I think it could be Vipera aspis, but that leght what did you descripe is really rare. Anyway it can be Smooth Snake(https://en.wikipedia.org/wiki/Smooth_snake) too. But you know personaly i cant do more from this point of view. The smooth snake is much more common and longer so there is a bigger possibility.


Under what conditions do dendritic spines form?

Dendritic spines are thought to grow and recede under LTP and LTD, respectively. See (Bosch and Hayoshi 2011) for a review.

From there, much of the synaptogenesis occurs due to surface molecules present both on the dendrite and the presynaptic axon in the growth cone.  Localization and guidance are achieved through gradients of growth factors in the developing nervous system  See (Kolodkin and Tessier-Lavigne 2011) for a review of all of these mechanics.

How this maps back onto the human CNS and thinking/learning/memorizing is still up for debate, but some of these mechanisms must have been preserved in higher species.

References:

Bosch M, Hayashi Y. (2012) Structural plasticity of dendritic spines. Curr Opin Neurobiol.,22(3):383-8. (Epub 2011 Sep 28).

Kolodkin AL, Tessier-Lavigne M. (2011). Mechanisms and molecules of neuronal wiring: a primer. Cold Spring Harb Perspect Biol., 3(6). [DOI]


The most popular theory is the ‘hydraulic limitation hypothesis’ (Ryan & Yoder, 1997), which suggests that as trees grow taller, it becomes more difficult to supply water to their leaves. This hydraulic limitation results in reduced transpiration and less photo-synthesis, causing reduced growth.
It is known that in larger/taller trees water supply is limited by two factors — distance and gravity. Larger trees have a longer pathway of transporting tissue, this tissue is known as xylem. This is known as hydraulic resistance and makes it more strenuous for the water to move around in the tree. So now not only is the pathway long, but the water also has to beat gravity. Increased force is necessary to pull the water up to the highest leaves. Additional difficulty comes from the trees growing upright. Fast - growing/short trees frequently have shorter life-spans. They achieve their expeditious growth by having broader, wider xylem vessels, this increasing their hydraulic efficiency. At the same time this provides space for embolisms. An embolism makes it unable for a xylem vessel to transport water. Taller, slow-growing trees are longer-lived, this is caused by them having multiple xylem vessels, rather than having only a few wider ones like the fast-growing trees. Short-growing trees also have a more secured hydraulic system, preventing the forming of air-locks.


Isoprenoid Diphosphate Concentration in Yeast saccharomyces cerevisiae

Although this information doesn't provide a direct answer to your question, I hope that it sets the scene for what is achievable in metabolic engineering from IPP. It should also provide a jumping off point for further literature research.

This is a fairly recent review of metabolic engineering of relevant pathways in various microbial systems, including Saccaharmoyes:

  Ajikumar  PK et al. (2008)  Terpenoids: Opportunities for Biosynthesis of Natural Product Drugs Using Engineered Microorganisms. Molecular Pharmaceutics 5:167–190

The review refers to:

  Ro, D. et al. (2006) Production of the antimalarial drug precursor artemisinic acid in engineered yeast. Nature 440, 940–943.

In this work, the introduction of a pathway-specific gene led to the production of 4.4 mg L-1 of product. This was increased to 153 mg L-1 by several manipulations including:

Increasing flux through the pathway by expressing a modified HMG CoA reductase

Decreasing flux into sterol synthesis by downregulation of the ERG9 gene combined with expression of a dominant negative allele of the transcription factor Upc2.

UPDATE

After posting my answer I found this paper:

  Huang, B. et al. (2011) Metabolite target analysis of isoprenoid pathway in Saccharomyces cerevisiae in response to genetic modification by GC-SIM-MS coupled with chemometrics. Metabolomics 7:134–146

The paper includes a detailed discussion of methodologies, which I won't go into here.

Although there are no measurements of IPP, in Table 7 they present this result: geranyl pyrophosphate 32 ng ml-1 in a 48 h culture, A600 ~ 2.3. ERG9 disruption increased this to 56 ng ml-1

As far as I can tell these values are presented as ng ml-1 original culture. Using 1 U of OD600 corresponds to 0.41 g of dry cells liter−1 taken from here I calculate a value for GPP of 34 µg g-1 dry weight in the wild-type strain.


