used only to a limited extent due to limited amount of substrate ($\alpha$-keto glutaric acid and glutamate) in the body. Also, excess glutamine in the body can have many major and minor side effects like skin rash, vomiting, etc. (see here for full list). Also, excess glutamate has much more pronounced effects. Since glutamate is a neurotransmitter, its excess causes cellular damage. This is what makes it an excitotoxin (see this for more details). Apart from this, the substrate ($\alpha$-keto glutaric acid) is an intermediate of Krebs cycle and is important in many other cellular activities (see here for details). So, its deficiency (caused due to conversion into glutamate) can easily affect many crucial metabolic activities. Thus, though this process seems an effective way of recycling nitrogen, it has many side-effects and is not much reliable i.e. can only be seen as an immediate solution. This is why when glutamate and glutamine build up in body, they are converted back to $\alpha$-keto glutaric acid and glutamate and the ammonia released via urea cycle.


is there an easy way to remember taxonomy?

Have a look at Wikipedia > List of mnemonics#Biology.

Dear King Philip Came Over For Good Soup
Do Kings Play Chess On Fine Green Silk?
Dumb Kids Prefer Cheese Over Fried Green Spinach
Do Kindly Place Cover On Fresh Green Spring Vegetables
Donald Kills People Cause Other Friends Get Sad

Given the current political situation I would go with the last one but it is up to your personal preferences. You can as well make up your own. Mnemonics are like soups; it is always better when homemade. For example, extending upon the last and inspired by @John's comment, here is a homemade mnemonic

Donald Kidnaps People's Children Causing Outlaw Foreigners Great Suffering

Enjoy the game!


Also, what is a hot pepper phenotype? What makes a phenotype a phenotype?

Phenotypes are the quantitative or qualitative characteristics that arise from the interaction of an organism's genetics with the environment.  For pepper plants, height is a phenotype, as are leaf color, average fruit weight, and pretty much every other characteristic you can measure. Capsaicin concentration (mass of capsaicin per unit mass of fruit) is a phenotype that is relevant to hot pepper enthusiasts.

  What causes significant variation of pod shape and size on the same plant? Environmental factors? Genotype/genetic factors?

It's hard to know.  There could be a genetic component that results in inequitable distribution of resources to individual fruits during plant development. There could be environmental factors that determine why one fruit is larger than another -- perhaps the larger fruit developed during a time when water and sunlight were plentiful to the plant.

  Are peppers on the same plant genetically identical?

See this excellent answer given by mgkrebbs to the question Are the seeds in a single capsicum fruit genetically identical?


Why would it evolve?

No research (that I can find) is consistent with specific time of day mating across many species. I can't think of any reason why even just a few quite different mammals (e.g. mice, bats, lions, whales, and humans) would all find a fitness benefit of mating at the same specific time of day and therefore it is highly unlikely to evolve. I would suggest that if there are consistent patterns they are no reason other than coincidence (correlation over causality).

For example, dawn and dusk peaks in activity...

I have no references to back this idea up but lets see how this goes. The majority of mammals will be awake around dawn and dusk because there is likely an over lap between nocturnal and diurnal species at these times. Given that mating (normally) requires the participants to be awake then this would be a time when more animals are awake it is therefore a more likely time for mating to occur. But, as I already mentioned it would purely be because of the increased numbers awake.

Simple statistical illustration of the dawn & dusk idea...

Imagine a raffle with 2000 winning tickets. You buy 1000 and put 500 hundred of these in a box called nocturnal and the other 500 go in a box called diurnal. The raffle is drawn 24 times (perhaps every hour). The first 14 times it is drawn you can win if the ticket is from the nocturnal box, the latter 14 times you can instead check the diurnal box. This means during the first 10 draws you have a 25% chance of winning, and likewise in the latter 10 hours, but in the middle 4 hours there is a 50% chance every draw.

This comes down to a simple statistical phenomenon, if you don't buy a ticket you can't win the raffle.


Is the basic reproduction number unique?

It should be noted that many of the methods you talk about aren't necessarily for getting a number but rather a formula for $R_0$, all of which should be equivalent.

However, when those methods step into the realm of getting a number by fitting parameters, they may give different results as they handle certain aspects of the data differently.

You are certainly "allowed" to use any formulation of $R_0$ you want - just document what you did.


This fish called neon velvet damsel fish (Neoglyphidodon oxyodon)

Check wikipedia


Duration of selection and survival of the fittest

Could not fit in a comment..

Welcome to Biology.SE! Here are a bunch of comments.

The sentence until it evolves into a new species and / or the old ones become extinct sounds weird and there seems to be some confusion between evolution and speciation. Also it seems that you have a very static view of what is a species, as if species were predetermined categories into which evolution came to show itself!
I am not sure but I think your question has to do with "valley crossing", that is "how can a population evolve toward some phenotypic trait if intermediate phenotypic traits are not fit?" Is that your question? You may be interested in "shifting balance theory" but it might be a bit too advanced.
It is common to overconsider the valley to cross (the deleterious impact of interemediate traits) and those traits are not necessarily so deleterious
Mutations do not always have small effects on traits. One mutation may have some very important impact and therefore, one mutation alone might be enough to cross a whole valley! You amy be interested in Fisher's geometric model. Fisher's geometric model is just some very arbitrary model and is not much inspired by any biological observation but it helps getting the concept of how mutations impact fitness (=function of survival and reproductive fitness).
When you say how do animals who are not well adapted get enough time to evolve to survive? I may use the word animals to refer to populations or to individuals in a population (extinction of genotype is a population and extinction of populations are two different things). If you referred to individuals then, your interest seems to be into "valley crossing" and "mutational effect"(effect of a mutation on phenotype or fitness). If you referred to populations, then you may be interested in "evolutionary rescue" or more broadly speaking in the so-called "theory of extinction".
There are probably other posts (or part of answers) on this site that will help you. A very good answer would be very very long. But maybe a moderately good answer may be relatively short!


The latin name for this animal is Leiobunum rotundum and Nelima fuscifrons, order Opiliones.

examples:
link


Is it possible to feel pain in some part of a body, but the pain "feeling" is introduced somewhere else?

Yes, this is pretty common.  Examples include

sciatica, pain felt down the back of a leg to the foot, from irritation to components of the sciatic nerve but commonly at the level of the sciatic nerve roots
angina pectoris, pain from myocardial ischaemia felt in the throat (Latin angina "infection of the throat"), arms, chest etc
shoulder tip pain from a subphrenic abscess

The clearest possible example of this is phantom limb pain, where pain is perceived to be arising from an amputated limb indicating that the pain is arising from central mechanisms.


What information does the KEGG Module statistics page show?

My understanding is that these statistics show the coverage for each KEGG Module in the particular phylogenetic group. For example, M00001, is found in 275 of the eukaryotic organisms in KEGG (which represents 90.5% of the eukaryotes in KEGG). The same logic applies for other groups.

An quick example demonstrating this hypothesis, done with the Protists group found in KEGG Organisms (since it is easier to count by eye). There are 43 protists, and in the statistics it says (as of 2015/7/9) that module M00001 is found in 33 of them, hence: $33/43=0.7674419$ which agrees with the 76.7% shown.


Why did viruses evolve in the first place?

The are different theories about virus evolution, some speculate that they were evolved before the cells, some speculate they are evolved to spread genetic information, a sort of specialized conjugative pilus others say that they are cellular parasites. Still, none has the final answer yet, but thanks to the boost of DNA sequencing, many new pieces of the puzzle come out lately so keep updating your knowledge!

Whether they are alive or not is also matter of discussion and it pretty much depends on the definition of life itself.
If you define life as the property of reproducing, transmitting genetic information and evolve, then viruses are life forms. But if you want to include in the definition that a life form must have all the biomolecular machinery encoded in the DNA (I really disagree on this point), then they are not. To me, they look quite a living thing.

About your sentence:

  So what's the point of all this? Infecting the host and causing so
  much trouble for the host...

I think you are looking only at the "negative" side. Viruses can transfer useful genetic information, plus they are involved with the evolution itself. We humans have lot's of viral DNA in our genome, so no viruses, no humans as we know them. Think about it ;)

There are plenty of resources around to get a better insight please have look at the following links to get started.

https://en.wikipedia.org/wiki/Viral_evolution

https://en.wikipedia.org/wiki/Evolution_of_influenza

http://www.sciencedirect.com/science/article/pii/S0042682215000859

https://link.springer.com/article/10.1007/s00239-013-9601-0

https://www.nature.com/search?order=relevance&q=evolution%20of%20viruses


I think that there are a few things going on in this question, I'm going to try to answer the ones that I think are most pertinent:

We should not expect "topology" as used in the Hi-C field to have a rigorous mathematical interpretation. Most of the people thinking about it are ultimately biologists who are interested in biological problems. As suggested in the comments, they are basically interested in the shape of DNA in the cell; e.g. which pieces of DNA are close together and which are far away. You can use this information for a lot of different purposes of course, but most people using the technique are satisfied with viewing topology as "the set of pairwise distances between all DNA chunks" (and whatever things you can infer from that set).