According to the Mayo Clinic website:

As you age, the tissue structures and muscles supporting your eyelids weaken. The skin may start to sag, and fat that is normally confined to the area around the eye (orbit) can move into the area below your eyes. Also, the space below your eyes can accumulate fluid, making the under-eye area appear puffy or swollen. Several factors can lead to this, including:

Fluid retention due to changes in weather (for example, hot, humid days)
hormone levels or eating salty foods
Not getting enough sleep
Allergies or dermatitis, especially if puffiness is accompanied by redness and itching
Heredity — under-eye bags can run in families

Of the list above, the most common reason is likely heredity.
Sources:

Mayo Clinic, as linked above
http://www.allaboutvision.com/cosmetic/puffy-eyes.htm


Does a bird nest out of its breeding range?

An all-year range for a bird species is obviously a range where a population exists year round, and since birds generally breed each year, there will be individuals of the species breeding within this range.  Precisely speaking, this is part of the breeding range of the species, but maps of bird ranges commonly call this range the all-year range, and will reserve the term "breeding range" for that part of the range map where birds breed but are not present during part of the year.  This is helpful since it communicates which times of the year the birds can be expected to be present.

Because in temperate zones summer is the time when breeding most always occurs, maps commonly show the summer-only breeding range in a warm color such as red. For migratory species, a range where they spend the winter but do not remain during the breeding season is usually shown in a cool color such as blue.  Typically such maps will show the year-round range in a combination of these two colors, e.g. purple.  (Some maps also show a migratory range, where birds transit but do not stay for long periods, in some other color.)


Neomycin resistance gene in E. coli stb3 cells

PGK is mammalian (murine) phosphoglycerate kinase promoter. It will therefore not work in bacterial systems. Why don't you select using ampicillin only? You can increase the ampicillin concentration if you want.

Regarding:

  I can't find anyone selecting bacteria by Neomycin anywhere.

Kanamycin is generally used for bacterial selection. The Neomycin resistance gene works on Neomycin, Kanamycin and G418 (a gentamycin variant). The gene basically codes for an aminoglycoside phosphotransferase and different variants of the gene have different affinities for different aminoglycoside substrates. For a basic reference see this.


What is the role of triton in buffer for western blot assay?

That's exactly it. Triton is a detergent and incorporating it just makes it a little more difficult for everything to bind. Here's how I imagine blocking buffer working:

PBS/TBS: buffering pH

milk/BSA: uniformly interacting with the entirety of the blot. The idea is that these will a) adsorb to the parts of the blot that don't already have much sample in them (since "empty" areas of the blot would otherwise adsorb the detection antibody/ies (this is a source of nonspecific binding).

Triton (or, more commonly, Tween-20): OK, now think about what's on your blot. Your antibody will have weak interactions with just about anything there. A detergent interacts with everything it touches (antibody and adsorbed proteins on the blot) to reduce binding affinity in lots of these interactions (although, some interesting counterexamples can be found here), thereby making the less-favorable binding even less favorable, decreasing the chances of your detection antibody retaining these weaker (off-target) interactions. The preceding article also suggests that the use of nonionic detergents lowers the signal intensity of the Western (and to a different degree across proteins).


I am not a botanist but looking at the flower in the second picture and the thorny trunk and pods it is likely to be part of the Ceiba genus. I cannot however be sure of the exact species.


Why do oncogenes show genetic dominance?

A tumor suppressor is an essential gene that regulates the cell cycle at different checkpoints. If one allele is lost due to a mutation then the function of that gene can be carried out by the other allele (There might be a less expression of that gene because of copy number reduction but it is not necessary in all cases- cases where there are feedback controls).

An oncogene is a gene that promotes cell division. Different kinds of mutations will have different kinds of effect.

Mutation leading to loss/reduction of function: Nothing is likely to happen unless both alleles are affected.
Mutation leading to hyperactivity: In this case one rogue allele will always remain active leading to uncontrolled growth stimulation.

So, it is the second type of mutation that you are referring to as in the case of Ras.
Note that any mutation leading to formation of a toxic or hyperactive protein (rogue allele), will show genetic dominance. Also see the case of Huntington's disease.


Can you name this plant that likes shade on Asturias?

You have found a helleborus, possibly helleborus viridis.
https://en.m.wikipedia.org/wiki/Helleborus_viridis


It looks like a whip snake, either a Balkan whip snake or a green whip snake. They are both present in the very north of Italy, close to Slovenia. They both vary in color, but the coloration of this one seems to be more similar to the Balkan whip snake.

See also this discussion.