Your sense (from the comment) that the linear chromosome ordering is the main interesting feature of topology is (IMO) absolutely correct. However, it is not a given that every chromosome is put together the same way. This is related to the most useful application of Hi-C data that I know of, which is to either (A) scaffold genomes (put discontinuous sequences into the right order) or (B) deconvolute mixed populations of genomes into groups of sequences that belong to the same cell. The linear order of DNA is by at least an order of magnitude the dominant signal in the data, and is therefore the most trustworthy thing in there.

Network topology is sometimes implicit but generally central as a feature of algorithms using Hi-C data. I don't know that we can say that all workers in the field are thinking of this when they talk about topology, but I certainly am. Some random papers that make it fairly obvious: here, here, here.

(Full disclosure: I work for a company that sells Hi-C kits and services.)


Gene expression for mathematicians: where to start?

I suppose you first need to learn the basics of genetics before investigating the stats behind gene expression clustering. I will based my recommendations on Khan Academy, that is generally speaking a good very introductory source of information for biology and other fields.

Basics of genetics

Here are a few questions for you:

What exactly do we call the genetic code?
Are you aware that genes are transcribed into mRNA that are translated into proteins?
What is an allele?
Do you know what is an exon and an intron?
Do you know what is a TATA box?

If you answered no to any of these question I would recommend that you have a look at Khan Academy > Central Dogma.

Gene regulation

Then, you should have a look at Khan Academy > Gene regulation

Other

Don't hesitate to have a look at other sections in the biology series of khan academy if you want to broaden your understanding of e.g. what DNA looks like, what is happening at reproduction, how do genes segregate, or other things such as evolution. Typically, Khan Academy > biotechnology could also be helpful as to give you a rough feeling of the methods used to investigate gene expression

Gene expression clustering

The literature on clustering gene expression is very rich (see google scholar).


Meaning of the word "targeted" in a description of chromatin immunoprecipitation

Looking at the article, I think they could leave out the word "targeted".
I think they used it because what is being enriched is not a promoter DNA, but the section of promoter DNA bound to the protein and antibody.
I suppose they could use  "...enriched 4.1-fold more FOLR1 Promoter DNA-CIC protein complex,..."
It is a little awkward or clumsy because the protein targets the DNA, and the antibody targets the protein.
So it is not always very obvious what the word "targeted" is referring to.
But without "targeted" I think the meaning is still clear enough.


What would happen if VEGF was injected into a person?

VEGF is a family of growth factors that promote angiogenesis and vasculogenesis.

Vascularization is a key step in the progression of cancer, so the VEGF family has often been a target for suppression: preventing vascularization of tumors can stop their further growth.

That said, your premise that VEGF hasn't been tried clinically is false: there have been several clinical trials of VEGF (and no doubt more that I didn't find).

Hedman, et al 2003 used catheter-based VEGF gene transfer at the time of angioplasty/stenting, though they found it did not prevent restenosis they did see increased perfusion (it seems to me that further research didn't show sufficient effects on long-term outcomes). Ripa, et al 2006 used VEGF gene transfer as part of a treatment for ischemic heart disease. It seemed like the treatment was safe, but the efficacy was limited. Ropper, et al. 2009 attempted VEGF gene transfer for the treatment of diabetic polyneuropathy. They found some improvement of pain, and report a fairly high rate of adverse events but their control group also experienced adverse events.

It seems like a similar VEGF plasmid is available in Russia as Neovasculgen for use in limb ischemia; the company developing the drug is in the process of beginning to get approval elsewhere.

VEGF as a topical application has been studied under the name telbermin, for example Hanft, et al 2008.

There may be others, but I stopped my search there. https://clinicaltrials.gov/ is a good place to start looking for what research has been done in humans if you have trouble finding journal articles at first.

Hanft, J. R., Pollak, R. A., Barbul, A., Gils, C. V., Kwon, P. S., Gray, S. M., ... & Breen, T. J. (2008). Phase I trial on the safety of topical rhVEGF on chronic neuropathic diabetic foot ulcers. Journal of wound care, 17(1), 30-37.

Hedman, M., Hartikainen, J., Syvänne, M., Stjernvall, J., Hedman, A., Kivelä, A., ... & Närvänen, O. (2003). Safety and feasibility of catheter-based local intracoronary vascular endothelial growth factor gene transfer in the prevention of postangioplasty and in-stent restenosis and in the treatment of chronic myocardial ischemia: phase II results of the Kuopio Angiogenesis Trial (KAT). Circulation, 107(21), 2677-2683.

Ripa, R. S., Wang, Y., Jørgensen, E., Johnsen, H. E., Hesse, B., & Kastrup, J. (2006). Intramyocardial injection of vascular endothelial growth factor-A165 plasmid followed by granulocyte-colony stimulating factor to induce angiogenesis in patients with severe chronic ischaemic heart disease. European heart journal, 27(15), 1785-1792.

Ropper, A. H., Gorson, K. C., Gooch, C. L., Weinberg, D. H., Pieczek, A., Ware, J. H., ... & Kirchmair, R. (2009). Vascular endothelial growth factor gene transfer for diabetic polyneuropathy: a randomized, double‐blinded trial. Annals of neurology, 65(4), 386-393.

Simovic, D., Isner, J. M., Ropper, A. H., Pieczek, A., & Weinberg, D. H. (2001). Improvement in chronic ischemic neuropathy after intramuscular phVEGF165 gene transfer in patients with critical limb ischemia. Archives of neurology, 58(5), 761-768.


Identify this tuber like object found on beach

It is spongy because it is a sponge, specifically a sea sponge. There are quite a large number of them native to the waters around england. I would guess Craniella cranium based on shape and location but I am by no means an expert on sponges.
Here  a cross section of a cleaned sponge

and sediment laden potato sponges after a hurricane.

you can see more images of collecting these here, http://www.vims.edu/newsandevents/topstories/archives/2011/irene_blobs.php

Here is a whole website dedicated to english sea sponges, http://www.aphotomarine.com/sponge_suberites_ficus_sea_orange_sulphur.html


Where can I find pdb files for macromolecules like receptors?

As pointed out in the comments, if you look for PDB files and you don't find them in the PDB, there is no solved structure. However, you can look in databases that contain models of proteins. Especially for the receptors the coverage has been increasing in recent years and so you may be lucky.

A good starting place to look for protein information is UniProt, where you find links to the Protein Model Portal and SwissModel. They contain models based on the PDB structure for Metabotropic glutamate receptor 3.


What is the difference between intials cells and meristems cells?

Meristems are undifferentiated plant cells. There are two types:

apical mesistem that occurs at tips or branches and roots as well as buds which produces elongation, and
lateral meristem or cambium that produces lateral growth (stem thickening).

As cambium cells divide, cells toward the inside differentiate into xylem (wood) - these cells are 'xylem initials'. Cells toward the outside that eventually differentiate into phloem tissues (inner bark) and are 'phloem initials'.

One could similarly label apical meristem cells that are in the postion and/or process differentiating into leaves or flower organs as x-initials.


What exactly happens to hydrogen atoms in step 4 of citric acid cycle?

Short answer:

There should have been an additional $\text{H}^+$ on the left-hand side.

Long answer:

You have rightly observed that the left side of the equation is deficient in one hydrogen atom. Let me draw your attention to another issue: the charges on both sides are different too. The left side has one negative charge too many. This gives us a clue: possibly there is a missing $\text{H}^+$ on the left.

This reaction is actually the sum of three reactions catalysed by a multi-enzyme complex. If you add the balanced equations for the reactions of $\alpha$-ketoglutarate dehydrogenase, dihydrolipoyl transsuccinylase and dihydrolipoyl dehydrogenase, you will see that there is indeed an additional $\text{H}^+$ on the left-hand side, which is omitted in your textbook.

But that is the case with most biochemistry/molecular biology texts. Biologists are very bad at balancing their equations, especially when it comes to $\text{H}^+$ and $\text{H}_2 \text{O}$. They balance out only the major reactants and products. The rest is often, er, left as an exercise to the reader.


Why doesn't surgical steel cause inflammation?

Some can
First the terms you are looking for is biocompatibility and bioactivity. The study of them is called biomaterial science. Both fields are relatively new so complete answers do not exist, there has been a certain amount of trial and error in find suitable materials.
There are a dozen factors that go into these things, toxicity, whether they corrode in the body, whether they are soluble, chemical reactivity, whether they trigger an immune response, whether they can bond with bone or other tissues, mechanical resilience, steric and electrical properties, wetting, even how smooth it can be made can have an effect. The other important thing is many materials have very different biocompatibility depending how and where they are used, different parts of the body can have very different conditions, for instance material used in a bone screw might be useless in a dental implant (different PH and chemical exposure) or a heart valve (different mechanical and electrical requirements).
Titanium has remarkable biocompatibility with internal bone implant, its already low reactivity actually gets better as its surface oxidizes as it becomes slightly polarized and will incorporate many cellular surface molecules(passivation). Many of the factors that make titanium useful in this way are still being studied.
Surgical steel is a broad term that covers several types of steel used for  multiple medicalpurposes, it includes steel implant and steel only used for instruments. Some forms of surgical steel work great for instruments but are rarely for internal implants, often because the same nickel content that makes them corrosion resistant is also bioreactive, triggering an immune response, but its superior mechanical properties means it still is sometimes used as implants, especially temporary implants were corrosion is less of an issue.  (paper, sorry it is only available in German). Nickel free surgical steels used in cutting implements is stronger and harder (what you want in a medical blade) but  without nickel it will quickly corrode in the body.
Part of the reason your doctor did not know was some aspects are still unknown in general and the study of these properties is rather specialized so a general practitioner may have never studied the parts that are known. Consider an  pilot still know very little detailed metallurgy of their engine components, and still be an excellent pilot becasue they don't really need to know.  Heck most of reason I know anything about it is I used to hang out with a guy who made titanium implant screws for a living and it just sounded kinda interesting so I read up on it.


Are B Cells unique to an individual's immune system?

Remember first that the human body nearly always, although there are exceptions, rejects any non-genetically identical graft placed into it, and therefore one cannot prepare a general colony of B-cells to confer immunity to the population at large. However, in principle, there is no impediment to removing B-cell progenitors in an individual, conditioning them to produce antibodies (which would be an artificial analogue of the natural process of 'Clonal Selection'), and re-injecting these differentiated B-cells into the patient. To my knowledge this process is currently beyond the capacity of our current cell culture techniques, as B-cell differentiation is controlled by an elaborate cell-signaling process, and even if it was feasible, it would remain impractical for several reasons. First, since the B-cell products, antibodies, can be transferred humorally, and should be tolerated by the general population, many existing treatments simply involve injecting antibodies into the patient's bloodstream. Examples of antibodies taken from volunteers' sera are the RhoGam preparations as well as IgG mixtures used to treat certain forms of immunodeficiency. There is a means of growing B-cells in culture to produce antibodies of precise specificity (i.e. monoclonal antibodies - note that clonal selection occurs in a living host for this technique, the B-cells are subsequently harvested then immortalized in culture). Adalimumab is a therapeutic monoclonal antibody.

There is however, very promising work being conducted involving T-cell vaccination, which is technically similar to what you described. The advantage in using T-cells is that these leukocytes can orchestrate an immune response, mobilizing the several, diverse elements of the immune system to respond to a specific antigen. These techniques are being principally researched as cancer treatment regimens.


Using exogenous genes to reduce the set of essential amino acids?

Decreasing the number of essential amino acids is frequently used as a selection marker during molecular biology experiments: An organism (usually yeast) that cannot synthesize a certain amino acid is first grown in the presence of said amino acid in the media. Then it is transfected with a gene of interest together with the gene that enables it to synthesize the amino acid. Now being grown in a culture medium that does not contain the amino acid, only individuals that were successfully transfected can grow, the others will starve.

A similar approach was also used in  Beadle and Tatum's Nobel prize-winning work on the one gene-one enzyme hypothesis.


How can two biological sequences be anything but homologous?

Homology in this context is always a matter of degree exactly because of shared ancestry. Measures of homology are often in terms of "percent homology" (or more often "percent similarity" as evidence of homology) or some other measure that allows representation of that degree.

To emphasize why this makes sense, think about a receptor family. In an extant organism, you might have 3 receptors that all are homologous. However, if receptors 2 and 3 are more similar to each other than to receptor 1, then you can make some better assumptions about the history of the evolution of receptors 1 to 3, that there is likely a "common ancestor receptor" to both 2 and 3. There is more "information" if you consider the degree of homology rather than just its existence.

At some extremes, sequences could be so different that even if they share a lineage they may have now diverged to the point that they are not distinguishable from independent sequences. However, selective pressures prevent such complete reorganization in key sequences and so at least some homology can be maintained across very distantly related organisms.

As far as deciding what is "homologous" versus "not homologous", that is somewhat of an arbitrary threshold that depends on levels of evidence and the purpose for recognizing the homology.


Distance to source populations and/or environmental gradients?

First of all, species richness is most likely the dependent variable (the one you want to explain), while distance to the source pool and pH are the independent variables (the ones you assume to have an effect on species richness).
The problem you are describing is termed multicollinearity and a common problem in regression analyses. The good news is that it does not affect the prediction of your model as a whole. The bad news is that the estimates for you individual predictors become increasingly erratic the higher their correlation is. You can estimate the severeness of multicollinearity in your model with the Variance inflation factor (VIF). Wikipedia explains nicely how to interpret the VIF:

The square root of the variance inflation factor tells you how much larger the standard error is, compared with what it would be if that variable were uncorrelated with the other predictor variables in the model.
Example
If the variance inflation factor of a predictor variable were 5.27 (√5.27 = 2.3) this means that the standard error for the coefficient of that predictor variable is 2.3 times as large as it would be if that predictor variable were uncorrelated with the other predictor variables.

You should calculate the VIF for your model. Many sources state that a VIF < 10 is still acceptable, but since there is no rule of thumb, I suggest to do some further reading on the topic if you get some critical value (just google "dealing with collinearity" and you'll find tons of material).


Are harmful gases abiotic or biotic factors in our environment?

Bez is correct, biotic and abiotic refer to the nature of the agent performing the stress.

biotic = living thing (lion that is actively engaging in catching you as food)
abiotic = non-animated (far from optimal temperature)

Now the example "shade" is trickier; because it depends on the perspective you choose.

There's always a context. Does the element creating the shade matter in your context?
If so, and this element happens to be animated/living:  stress = biotic (though you should reference at some point that the object at hand is animated).

If it doesn't matter what object generates the stress since you are only interested in the effect of the shade on a system: shade = abiotic

Pipeline: Analyze the context, choose and communicate your choice of perspective/angle and then remember what biotic and abiotic literally mean.

Coming back to "harmful gases": What is your context meaning harmful for whom? Specify that first. Carbon Dioxide is an example of something that may be deleterious at a specific concentration for one system and at the same time beneficial for another.

Does it matter how these gases were produced? CO2 may be a product of an animated system's metabolism and thus may be called abiotic. It may also be a product of oxidation of a multitude of carbohydrates.

I don't know of an example where Carbon Monoxide is produced by living things.

You could of course circumvent this discussion by analyzing what harmful effect the gases have on your system of interest. For example: they generate respiratory stress on humans, and then you use the effect of the gases on the system to characterize them.


Is the deep ocean fish look ugly because due to darkness there is no visual sexual selection?

I suspect the deep ocean fish look ugly to you because they are unfamiliar.  The iconic fish species with which humans have coexisted forever are all surface fish, with common adaptations for surface living in the light.  When one thinks of a fish the salmon or cod is what we think of.

The deep fish have different selection pressures.  They do not need to be streamlined or svelte.  A deep fish might think a surface fish is ugly because it cannot make its own light - how plain and dull.  How can the surface worlders find a good mate if everyone is dark?


Kinetic Vs Potential Energy in Biochemical Contexts

I think you are right and many examples are ambiguous.  Even D) is ambiguous as a molecule is always in motion due to entropy except, perhaps, at absolute zero (0 Kelvin). But normally, it does contain kinetic energy.

However, as you already identified the ambiguity, look at the best, or in this case least incorrect answer; The only option without any physical movement explicitly mentioned in the question description is D). All the others mention 'emit', 'flight', 'rushing down', etc.

Also ask your teacher :)


Why is a hippo so big if it has round about the same genes as a mouse

Genes are the "plans" for proteins in an organism; in turn, those proteins do all sorts of things, catalyzing chemical reactions and making up much of the structure of an organism.