MCQ - Independent assortment or Incomplete linkage

It doesn't really matter on which chromosomes the where concerned genes are located, Now coming to your question.
A> Complete linkage > Complete linkage says that the concerned genes are right next to each other and no crossingover is possible so the expected genotype of the offspring would be 100% parental type. 50% Wild (se+ vg+) and 50% Mutated (se vg)

B> Incomplete linkage > This is the correct answer. According to incomplete linkage, the genes are close but not right next to each other so there is space for crossingover to take place. However, they are still close, close enough to be considered as linked and thus chance of obtaining recombinant offspring would always be less than that of the offspring with parental genotype, parental type always remains over 50% and here the parental type offspring is 80% (40% wild type parental genotype + 40% mutated parental genotype) and 20% recombinant genotype [(10% se & wild type vg+) + (10%vg & wild type se+)]

C> Independent assortment says that there is no linkage and thus no crossingover, this is possible only when the concerned genes are located on different chromosomes but here in the obtained data of offspring it is clear that crossingover did take place and 20% of the offspring is result of the crossingover so this option is not correct

D> Epistasis : In your attempt you mentioned that it is not epistasis because two genes are controlling separate phenotype thus it is not epistasis. your explanation is wrong. Don't get me wrong, the answer is not epistatsis, I am just saying your explanation is wrong, epistasis is the phenomenon where one gene interferes with the expression of another gene, look at the term carefully. I am calling them as genes not alleles. Alleles are different version of the same gene that control the same phenotypic character. In epistasis two different gene that control completely different phenotypic expression are interacting. One gene if expressed prevents the other gene from getting expressed, this not about the dominant alleles where if the dominant allele expresses recessive allele wont express. For example, assume gene A codes for white flower colour and gene B codes for sweet smell. If B gene expresses then A gene wont express. This is epistasis


Is there a biological term for an activity period that is determined by temparature

I doubt there is such term.

Note that diurnal and seasonal are likely pretty well correlated with the temperature cycle. The temperature cycle is, I would presume, mainly affected by the daily and seasonal cycle.

You can talk about a behaviour that is dependent upon the temperature which fluctuates daily and seasonally. Looking for specific keywords on Google Scholar, it appears that most authors go through short phrasing of the kind to express this concept.


In eukaryotes DNA has a structural as well coding function. Parts of chromosomes called centromeres bind to proteins and form a scaffold which helps chromosomes attach to each other and correctly segregate during division. Technically this is still related to the transmission of genetic information though.

Since RNA can act as an enzyme (the so-called ribozymes), scientists have hypothesized that DNA can also have an enzymatic function, but no such function has been found in nature. Artificial DNA enzymes (deoxiribozymes) have been designed to cleave DNA, covalently modify proteins, ligate RNA molecules, and even catalyze reactions between small molecules. See this lab's website.


What is the morphological difference between Leydig cell in human and pig?

Perhaps what your teacher meant was not so much a difference in Leydig cell morphology, but in interstitial tissue morphology, ie. tissue which occupies the space in between seminiferous tubules. Leydig cells are its most interesting component, others being small blood vessels (a lot of them), nerves and connective tissue (mostly fibroblasts, mastocytes, lymphocytes and macrophages). In different species interstitial tissue looks differently, for example:

Leydig cells form clumps around blood vessels, and are surrounded by fibroblasts (which makes them more difficult to isolate) in guinea pig, but not in mice or rat;
in human a lot of interstitial tissue is extracellular matter, Leydig cells are not so frequent, but more active;
and, last but not least, in pig, there is little extracelluar matter and a lot of Leydig cells that are very easily isolated (and produce large amounts of estrogen).

I found all this in some old lecture notes; I couldn't dig up any sensible reference, though.


Is it possible to condition the body to reduce bruising?

Bruises are a type of hematoma of tissue in which capillaries and sometimes venules are damaged by trauma, allowing blood to seep, hemorrhage, or extravasate into the surrounding interstitial tissues (reference).  From what I read there seems to be two reasons why you notice a reduction in bruising.

The first would be because there is a deadening of nerve cells where they get used to the pain and eventually less sensitive. There could also be the development of some scar tissue from the bruising which has irregularly developed nerve endings leading to lesser stimulation. (reference 1 and reference 2)

The second reason could be because you yourself get stronger. The Wolff's law states that:

  Bone in a healthy person or animal will adapt to the loads under which
  it is placed.1 If loading on a particular bone increases, the bone
  will remodel itself over time to become stronger to resist that sort
  of loading.2 The internal architecture of the trabeculae undergoes
  adaptive changes, followed by secondary changes to the external
  cortical portion of the bone,3 perhaps becoming thicker as a result (reference).

So, repeated stress on the bones of your face/hands should be make them stronger. I don't think your body can adapt to heal faster in an area from repeated bruising as most likely scar tissue will develop from repeated stress on the skin. You can however improve your nutrition and diet to help your body heal better (reference).


Can the Na+/K+ pump backwards to generate ATP?

All enzymes can theoretically catalyze the reverse reaction.

Researchers have driven the Na+/K+ ATPase to synthesize ATP with artificial ion concentrations:

  We have studied the apparent affinity for K at its intracellular discharge sites by measuring the rate of ATP synthesis as a function of the internal K concentration in resealed red blood cell ghosts, where the Na-K pump is driven in reverse by the downhill efflux of K and influx of Na…


Why aren't the antibodies in the mother's milk digested by the infant's digestive system?

Demers-Mathieu et al. 1 used ELISA to quantify immunoglobulin concentrations from milk after 2 hours of digestion in the stomachs of preterm-delivered and term-delivered infants.  From the abstract:

Total IgA concentration decreased by 60% from human milk to the preterm infant stomach and decreased by 48% in the term infant stomach. Total IgM and IgG concentrations decreased by 33% and 77%, respectively, from human milk to the term infant stomach but were stable in the preterm infant stomach.

The authors note that the infants enrolled in this study had a variety of medical conditions, but "no overt gastrointestinal tract issues or other medical conditions that have been associated with an effect on gastric emptying or digestion capacity." Two hours of digestion was chosen to ensure recovery of sample from the stomach while maximizing digestion time, per the gastric emptying times observed in Siegel et al. 2
So, it appears that term infants are digesting antibodies from their mothers, but a substantial portion of immunoglobulins remain intact.  Weaver et al. 3 report IgA concentrations between 0.311 and 1.247 g/L across 1600 breast milk samples, with negative correlations to maternal age and parity.
Taking the median IgA concentration of 0.708 g/L, a 48% reduction gives 0.368 g/L post-digestion.  Dewey et al. 4 report that 3 month-old infants consume 818 mL of breast milk (assuming 1 g/mL) per day, on average, which suggests that ~300 mg IgA are available to the infant intestine from daily breast milk consumption.  If the adult human gut produces 40 to 60 mg IgA per kg body weight per day 5, then ~300 mg IgA is in the ballpark of what a 6 kg infant would need to phenocopy IgA concentration in the adult gut, assuming limited immunoglobulin production by infants themselves.
So, it seems like hypothesis #2 is close to the truth, at least for highly abundant antibodies like immunoglobulins:

Antibodies are present in such large amounts that many of them are undigested by chance.

Demers-Mathieu V, Underwood MA, Beverly RL, Nielsen SD, Dallas DC. Comparison of Human Milk Immunoglobulin Survival during Gastric Digestion between Preterm and Term Infants. Nutrients. 2018 May 17;10(5):631.
Siegel M, Lebenthal E, Topper W, Krantz B, Li PK. Gastric emptying in prematures of isocaloric feedings with differing osmolalities. Pediatr Res. 1982;16(2):141-147.
Weaver LT, Arthur HM, Bunn JE, Thomas JE. Human milk IgA concentrations during the first year of lactation. Arch Dis Child. 1998 Mar;78(3):235-9.
Dewey KG, Heinig MJ, Nommsen LA, Lonnerdal B. Maternal versus infant factors related to breast milk intake and residual milk volume: the DARLING study. Pediatrics. 1991;87(6):829-837.
Jacob Campbell, James Berry, Yu Liang. Chapter 71 - Anatomy and Physiology of the Small Intestine, Editor: Charles J. Yeo, Shackelford's Surgery of the Alimentary Tract (Eighth Edition). [via ScienceDirect]


Meaning of red blood cell volume expansion

Red blood cell volume is the percent of blood taken up by red blood cells (also known as the hematocrit), and is expressed as a percentage (so, normally, RBCs should comprise x% of blood by volume.) It says nothing of the size of the red blood cells.

That needs to be done by measuring the mean corpustular volume either by special machine or by looking at a slide of cells. So if the MCV is not mentioned, you can assume that expansion is referring to increased number of RBCs.

Smaller than normal RBC's are called microcytes, larger than normal are called macrocytes.

Recombinant EPO just increases the production of RBCs (and, unfortunately, it has some other effects as well.) It should not affect the size of the final erythrocyte.


Is it possible to use microalgae to produce food and live on it?

I don't see why microalgae couldn't be a main food source (putting aside the taste factor).

It contains many different lipids, carbohydrates, proteins and other essential nutrients that are digestible and would be beneficial to humans. I do know that microalgae has a very high lipid content (hence why they're often harvested for biofuels), but it can nonetheless provide nutritional value (ie. feed a starving man).

However, not how this is completely different from living solely off of microalgae. This likely wouldn't be possible, as us humans cannot synthesize all nutrients that we need from scratch. These nutrients are deemed essential nutrients. This problem usually arises when your diet is too restricted to certain types of food. So whether it's microalgae or any other type of consumable, you wouldn't be able to live by only eating that thing.