A hippo is much bigger than a mouse, but it isn't that much more complex: both are going to have the same sorts of organs like a heart, lungs, kidneys, liver, brain. If you look at an individual cell from each animal from the same tissue, they will probably look almost identical! They are going to have similar metabolic pathways, etc. Their genes will be different, because some differences in proteins are necessary to build organisms of different structure and size, but the number of genes doesn't have to vary much, the hippo just needs to produce a lot more of the gene products, not have more plans.

A hippo will of course have way more genetic material, because it also has more cells and there is a copy of the DNA in every cell, but what your teacher is talking about is the number of genes within each cell.

Ultimately, genes come from evolution. You can read more about the basics of evolution somewhere like Berkeley's Evolution 101.


Here are two free articles that go into the subject very nicely, I think:

Major Histocompatibility Complex (MHC)
How pathogens drive genetic diversity: MHC, mechanisms and misunderstandings

The MHC loci are the single most important determinant of our immune system's response to foreign invaders and are absolutely necessary for discrimination between self and non-self.  Because of the massive diversity amongst those pathogens, no one single MHC allele will allow the best response.  For example, the delta-32 deletion that bears resistance to HIV also increases susceptibility to West Nile; if you're more likely to suffer from the latter, that is a fitness reduction that could be selected against.  Thus, more alleles will survive in the population as all can be advantageous.  This is called balancing selection.

Additionally, the microbial invaders mutate and evolve much, much faster than our genome does, so you want to have the greatest breadth of MHC present in the population and in an individual in order to maximize resistance to whatever may arise.  At a population level, it is also advantageous because it means that the entire populace won't succumb to a certain infection.  If everyone has similar alleles one virus could wipe everyone out; we observe something similar happen with our crops, for example, when grown in massive monocultures.  There is also a fair amount of evidence, mainly in humans and mice I believe, supporting a role for MHC in mate selection.  Individuals seem to find potential mates with different MHC alleles more attractive, presumably to maximize the fitness of their offspring.

MHC is an absolutely fascinating subject (I'm researching it at the moment!).


Can you still contract a disease after being vaccinated and be able to spread it?

I tried to break down your question into smaller parts and answer them individually:
Q. What is immunity?
A. Simply put, immunity is the ability to react to an infectious agent and stop it from causing disease.
Q. Do vaccines make you immune to infectious diseases?
A. Yes, by definition. If it doesn't make you immune, it's not a vaccine.
Q. Can we get disease even after being vaccinated?
A. Yes, because no vaccine is 100% efficacious. For example, the MMR vaccine has about 97% efficacy in preventing measles.
Q. Do vaccines prevent infection?
A. It depends on how the vaccine works. Some vaccines enable the immune system to actually reduce survival and multiplication of the infectious agent. The polio vaccine is an example$^1$. It leads to generation of antibodies that neutralise the virus$^2$.
Other vaccines prevent disease (or reduce its severity) but do not prevent infection. The diphtheria toxoid is a good example of this$^3$, because the antibodies generated by vaccination neutralise the toxin while leaving the bacterium unscathed. (I believe all toxoids behave like this.)
Q. Can we spread infection even after getting vaccinated?
A. Yes. This is easy to see for those vaccines (like diphtheria, mentioned above) that prevent disease but not infection.
Vaccinated individuals can spread infection with the other, multiplication-stopping kind of vaccines too. Again, this happens because no vaccine is 100% efficacious. Note that chances of spread are reduced (as compared to the unvaccinated scenario), even if they are not zero. For instance, see the work of Seward et al$^4$ on breakthrough varicella.
Q. The big question: is getting vaccinated more dangerous than not getting vaccinated?
A. Sorry, but this is not the place to discuss it. It requires a careful look at the risks and benefits of vaccination, not just for the individual but also for the community at large. That would be a discussion more appropriate for Medical Sciences Stack Exchange.
To summarise: yes, we can catch a disease and spread it even after being vaccinated. The chances of this happening vary with the kind of vaccine.

Journal articles cited

Howe HA. Am J Public Health Nations Health. 1957 Jul;47(7):871–5. https://doi.org/10.2105/ajph.47.7.871
Faden H, Modlin JF, Thoms ML, et al. J Infect Dis. 1990 Dec 1;162(6):1291–7. https://doi.org/10.1093/infdis/162.6.1291
Miller LW, Older JJ, Drake J, et al. Am J Dis Child. 1972 Mar;123(3):197–9. https://doi.org/10.1001/archpedi.1972.02110090067004
Seward JF, Zhang JX, Maupin TJ, et al. JAMA. 2004 Aug 11;292(6):704–8. https://doi.org/10.1001/jama.292.6.704

Suggested reading

https://www.who.int/health-topics/vaccines-and-immunization
https://www.ncbi.nlm.nih.gov/books/NBK27131/


Do all RNA polymerase in Eukaryotes share the same transcription factors?

Except for the TATA-binding protein (TBP), there are no common transcription factors for each RNA polymerase. However, there are homologies between many of the factors used by the different enzymes.

The paper Conservation between the RNA Polymerase I, II, and III Transcription Initiation Machineriesa gives a good overview over the different initiation factors of each RNA polymerase enzyme. It contains a comparison of various transcription factors in yeast.

Here is an excerpt form the paper showing the homologies between some of the initiation factors of the TFII group and their homologous counterparts. (The first schematic is RNA poly II, the second RNA poly I, and the third RNA poly III):

Source:

a Alessandro Vannini, Patrick Cramer, Conservation between the RNA Polymerase I, II, and III Transcription Initiation Machineries, Molecular Cell, Volume 45, Issue 4, 24 February 2012, Pages 439-446, ISSN 1097-2765, https://doi.org/10.1016/j.molcel.2012.01.023.


Why is cartilage replaced by bones in a vertebrate adult?

Bones are complex organs, made of more than just a structural element. Cartilage is just a tissue, usually devoid of nerves and blood vessels.

Chondrichythes live in water (ἰχθύς ichthys is Greek for 'fish'); the difference in specific gravity and buoyancy is considerable, and cartilage is not robust enough to mechanically support your body out of the water.

Vertebrates have evolved to have a bone marrow, which is part of the bone. If the structural element of the bone (the dense mineral matrix) was replaced by cartilage only, then the hollow structure would make things even worse.

Additionally, cartilage has about the same density as water (Pan et al, 2016) whereas dense bone is 60-90% more dense, which means extra weight pulling aquatic animals down.


It's a phenomenon called Frisson.  From the wikipedia page.

  Frisson (French for 'shiver') is a sensation somewhat like shivering, usually caused by stimuli. It is typically expressed as an overwhelming emotional response combined with piloerection (goosebumps). Stimuli that produce a response are specific to the individual.

  Frisson is of short duration, usually no more than 4–5 seconds, usually pleasurable.1 Typical stimuli include loud passages of music and passages that violate some level of musical expectation.[2]

There is some interesting research that shows it occurs when a sound contains certain chords or has certain notes because of how our biological setup reacts to those specific notes.  See the "crying chords" that were supposedly present in Adele's song "Someone Like You". npr article about crying chords


Why are different lengths of nucleotides taken for structure prediction from an miRNA match area after BLAST analysis?

There is no hard and fast rule for how many nucleotides you have to select. If your miRNA is ~20nt and you take 70nt from both sides (average length of hairpins is ~84nt in humans), your total length will be 160nt. The point of taking $\pm70nt$ is that you don't know if your read is -3p or -5p. So take 70nt from both sides.

The maximum length of a human miRNA hairpin is 180nt for mir-3648 (90nt per half hairpin). In such cases you may take more flanking residues. But these cases are rare.


Why are riboswitches mostly present in bacteria and not in eukaryotes?

You get higher accuracy and more timely control at a post translational level (think about the time it takes to affect a pathway with cofactor stimulation compared to gene expression stimulation). You also have more points of control throughout the pathway if you affect activity post translationally allowing for a more complex interaction between stimulating and repressing factors.


Are there known life expectancy differences in non human mammals by sex?

Yes, there are. It is not well studied in general, but for certain species it is. Here is a relevant excerpt (Austad, Fischer, 2016):

Females live longer than males in humans and all Old World monkeys and apes for which we have the best data. . . This appears to be true in both wild and captive populations. . .  Yet whether there is a general mammalian pattern of greater female longevity under protected, captive conditions where intrinsic physiological aging dominates mortality patterns, is not known because so few species have been rigorously investigated. What is known about the best described species indicates that all show a substantially different pattern from humans.