Another related problem is that growing microalgae is more difficult than it would seem, as is once again usually encountered in second-generation biofuel manufacturing. Temperature, light, cell density, nutrients, and much more must be precisely managed to obtain a increasingly growing population of microalgae. The pros and cons of farming microalgae for billion of hungry people would have to be contrasted with other current agricultures, like corn, soy and rice.


How can I avoid digesting protein-bound DNA?

Well, it depends if you just want to sequence your protein bound fragments.
If that is the case, I suppose you could go for a FAIRE-seq.
Basically, you perform several iterative phenol/chlo extractions, thus separating the bound and unbound fragments.
Then you sequence the unbound fragments that are present in the aqueous phase, and after the mapping, you can deduce the regions that were actually bound to proteins.

I don't know if it is possible to treat your bound fragments (that you isolate after a phenol/chlo extraction in the organic phase) with proteinase K, then perform another phenol/chlo extraction to purify your formerly bound fragments and sequence them.
Could be worth trying.


History: Building a "Phylogenetic network" of famous evolutionary biologists

Maybe not exactly what you are searching for, but you should look at the evolutionary biology version of Academic tree. This provides family-tree type relationships between researchers, but mostly (only?) of supervisor-student relationships.

As an example, the tree for Joe Felsenstein includes links to e.g. Dobzhansky, Lewontin and Sewell Wright. You should be able to find much of the information you are looking for at this site.

Here is a small cutout of Joe Felsenstein's tree, just as an example:


Help identifying a mushroom found in Raymond, WA, USA

To me that looks like Chrysomphalina chrysophylla, which is one of several fungi superficially similar to the chanterelles.
(The chanterelle in contrast has gradual increase in the diameter of the stalk rather than a sharp demarkation between the stalk and cap.)
Chrysomphalina chrysophylla is a species that has been reported in Washington:
 Source: Burke Herbarium Image Collection (for Washington state)


Yes, Horizontal gene transfer (HGT) can happen in both ways, from prokaryotes to eukaryotes and vice versa. So far less attension is given to from eukaryotes to prokaryotes HGT. It has played very important role in eukaryotic evolution also. Following figure from (Patrick and Palmer 2008) shows some potential cases in eukaryotic phylogeny.

You can find many such examples from above reference. Coming to human part, there are few cases like From Humans to Plasmodium vivax and From human to Neisseria gonorrhoeae , where researchers have shown evidence of HGT from humans to prokaryotes. Unfortunately , there is very little on mechanism by which they transfer. It is matter of speculation right now as these studies are controversial.


Why are some scorpion species fluorescent under UV light?

As far as I can see from different articles, this seems to be a study in progress. Dr Kloock from the California state University states that scorpions might be more active when not exposed to UV light. If not fluorescing, they know that they are hidden and have a lesser chance of being preyed on. He argues that scorpions are less active on full moon nights rather than other days. (reference) Dr Kloock has also stated that the pigment could get used up on repeated exposure to UV light. He made an observation that scorpions whose pigments got used up were more active than those still fluorescing when exposed to UV light mimicking the moon and the stars. (reference) Dr Gaffin from the University of Oklahoma, in his studies have reported that scorpions might be converting UV light to turn it into the colour blue-green which is what they see best effectively turning their body into one big eye. His studies are consistent with Dr Kloock in that scorpions try to hide and avoid UV light (reference). Some scientists have also hypothesized that scorpions might glow to warn predators or that the pigments that make it glow are the accidental by products of certain chemical reactions in its body (reference). There is no definite proof on this subject though.


The T7 tag is the first 11 amino acids of the T7 gene 10 protein. Basically, if you engineer a protein with the T7 tag, you've engineered a small, known epitope to the protein of interest which may be detected immunologically. The small size of the epitope reduces the chance it will disrupt the protein's normal function (to which it's tagged). If we look at the affinity purification kit on the following product page we can see that specific vectors can be used to express T7-tagged proteins, and an immunoaffinity column can be used to purify the protein of interest. The T7 tag chemical structure is denoted here.


why can proteolysis only occur once on a enzyme?

Because you mention zymogens, I assume the proteolysis you are referring to is the conversion of the inactive to active form of an enzyme by cleavage. The reason this would only happen once is that there isn't any process to put the two cleaved halves of the protein back together, so once cut in half it stays that way until degradation.

The proteolytic enzyme that is doing the cleavage of the zymogen will repeat this process over and over with multiple copies of the zymogen: it is the zymogen itself, the target, for which this is a once-in-a-lifetime event.

It would certainly be possible for a zymogen to require multiple cleavage events, but each of those events could only happen once.


It looks like two insects there, with the one in the background (top) impossible to see. But the one in the front, with its head down looks very much like the American cockroach, Periplaneta americana (Blattodea, Blattidae)


Interesting question.

As a prelude, I should probably mention that single celled organisms cannot get cancer as we understand and define it. Mitochondria are not, of course, single celled organisms, they are organelles, but this interesting question involves treating them as if they were autonomous. We'll come back to that later. First, single-celled organisms and cancer...

Of all the hallmarks of cancer, unregulated replication is probably the most fundamental, but all the same, cancer is necessarily a disease of multicellular organisms with differentiated tissues. Bacteria do not get cancer. Protozoa do not get cancer. Yeast do not get cancer. I'm spending too much space on my prelude here, but let's pretend like this isn't an issue and just address unregulated replication. Incidentally, the review I linked is an updated version of the classic review of cancer biology. If you're interested in cancer biology, I highly recommend reading it, and perhaps the original 2000 review.

Ok, now to the question. Let's put aside the problem of a single organelle or single celled organism getting cancer, and consider whether mitochondria can develop mutations in their DNA that cause them to replicate in an unregulated fashion.

Yes, mitochondria do have their own DNA, but they are not fully autonomous.  They do "replicate independently", but what is meant by this is that mitochondria replication (via fission) is a process that occurs independent from the replication (via mitosis) of its enclosing cell. The process is regulated by proteins encoded in the nuclear genome (not the mitochondrial genome)

Both fission and fusion are regulated by dynamin related proteins, which you can read about in this, fairly dense review. The mitochondrial genome encodes very few genes, 14 at last count, and while problems with those genes and proteins are implicated in a few diseases, uncontrolled replication is not one of them.


Yes, it is possible to extract adrenaline from the adrenal glands.  This was done in 1901, a patent was filed, and it was marketed under the name Adrenalin.  It is also known as epinephrine.  It is synthesized nowadays for most uses.


How do castes evolve in eusocial species?

Does a fertile queen have the code for soldiers/workers in its own genes, so only a mutation to the queen results in change of the whole coloniy's castes?

Yes.

  But how that would protect them from just going extinct due to one unfavorable mutation to a queen?

One unfavorable mutation to a queen could make that queen and her lineage "extinct". It wouldn't necessarily have any effect on the rest of the population (i.e. other queens and their lineages).  There's no difference here between eusocial and other species.


The main abnormality in prolactin levels is hyperprolactinemia, meaning blood levels of prolactin above the normal range, not during pregnancy or lactation.

The major cause of these abnormal prolactin levels are tumors consisting of pituitary lactotroph cells--called prolactinomas--which secrete prolactin. This is generally corrected with synthetic dopamine analogues, as dopamine negatively regulates secretion of prolactin in lactotroph cells.

Here is a 2010 review with further detail:
http://joe.endocrinology-journals.org/content/206/1/1.full.pdf


What happens if both forward and reverse primers have same Tm?

It is actually good if both the primers have the same Tm (Melting Temperature) because you would basically want both primers to anneal at your Ta (Annealing Temperature) which is generally set as Tm-5. If the Tm(s) don't match, then your Ta should be set according to the lower Tm.


A biomechanical analysis can be done to determine how much support comes from the muscles vs other (skeletal) support structures. Assume the body is standing upright, in static equilibrium. Consider this (over simplified) free body diagram of the upper torso where the sum of the forces equals zero in static equilibrium.

Here the diagram over simplifies the analysis with one general equation: Fsupport = sum of all the weights. Since we are considering only how much weight muscle supports, we deduct Wbones from Fsupport.

A spine by itself would not be able to support itself because the sum of the forces do not equal zero in static equilibrium. (Wgravity + Wspine) > Fsupport.

In reality, each muscle, bone, and organ has many more forces with specific magnitudes in different directions that altogether equal the weight of the specific region of mass it supports. I imagine these forces as many vectors over an area/field. A more detailed analysis would require a program like MATLAB that uses triple integrals in calculus to visualize these forces in 3D. This kind of visualization can help us color code only the muscle vectors which answers your question, "to what extent is our ability to support our spine to remain upright due to muscles," as a percentage of the sum of all the forces input into the program. How the muscles keep the spine erect can be determined from such visualizations as descriptions of directional forces.

For an example of how this kind of analysis is done, see this paper on lumbar spinal support. http://www.uvm.edu/~istokes/pdfs/stab-model.pdf


Why don't humans typically drink human milk after infancy?