See the linked study for more information. There is a whole section on sex differences in lifespan in mammals.
In general, in any species where males fight fiercely amongst each other for status, I would also consider it likely that males have shorter lifespan on average than females. Although I don't have a good citation for this at the moment.
In a more recent review, Lemaître et al (2020) confirmed the tendency for females to outlive males across many mammalian species:

In human populations, women consistently outlive men, which suggests profound biological foundations for sex differences in survival. Quantifying whether such sex differences are also pervasive in wild mammals is a crucial challenge in both evolutionary biology and biogerontology. Here, we compile demographic data from 134 mammal populations, encompassing 101 species, to show that the female’s median lifespan is on average 18.6% longer than that of conspecific males, whereas in humans the female advantage is on average 7.8%. On the contrary, we do not find any consistent sex differences in aging rates. In addition, sex differences in median adult lifespan and aging rates are both highly variable across species. Our analyses suggest that the magnitude of sex differences in mammalian mortality patterns is likely shaped by local environmental conditions in interaction with the sex-specific costs of sexual selection.


Why does excess dopamine activity in the pleasure centers results in less pleasure in schizophrenics?

Short answer
The dopamine hypothesis includes brain regions with reduced dopamine transmission as well. The prefrontal cortex in specific has reduced dopaminergic activity and is implicated in anhedonia. It affects pleasure seeking behavior through interactions with the nucleus accumbens.

Background
The negative symptoms of schizophrenia are less well understood as the positive counterparts. One thing is for sure, the dopamine hypothesis cannot explain everything. It is a very useful working hypothesis, but primarily based on the first generation antipsychotics such as haloperidol with mainly dopaminergic mechanisms of action. In turn, these drugs mainly and effectively target the positive symptomatology (excessive dopaminergic transmission).

Second-generation antipsychotics are more effective in treating the negative symptoms and are thought to actually increase cortical dopamine, as well as and acetylcholine release, as well as have a variety of effects on the glutamatergic system not shared by the typical agents first-generation antipsychotics (Meltzer, 2004).

In fact, the dopamine hypothesis has been improved and adjusted during decades of intensive research. One of the important things that has come out of this is that dopamine neurotransmission is regionally affected, with a prefrontal hypodopaminergia (prefrontal cortex, or PFC and a subcortical hyperdopaminergia (e.g. in the pleasure centers). An excellent review of the historic developments in the dopamine hypothesis was published by Howes & Kapur (2009)

Now on to anhedonia. Pleasure perception per se seems largely unaffected in schizophrenic people, it is the anticipation of pleasure that seems negatively affected. This is accompanied by reduced motivation and goal-directed actions to seek pleasure. Anhedonia is primarily attributed to disturbed interactions between the ventral (nucleus accumbens) and dorsal striatum (mainly the caudate) and the PFC and not so much in the experience of pleasure per se. In addition, insular cortex, amgydala and hippocampus may be involved. A dysfunctional coupling between the anterior cingulate and the insular cortex (the “salience network”) has also been linked to the failure to appropriately process reward in schizophrenia. Lastly, goal-directed actions needed to obtain the reward and dependent on the PFC is dependent on not only dopaminergic, but also adrenergic and other mechanisms. This is all nutshelled information and I would encourage you to read Milan et al. (2014), who have written an extensive and excellent review focusing on anhedonia in specific as a negative symptom. Fig. 1 is obtained from that paper and shows the complexity of anhedonia.

Fig. 1.  Cerebral circuits involved in negative symptoms, with a focus on deficits in anticipatory reward. source: Milan et al. (2014)

Reference
- Hows & Kapur, Schizophr Bull (2009); 35(3): 549–62
- Meltzer, Curr Opin Pharmacol (2004); 4(1): 53-7
- Milan et al., Eur Neuropsychopharmacol (2014)24(5): 645-92


What portion of America needs the Flu vaccine for herd immunity effects to become substantial?

Quoting Jhung et al. 2011 talking about H1N1 2009 epidemics

  Although estimates of R0 from past pandemics vary, the R0 of previous pandemic influenza viruses generally range from 1.5 to 1.8 for the 1957 H2N2 and 1968 H3N2 pandemic viruses, and 1.8–2.4 for 1918 H1N1 influenza A strain, with a high estimate of 5.4 by Andreasen et al [see also White et al]. During the current pandemic, White et al used CDC case-based data from 1368 confirmed and probable cases with a date of report on or before 8 May 2009 and estimated the reproductive number of pH1N1 virus to be between 2.2 and 2.3. Estimates decreased to 1.7–1.8 after adjustment for increased case ascertainment during the initial pandemic period. In a sensitivity analysis making use of previous estimates of the mean serial interval, White et al estimated that the reproductive number was between 1.5 and 3.1. Fraser et al used data from the initial outbreak in Mexico to estimate R0 in the range of 1.2–1.6. Yang et al used reported case clusters in the United States to estimate R0 to be 1.3–1.7. Most estimates of R0 for pH1N1 virus, therefore, have indicated that the virus was at the low end of transmissibility, compared with the strains that caused the 1918 pandemic, and was comparable to or slightly less transmissible than the strains that caused the 1957 and 1968 pandemics.


Your spider shows an apparently large size, a large round cephalothorax, with smaller and thinner abdomen, very long and sturdy legs, with a long 'foot', and is a general brown color, with some darker markings on the legs.
This is consistent with one of the larger varieties of spider found in the warmer areas of the world, and trading under the name of Huntsman Spider, or Giant Crab Spider.  There are a number of species of these spiders in the family Sparassidae.
As it happens, the most common variety of Huntsman, Heteropoda venatoria, is found pretty commonly in southern India (reference link example included: http://www.southindianspiders.org/south-indian-spiders2.htm ), and I'm quite confident that this is what you have there.  Here is an example, from the US website Bug Guide, of this species:

Like almost all spiders, this spider is venomous, but like almost all spiders, its venom is not particularly troublesome to us humans.  A bite from a spider this big would be moderately painful simply from the large fangs, and the venom doesn't appear to usually add too much to it.  Here's a short but amusing discussion of such bites, from an Australian website: http://sciabc.us/IL2pR

These are sort of the spider equivalent of Geckos - commonly foraging in human homes for the various critters that like to make pest of themselves (cockroaches, mice, etc.) - but they never try to sell us insurance.


How do sarcomeres coordinate contraction?

I'm answering question 1, I think it'd be better to post these questions separately.

Consider action and reaction: myosins (thick) filament is experiencing force F towards Z line.

If the muscle is acting on something that is movable (e.g. you're pulling on a drawer which isn't locked), the force F towards Z line is greater than the force that maintains your thick filaments in place, and they'll slide towards Z line. The speed at which they slide is limited by the rate at which myosin heads can detach once they have performed power-stroke.

If the drawer is locked, then force F cannot overcome the external force. This force however is normally lower than the force required to tear actin or z-line, it is limited by two molecular factors: myosin will stall and not effectuate power stroke under too strong an opposing force, and myosin heads  will detach after some time and relax the tension they have built up. This is how you get the maximum force under clamped conditions.


Why are C4 plants mainly tropical plants?

This is not my field, so the following is based solely on a brief reading of Internet sources.

The Wikipedia entry on C4 carbon fixation states:

  When grown in the same environment, at 30°C, C3 grasses lose approximately 833 molecules of water per CO2 molecule that is fixed, whereas C4 grasses lose only 277.

However it does not explain why this is so.

In contrast, the section in Berg et al. focuses on the energy losses caused by photorespiration and makes the following initial point:

  …the oxygenase activity of rubisco increases more rapidly with temperature than does its carboxylase activity. How then do plants, such as sugar cane, that grow in hot climates prevent very high rates of wasteful photorespiration?

The answer to this (didactic) question is the C4 pathway (as described in full in that text), but the answer to the question posted here  is that “tropical plants employ the C4 pathway because of this increased wastage of energy through photorespiration at the higher temperatures in which they live.”


During exercise muscles are put under stress which eventually causes micro tears in the muscle fibres.

These micro tears put pressure on the nerve endings which causes the pain.
The body will then repair the tears during rest and recovery using proteins and sufficient fuel. The muscle will then become slightly bigger and stronger.

Energy systems used to repair these lesions are the following

There are three different types of energy systems:

Phosphocreatine
Lactic Acid
-Aerobic

1.Phosphocreatine Energy System

The ATP-PC system lasts for 8-10 seconds.
During the ATP-PC system a phosphate breaks off of the ATP to form ADP and a lot of energy.
ADP will then bind with another free phosphate to form ATP.
The ATP-PC system is an anaerobic energy system as it dose not use oxygen.

Lactic Acid Energy System

Glucose is broken down sustain performance for a longer amount of time than the ATP-PC system.However this system does not use oxygen so is not suited for events over 90 seconds.
When the ATP-PC system starts to fade the process of anaerobic glycolysis begins.
Glycogen is stored in the liver and is broken down without the presence of oxygen.
This produces lactic acid which limits energy production.