Giving a woman food for her to inefficiently convert to different food is a waste of time and energy; it only makes sense for infants that can't eat much else (and even there, plenty of people find substitutes so the woman can get back to work).

Turning grass, which people can't eat, into a food people can eat makes a whole lot more sense.


How does ultraviolet light influence the decay process of wood?

Ultraviolet light is microbicidal. See this post.
As I answered in this previous post, micro-organisms are essential for rotting. Since UV kills these microbes it will reduce the rate of rotting. The heat from sun will also dry the wood and further decelerate rotting.


The question is a bit unclear

  Can you produce haploid cells without meiosis?

The question is a bit unclear. for two reasons

What do you mean by "you". You mean can we do such thing with modern technology or do you mean does it ever happen or do you does it ever happen in human cells.
It is also unclear what from. Are you implicitly asking whether "you" (whatever 'you' mean in your sentence) can make a haploid cell from a diploid cell or form anything?

Answer

In this answer, I will assume that the question is

  Does any lifeforms can make a haploid cell from any other cell without meiosis?

The answer is yes. Many organisms have a long haploid stage during which many mitosis occur. Haploid cells undergoing mitosis results into two haploid cells.

You might want to read more about life-cycle (wikipedia), especially the sections on haplontic life-cycles and haplo-diplontic life cycles.


How are individual neuron firing rates characterized?

However, upon reviewing these papers, it appears that the neurons were
  stimulated while still inside the tissue, but after the tissue had
  been sliced. However, this seems so absurd that I must be misreading
  it.

You're not misreading it. I can't access the paper you refer to, but this is a standard way to measure the electrophysiological properties of individual neurons, and has been for more than 25 years. (I'm really curious what you find "so absurd" about this).

I'll take an educated guess (since I can't read the methods online) that these recordings are from rats (or possibly mice), using whole cell patch clamp technique in thin slices of the young rat neocortex. Briefly put: the animal is sacrificed, the brain is removed, it is sliced into about 400 micron thin slices using a vibrating razor blade, and the slices are kept in a artificial cerebrospinal solution that allows the neurons to remain functional for a day's worth of experiments. Then individual neurons are imaged under a microscope and "patched onto" with a glass micropipette that contains a silver wire. Electrical events in the neuron can thereby be recorded into one's computer and plotted as shown in the figure you provided.

In this case, what's shown are what are known as current clamp recordings, in which current is injected into a neuron and the resulting voltage changes are recorded. Here, they are injecting a depolarizing current to make the neurons spike (have action potentials) and seeing that the neurons they sampled vary in their spiking properties. Some are fast spiking, some are slower spiking, some have different spike waveforms or patterns of spiking.


What effects does being cryogenically frozen have on a person's body?

Short Answer
Death!
Longer Explanation
In terms of the cellular and molecular level, many of the relatively weak interactions holding a person together are disrupted by cold temperatures. As a cell freezes, most of its  proteins and lipid membrane content will denature and "fall apart", the same as if you boiled it.
As with many things in biology, the problem is water. At room temperature, the lipid bilayers and proteins of a cell are held together largely by way of a complex network of interactions with the surrounding water. If the cell gets too hot or too cold this network of interactions between biomolecules and water falls apart. This leads to a disruption of the cell's overall organization*, which in turn can cause problems up to and including complete cell rupture and death.
So in order to preserve a living creature under cryonic conditions you need to replace the water in and around its cells with a different molecule that will maintain most of the normal intermolecular interactions even under conditions of extreme cold. There are protocols for freezing cell cultures that use various different substances as replacements for water, such as glycerol or DMSO, and there's a frog that loads its own blood with carbohydrates at low temperatures in order to turn it into a better cryonic medium.
footnote
*The disruption of a cell's organization at extreme cold is likely to persist even if the cell is brought back to room temperature. See Gulevsky, et al for a complete review of the thermodynamics of cold denaturation.


Is there a vaccine against the plague (Yersinia pestis)?

There is little motivation right now for vaccination against plague because:

Human infections with plague are fairly rare. A vaccine administered to the general populace would have to be very cheap and extremely safe to make it cost-effective and have a net benefit given the risks of plague are so low, and because
Antibiotics are effective against plague - this makes the likelihood of a widespread outbreak fairly low. Antibiotic resistance could be a concern, but plague would not be one of the most concerning pathogens from that perspective - there isn't much exposure to antibiotics in the reservoir species that the bacterium lives in, so there is less selective pressure towards resistance compared to other bacterial pathogens.

Additionally, plague lives in reservoir species, so extensive human vaccination is not a plausible way to eradicate the bacteria entirely, unlike pathogens that have humans as a primary host.