Aerobic Energy system

The aerobic energy system is constantly being used in your body to supply the muscles with energy.
In sport the aerobic energy system is used for events that last anything over 90 seconds.
The aerobic system can be used constantly but only if there is a constant supply of glycogen and fatty acids.
The aerobic system uses oxygen, glucose and fatty acids to yield large amounts of ATP.
The system takes place within the mitochondria and produces two bi-products, carbon dioxide and water.


Why exactly are the reflections of sunlight in this dragonfly's eye hexagonal?

Here is the image in comments. The direction of the sun can be seen from the shadow of the left antenna. I just sketched this image to note some observations, it's the best answer that I can find at this time.

source


Finding phylogenetic distance between sequences?

No, because it is really not a binary decision. There are attempts to associate percent pairwise difference with taxonomic ranks (particularly species), but this is problematic because every independent lineage can vary according to its own rate. You could use sequences from different families, or orders, or even phyla, but these two can depend on whether specialists in the field are lumpers, or splitters. For example, all ants are in the same family, and Formicidae is over 100 million years old, while birds that may have diverged from a common ancestor within the last 10 million years are in a different family. You can use pairwise distance OR higher-level taxonomy as a proxy. But it would be crude. Why not program your software to make hard decisions about homology, and then find the closest most distant homologue in terms of pairwise differences?


Why is ATP used as a source of energy rather than glucose?

Well the mechanics of this can actually get pretty complicated, depending on how far into the biochemical weeds we want to go, but there are a couple of very simple reasons at the core... Well they actually aren't that simple, but they can at least be analogized in simple ways.  The first, and easiest to illustrate is this.  This is a glucose molecule:

And This is an ATP molecule:

If you want to get some energy out of an ATP molecule, all you have to do is break off one of those phosphate groups.  If you want to add more, you just stick another phosphate group back on.  This can be done without significantly changing the structure of the molecule itself.  That Adenosine base never gets touched.  Only the chain of phosphates is manipulated.  It is much more energy efficient to add and remove those phosphate groups than to add and subtract elements from a glucose molecule, as there is no way to effectively break it down without significantly changing its structure, which makes it harder to build back up.  We want a molecule that it is just as easy to add energy to as it is to pull energy out.  The glucose molecule just doesn't have a chain sticking off that's easy to remove and put back at will.  The CH2OH group on the end looks like an attractive energy sink on its face but getting the whole thing off isn't nearly as easy as it looks, and it doesn't contain as much energy as a phosphate group either, which brings us to the second easy to illustrate reason ATP is more attractive than glucose as an energy carrier.

If you look at that chain of phosphates, you will notice that they are each separated by an oxygen atom.  There are also a bunch of convenient hydrogens and OH groups floating around that make hydrolysis and dehydration very easy.  Where would you hydrolize the glucose molecule to produce a low energy molecule that can be converted back to glucose more efficiently than ADP can be converted back to ATP?  Just compare this process:

To this one:

The ATP hydrolysis looks more like the breaking down of polysaccharides into glucose than the catabolism of glucose itself, and this is at the core of the difference between the two molecules.  It is always easier to add and subtract links from a chain than it is to make direct modifications to one of the links themselves.  Glucose is great for energy storage.  You can pack a lot of energy into a glucose molecule, but once you get it out, it's very hard to put it back.  It's much easier just to throw out the waste and start over by making or eating another one.  We don't have this luxury with ATP.  It has to be able to drop off its energy load and go pick up more.  For this, the structure of ATP is much more appropriate than the structure of glucose.


The main plant in the photo (with the larger leaves) is called Virginia creeper. The botanical name is Parthenocissus quinquefolia.   The leaves are very distinctive in leaf groups of 5 to 7 leaflets.  It is an aggressive woodland vine in the grape family Vitaceae.

Links:
https://en.wikipedia.org/wiki/Parthenocissus_quinquefolia

https://plants.usda.gov/core/profile?symbol=paqu2


Online repositories of scanning electron microscope photographs?

First off I'd like to reccomend the University of Dartmouth's publicly available collection located here.  They have both SEM and TEM images of a wide range of organisms and cells from algae to see urchins through everything from cholera to mammalian cells.  Images are high quality, fully captioned and properly attributed.

I'm a little confused as to the problem you're having with google - see my original comment on your question.  However I have looked at the photos of Wikimedia Commons in the SEM category and see that they are either images taken with, images of SEM Microscopes or technical drawings regarding their function.  I assume that you're looking for the images taken with SEM.

I was able to find a great number of similar images to those in the commons with a Google Image search - I read above that you were having problems with this approach so perhaps try the search term "SEM images" in image search (or this search to avoid duplications from images you have already seen on Wiki Commons)?

Examples found on just the first page:


The pressure you need to apply is equal to your systolic blood pressure, about 120 mmHg. This is about 163 g/cm^2.


What is the significance to life of the anomalous properties of water?

This is a brief treatment of your question, specifically:

  the fact its solid form is less dense than its liquid form - is extremely important. ...crucial for the development of life.

I can't speak to the importance of this property in the development of life (as I don't know the exact conditions of the world when life began, and therefore the role expansion of ice played in it) but life would not continue without it.

Water does not conduct heat very well, therefore water temperature fluctuates more near the surface of a body of water (say a lake, an ocean, or even a river) than in the deeper regions. In the winter, surface water freezes.

If water were denser on freezing, it would sink to the bottom, and liquid water would replace it. That liquid water would freeze, sink, be replaced, etc.

When it became warmer, the frozen water at the bottom would be less affected by surface temperature, i.e. it would be less likely to melt.

Even with summers, because of the failure of deep ice to melt, eventually you would be left with a mostly frozen body of water, and life doesn't carry on well in those conditions (freezing of the cells of plants and animals in the water would cause cell lysis, again, because of the expansion of water within), whereas life in a liquid under a frozen surface carries on much better. Life in the water would die.

If there were no life in water, then life on land would be most difficult. (Consider most of our oxygen comes from phytoplankton in the oceans. Even if the phytoplankton didn't happen to die from being trapped in frozen water, their nutrient supply would be cut off, frozen below.)

That's just the tip of the iceberg, really. The anomalous expansion of water also affects ocean currents and weather in ways that enrich life on earth.

Since you didn't ask about the other properties of water, this answer doesn't address surface tension, etc.

Edited to add: Corrected an error about the thermal conductivity (insulating properties) of ice. Ice does conduct heat more than water. It may be advantageous to the temperature of the water below possibly by holding snow (which does insulate well).

Source
Thermal Conductivity
Plankton: Ocean Drifters


Is there any biological evidence that is not suggestive of or seems to disprove evolution?

Evolution is a broad field of knowledge. There are definitely a few elements of our current theory of evolution that does not perfectly match observations. However, those concern small details and might not of much interest to you. Here are a few examples

We don't know the relative importance of background selection and selective sweep at explaining genome-wide variation in genetic diversity.
We don't really have much of an idea what fraction of speciation happen in sympatry.
We don't understand well how recombination rate evolves to differ in different genders.
We don't really understand what are the limits and/or costs of phenotypic plasticity that makes phenotypic plasticity less frequent that we would otherwise expect.
We don't really understand the patterns of genetic diversity on sexual chromosomes at the intersection with the pseudo-autosomal region (PAR).
We don't fully understand how much expansion load (a type of mutation load caused by the sampling of individuals at the expansion edge of a population) there is in human population.
We don't really know whether the mitochondrion (and other double membranes organelles) was first a endo-parasite or a endo-symbiont.

If you are asking whether there are evidences suggesting that evolution is not happening or that humans and chimpanzee do not actually share a common ancestor but were created independently, then no, there is no such evidence.

You should have a look at the related post Is Evolution a fact?


This is a Privet (Genus Ligustrum). It appears to be Ligustrum vulgare which is known as Common Privet, or sometimes European Privet.

It is a common woodland understorey shrub in Europe, often planted as garden hedging in urban areas as it is semi-deciduous and responds well to repeated pruning. You could never really call it a tree, it is a shrub species.

The white flowers as you say are quite fragrant and pleasant. They develop into shiny black/dark purple berries.


What are the distinct neurochemical components of sexual pleasure?

Sexual response is primarily related to nitric oxide and its products. All of the systems you mentioned play a role, however the core pathway is from touch stimuli, to oxytocin release, to nitric oxide and dopamine accumulation, to motor response (orgasm) followed by prolactin to counteract said neurochemicals and temporarily suppress sexual response.


What problems do invasive species cause ?

Here is an attempt at a partial answer.

  What is so bad about invasive species ?

Invasive species have been introduced to a new habitat by humans (or by natural means).

They usually do not have a predator in a new area nor are the pathogens in the area very adept at infecting them. So, they may proliferate rapidly and compete with the native species. They may also be ferocious predators as their preys do not have defenses against them.


Explain a gene network to a first year undergrad

There is no single answer, because networks (or graphs, as they are called in discrete mathematics) are flexible tools that can be used to model all sorts of relationships between genes, transcripts, proteins, or other entities in biology. (And networks are useful models in many other disciplines too, like sociology.) Depending on the type of network you're considering, there are various experimental methods for determining connections. I give only a couple of examples below. For general information on networks as abstract models, look into graph theory.

Gene regulatory networks

A gene regulatory network is a directed graph where one gene (A) regulates another (B). In this case, the connections between genes are directional and can be represented by arrows A $\rightarrow$ B. Depending on exactly how you define "regulation", a connection A $\rightarrow$ B can mean different things, for example:

Gene A encodes a transcription factor that binds to gene B. In this case, evidence for A $\rightarrow$ B comes from assays of proteins binding to DNA, such as chromatin immunoprecipitation (ChIP). Large collections of such data are available in databases like Transfac.
Expression of gene A causes regulation of gene B, by any mechanism (possibly indirectly). In this case, data for an interaction can come from experiments where gene A is induced (forcibly expressed) or suppressed/deleted and the resulting changes in other genes are measured, for example by microarrays or RNA sequencing. A famous early example of this is the "Rosetta" data set on yeast deletion mutants.

Inference of gene regulatory networks is a large and complicated topic that I cannot cover here. It depends on many factors, such as how you model the time dimension (do you have steady state or transient data), and how you parameterize the network to model expression data quantitatively. The review suggested by @CMosychuk looks like a good place to start.

Coexpression networks

This type of network represents coexpression between genes (or more accurately, between mRNAs or proteins). This is typically a representation of pairwise correlations between genes across some set of conditions, so the data source can be any collection of mRNA or protein level expression data. (Here is one example.) Because correlations are symmetric, connections in this type of network have no direction, and can be represented simply as a link A$-$B (not an arrow). Partial correlations are sometimes used to filter out indirect associations, but still these networks contain no causality information, and should not be confused with the directed type.

Protein-protein interaction networks

These are undirected network models where a link A$-$B means that two proteins interact physically. Data supporting such connections come from various biochemical assays for protein interaction, such as the two-hybrid assay or immunoprecipitation. There are large databases collecting protein-protein interaction data that can be used to build these network models, for example BioGRID.

There are many other types of networks, but this is already a long answer :) As you can see, it's important to be clear on what type of network you are working with. Often the data you have available will determine what network model is suitable --- for example, if you have only a collection of unrelated transcriptome profiles and no causality information, a coexpression network might be the best model.


I think you probably mean insect and pest control from plant extracts.

I have seen posters where extracts from herbs were pretty effective in killing insects.  Really common herbs - rosemary, basi.   It makes sense that plants (and animals) would evolve chemical defenses against insects.

For instance, a quick search under google scholar talks gives you an idea of the research going on (mostly not in the US) here.  Pestoban, an Indian herbal preparation is quite effective against some pests while less effective (~50% effective) in removing fleas from treated livestock.

It also stands to reason that the compounds found in edible herbs and plants would tend to be selectively effective against insects found in the environment local to the plants.

Another related topic is the search for antibiotics in herbs and spices.  Tumeric is a common topic of research, which explains one of the possible reasons its used in cooking. Garlic components show interesting medical properties too.

While this may seem suspect to some, the research is done in the West too, but it is usually spun a different way. In general if you are looking for bioactive compounds that are not completely toxic (like heavy metals or cyanide for instance), you would want to look at compounds which are made by living things.  Nearly all pharmaceutical designs come from or are derived from plant or microbial / fungal extracts.   This is in fact the field of Natural Products Chemistry which is still a big thing in chemistry and biochemistry.  Few if any of the hot targets of organic synthesis are not some fancy compound found in a plant, fungus or sponge extract.  E.g. the surreally complex Palytoxin, the miracle breast cancer drug Taxol, and the venerable cholesterol control drugs, the Statins.


How does the original ionic distribution restore after synaptic transmission

Most of the depolarization in the presynaptic terminal is still sodium-based, it's just that there are also calcium channels there. Very little calcium actually moves, as these channels are closely coupled to the synaptic release machinery (see for example Stanley 1993 Single calcium channels and acetylcholine release at a presynaptic nerve terminal).
The calcium concentration gradient has to be established everywhere in cells that have this gradient (all animal cells, as far as I know), not just at a synapse, since calcium is typically a powerful "second-messenger" signal.
The two common mechanisms for transport are by using the gradient of sodium via calcium antiporters (this mechanism: using sodium or proton gradients to move other ions/molecules, is quite ubiquitous in biology), and via a calcium ATPase. Calcium transport involves both the external space and intracellular calcium stores such as within the endoplasmic/sarcoplasmic reticulum.
In the short term, calcium concentrations are also dealt with via chelation by calcium-binding proteins.


Is cell senescence in culture comparable to that in vivo?

Senescence does not equal cell death, but is simply an arrested state in which the cell still remains viable (1). It has been shown throughout the literature that this state corresponds with an altered cell cycle profile different from contact inhibition or damage-induced arrest (2). This corresponds with an enlarged cell size, altered gene expression (3, 4), and the pH-dependent expression of β-galactosidase (5). This has been shown both in cultured cells and in animal models (6, 7).

Goldstein, S. (1990) Science 249, 1129-1133.
Sherwood, S. W. et al. (1988) Proc. Natl. Acad. Sci. , USA 85, 9086-9090.
Cristofalo, V. J. et al. (1998) Crit. Rev. Eukaryot Gene Expr. 8, 43-80.
Linskens, M. H. et al. (1995) Nucleic Acid Res. 23, 3244-3251.
Dimri, G. et al. (1995) Proc. Natl. Acad. Sci., USA 92, 9363-9367.
Swarbrick, A. et al. (2008) Proc. Natl. Acad. Sci., USA 105, 5402-7.
Efeyan, A. et al. (2009) PLoS One 4, e5475.


Does the string "...CATCAT..." appear in the DNA of Felis catus?

The Felis catus genome has been published, annotated, and updated quite a bit since 1996, including spans of so-called intergenic regions, which are basically scaffolding and other structures, along with perhaps some unidentified genes, pseudogenes, regulatory sequences, etc. Basically, pretty much the entire DNA sequence is available now, not just the gene sequence of the mitochondrial genome, which was what was published in the 1996 paper you referenced. Mitochondria are the power plants of the cell, but are just an organelle that happens to contain its own DNA; they are separate from the chromosomal DNA in the nucleus. All of this is available for free (if you know where to look) at the National Center for Biotechnology Information (NCBI), part of the National Library of Medicine (NLM) at the National Institutes of Health (NIH) in the United States. Other sites are also available, such as Ensembl, a joint project between the European Bioinformatics Institute (EMBL-EBI), part of the European Molecular Biology Laboratory (EMBL), and the Wellcome Trust Sanger Institute (WTSI). Both institutes are located on the Wellcome Trust Genome Campus in the United Kingdom.
So, to the genome. Genomic sequences can be searched in a couple of different ways, depending on what you're looking for, but the most common way is to use BLAST, the Basic Local Alignment and Search Tool. As the name implies, it takes sequences as input and searches one against the other, aligning the results as best as possible using certain algorithms that the user can define and tweak. The BLAST web interface to the cat genome is here. You don't need to worry about any of the other options here except the "Enter Query Sequence" box. FASTA format is just using the single-letter abbreviations for nucleotides (AGCT), all strung together.
The genome we're searching is of an Abyssinian cat named Cinnamon:

Cinnamon, the cat which was chosen to be the definitive genetic model for all cats in the feline genome project. Image courtesy of the College of Veterinary Medicine at the University of Missouri.
To start with, I typed in CATCATCATCAT and to my surprise got back over 200 hits, covering every chromosome the cat has. So, I doubled the length of the input to 8 CATs, and got back the same result set. Unfortunately, 12 CATs was too many (and really, it is too many), so I worked backwards.
The final results are here (sorry, link expires 10/13/16. To regenerate, go to BLAST link above and enter CATCATCATCATCATCATCATCATCATCAT). Apparently, popular wisdom is incorrect, and Felis catus chromosomes really contain 10 CATs each, one more than is needed for their 9 lives. No word yet as to why this may be, but scientists are presumably working on it.


Fruit identification - What is this green long fruit?

Could it be a Ceiba speciosa pod? We have a lot of Silk Floss trees near where I live and they grow these types of pods. When they are fully developed, they burst open and are filled with cotton-like floss and dark seeds. I have never seen an unripe one opened up, but it definitely looks like the ones on the trees. The trees themselves are easily identifiable as well. They are large with greenish trunks that have thorns growing along the surface. Also, if you had previously seen the tree with large pink-purple flowers, that would be a good indication.
https://en.wikipedia.org/wiki/Ceiba_speciosa


How to do research in bioinformatics without wet lab experiments?

Doing actually valuable bioinformatics research completely on your own after graduating from university (I am assuming that this corresponds to a master's degree) is somewhere between impossible and very unlikely - even for someone who actually studied bioinformatics.

In order to really do research (in almost any field) you will have to become a PhD student first - and for that studying the relevant topics on your own, like you are already doing, is probably the best preparation.

If there are truly no 'cross discipline' applications possible where you are from, you'll probably have to apply for programs or positions abroad. It is, however, becoming increasingly common for bioinformatic research groups to hire people from various different backgrounds - ranging from wet lab biology to physics. I would advise you to actively look for such interdisciplinary research groups (ideally purely computational groups as a physics background will be more valuable there than in a mixed dry/wet-lab group) and potentially directly contact the group leader if the university/institutes don't offer any programs that would allow you to apply.


Common Metrics of Assessing DNA Sequence Quality

As mention in the comments Phred scores are the quality scores for most sequencing platforms. This value expresses the probability of a base is being called wrongly. You can find more information here. This values can be found in a fastq file coded by symbols.

For example, a phred score of 30 means that there is a probability of 1 base being wrong every 1,000 (that is 99.9% accuracy). In general values around 30 are considered good enough, but it depends on your analysis whether you want to be more more or less restrictive.

Biopython has some examples on how to plot and filter phred scores. There exits lots of other software to do QA checks, for example this one.

You can also check length and distribution of the reads, duplication levels, etc.

In case you need to trim sequences from Illumina there are several stand-alone software like this that you can use.


Why does polyploidy give an evolutionary advantage?

First of all I am not sure if your examples are per se correct. But they might also be an additional bonus. Secondly, I would like to refer to two articles: "Polyploidy" and "The advantages and disadvantages of being polyploid".

One of the main benefits could be allowing organisms long-term evolutionary flexibility. Often adapted polyploids can undergo a proces that is called diploidization, during which genomic redundancy is removed. This means extra copies of genes will undergo less negative selection. Meaning alleles containing deleterious mutations at functionally important nucleotides are selected against. This allows more mutational freedom, leading to what is called subfunctionalization and neofunctionalization: new genes are created with slightly different or new functions. Other redundant genes are lost or become inactivated (pseudogenes).

Another example of benefits from polyploidy, this time not in an evolutionary, but in a more individual context, is the fenomenon called hybrid vigor or heterosis. Heterosis is a phenomenon in which a polyploid offspring of two diploid parents is more healthy and vigorous than its progenitors. One of the factors explaining this could be due to a protection against recessive characters, as being homozygous as a polyploid is even more 'uncommon'.


ID a marine creature found on a beach on the US east Coast

It's positively a sea anemone. It retracts the tentacles when disturbed and become quite rigid. It's hard to identify it in this condition, leave it for a whlie in a jar with sea water and you'll see.


How necessary is human zygote cytoplasm for generating a human?

The zygote itself is necessary because in the early embryo there is almost no transcription of its own genome, instead it uses mRNA deposited in the egg cell by the mother (see also maternal to zygotic transition).

That being said, I don't think any ethics committee would allow an experiment like this in the first place.


How does a neuron know to which one of the next neurons to pass the signal

The neuron that sends the signal does not know which neuron to send the info to. The job of the neurons getting the signal is to identify whether it is their turn to get activated by the signal.

This is controlled by a protein. Depending on how often the neuron is used, a number of channels are formed on the surface of the dendrites. The activation happens at an optimal level of the protein present in the cell depending on the number of channels on the surface.. Each time the cell receives the signal, this some of this protein is created.

First, the neurons with most channels is activated, but if the organism does not get the memory that is wants, the earlier neuron will continue with sending more signals. Then receiving-neuron-number-1 stops activating (because peak concentration has passed) and the next one starts. This continues for all neurons.

In layman's terms, from info-1 to info-2, info-2 is chosen in the order of thoughts most associated with info-1 to least associated.


If I stop consuming protein, will I still excrete urea?

Yes, you will still excrete urea, but the amount you excrete will be diminished. As you might expect, when the body is low on protein, there's a physiologic drive to hold onto as much nitrogen products as possible, in order to conserve the limited supply.

Normally, your kidneys excrete approximately 40% of the urea that is filtered through the glomerulus. (It's slightly more complicated, because there's both secretion and reabsorption that happens along the nephron, but that's approximately the end result.) However, in protein malnutrition, the kidneys reabsorb more of the urea, and that number can drop to excreting only 10% of the filtered urea. (Source) It appears that this is an active process to reabsorb the urea, rather than a passive effect from other effects that malnutrition has on the body.

However, the body isn't capable of stopping excretion of urea completely... there will still be some that is excreted. Urea transporters in the kidney aren't 100% efficient, but probably the bigger issue is that the body needs to use that urea to regulate other functions. Urea is important to the body's ability to concentrate urine, which in turn is related to the body's regulation of blood volume and sodium concentration. And in general, the body cares more about maintaining proper blood volume and tissue perfusion than anything else.


What causes feeling of feet falling asleep to be delayed?

This paper, while mainly dealing with chronic nerve compression, appears to explain the effects of nerve compression on the blocking the transmission of neural impulses (causing the "sleeping limb" syndrome).

This paper describes how the application of pressure on a nerve causes a miniature case of compartment syndrome, where the pressure causes the intraneuron pressure to increase, leading to paresthesia. Edema also occurs within the neuron, causing pain signals to be sent out. In the experimental rats which were unable to relieve this pressure, permanent nerve damage resulted.

When the effects from the nerve compression exceeds a certain level, the pain/tingling will result in you releasing the pressure from the limb in order to prevent nerve damage.

However, the nerves are still blocked from transmitting their impulses due to the  compression blockage described in Paper 1. When the blockage is resolved, the neurons are now capable of transmitting their pain signals, which continue for a period of time until the pressure within the limb falls sufficiently below the pain threshold.


EF1-alpha is considered a ubiquitous/constitutive promoter; it is effective in all animal cells and tends to provide strong expression. Embryonic (and other) stem cells are more difficult to target than other cells because they don't express genes under the cell-type specific promoters that are often used for other populations of cells, which is why you're seeing it used specifically for that application, but that's not the only use.
You'll find a lot of the promoter information on individual commercial sites and rather than promoting specific ones I'd suggest searches like https://www.google.com/search?q=ef1+alpha+constituitive or https://www.google.com/search?q=ef1+alpha+ubiquitous - use of EF1-alpha isn't "owned" by anyone so when they say these things it's not just because they're trying to sell you on some special method of theirs, they are just using a field standard approach.


Probably a moth larvae but better to confirm

This is probably a larvae of Tinea pellionella, the case-bearing clothes moth.
T. pellionella is a species of tineoid moth in the family Tineidae (i.e. the fungus moths).


psychological database with sequenced DNA records

You might want to look at the Danish Data archive:

http://www.sa.dk/content/us/about_us/danish_data_archive

I have never used their data and I don't know what barriers there might be to accessing it, but the impression I got at a talk by Soren Brunak (http://ctbr.hunter.cuny.edu/Brunak), was that this was one of the most complete databases for studying relationships between people's DNA records and other health information that might be available about them.


Can we artificially increase human growth using HGH?

You asked

  ... is it theoretically possible for someone (like a "fully grown" adult) to artificially grow beyond their genetic potential by providing them with regular doses of HGH?

For an adult, the answer is no. Human growth means skeletal lateral growth, which is indeed mediated by human growth hormone. But during normal human development bones ossify in the process, and in human adults the bones are completely ossified and can't grow in length anymore.

From the cancer.gov site on Bone development and growth:

  When cartilage growth ceases, usually in the early twenties, the epiphyseal plate completely ossifies so that only a thin epiphyseal line remains and the bones can no longer grow in length

Further reading: NEJM Osteogenesis: The Development of Bones

This point is usually reached around the early twenties in humans. The case mentioned in your question is different because in this case, the human growth hormone was "given" before this process had finished and thus the bones grew longer. He was 22 when he died, so we will never know if he would have finished growing in his mid- to late twenties.

Giving adults (that don't suffer from an HGH deficit) more human growth hormone has been done and does not result in lateral growth, but it does result in increase in lean body mass in both young adults and the elderly