That said, vaccines are available and can be used for certain individuals at high risk. However, they take a long time to show immune protection (>1 month) making them not that useful during outbreaks. From the same WHO report linked above:

  Worldwide, live attenuated and formalin-killed Y. pestis vaccines are
  variously available for human use. The vaccines are variably immunogenic
  and moderately to highly reactogenic. They do not protect against primary
  pneumonic plague. In general, vaccinating communities against epizootic
  and enzootic exposures is not feasible; further, vaccination is of little use
  during human plague outbreaks, since a month or more is required to
  develop a protective immune response. The vaccine is indicated for
  persons whose work routinely brings them into close contact with Y. pestis,
  such as laboratory technicians in plague reference and research laboratories
  and persons studying infected rodent colonies (23).

WHO plague manual:

https://www.who.int/csr/resources/publications/plague/WHO_CDS_CSR_EDC_99_2_EN/en/


Is there a difference in cytoplasmic pH between prokaryotes and eukaryotes?

In the article "pH of the Cytoplasm and Periplasm of Escherichia coli: Rapid Measurement by Green Fluorescent Protein Fluorimetry", by Jessica C. Wilks and Joan L. Slonczewski, the pH of E.coli cytoplasm was mentioned as 7.2 - 7.8. I just took E.coli's pH range as a common example of prokaryotes.

Reference link: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1951819/


Accurate Human Skull Model for Educational Purpose

The best way to ensure you're getting an accurate skull, near as I can tell, is striking the "model" part of your question, and go straight for a real skull.

A cursory search revealed, for instance, Skulls Unlimited International, The Bone Room, and The Evolution Store although other providers probably exist as well.

A regulatory board for model skulls probably doesn't exist, given the apparent ease with which real skulls can be obtained and kept.


Hepatitis is a condition of the liver where the cells of the liver organ are inflamed. Most often it is caused by a viral infection, hepatitis A, B and C are all viral forms of the disease.

Bacteria (and Fungi) can cause hepatitis of the liver, and two examples would be the Staphylococcal and Streptococcal bacteria. These can directly infect the liver, and are also responsible for some inflammations in other tissues of the skin and heart and elsewhere.

Prolonged alcohol abuse is another cause of hepatitis (as well as cirrhosis) and is not associated with bacteria virus or fungi, but instead from a damaging effect on the liver.


Why do we have such a wide range of responses to pathogens and carcinogens?

This answer will address only cancer.

There is no such thing as standardized exposure to carcinogens in humans; while it would go a long way to answering your question, it would be unethical.

Also, it is unlikely that two people who do consume identical amounts of a carcinogen have identical environments or identical genetics.

Cancer used to be thought of as a carcinogen-host interaction; expose a (rodent, in my studies) to adequate levels of a carcinogen and cancer will occur. We tried to figure out exactly why. Then it was thought of as a host + environment (This was decades ago.)  The immune system was found to play a role; another level of complexity was added.

Mapping the entire human genome has made us aware of how simplistic these (and most) models were. There are tumor-suppressor genes. There are genes that matabolize carcinogens differently from other genes. There are genes that direct repair of DNA better than other genes. The possibilities are just beginning to surface.

To answer your question more directly,

  Although many studies have focused on carcinogen metabolism and cancer risk, more recent studies are considering DNA repair.

I would not go so far as to label DNA repair as Immunology.

I don't know why my father, who had a 120 pack year history of smoking, had absolutely no ill effects (not a trace of COPD, and certainly not cancer, no heart disease, CVD or other) and why my mother had COPD at a 40 pack-year history, but I'm sure it was genetic.

  Sporadic cancers are caused by genen-environmentn interactions rather than a dominant effect by a specific gene, environmental exposure, or gene-environment interaction. New paradigms, where we categorize genes as caretaker or gatekeeper genes, will allow for new hypotheses to be tested and will require advanced methods of analysis.

And, in another study,

  Three meta-analyses report 35% to 50% increases in breast cancer risk for long-term smokers with N-acetyltransferase 2 gene (NAT2) slow acetylation genotypes.

Cancer Risk and Low-Penetrance Susceptibility Genes in Gene-Environment Interactions
Integrative Epidemiology: From Risk Assessment to Outcome Prediction
Active smoking and secondhand smoke increase breast cancer risk: the report of the Canadian Expert Panel on Tobacco Smoke and Breast Cancer Risk (2009)


Those appear to be the eggs of a species of apple snail in the genus Pomacea, probably the introduced invasive golden apple snail (Pomacea canaliculata), but there are at least two other candidates1,2.
You can learn more about this species and the problems it causes from this Columbia University webpage.
For comparison — Figure 3 from "The identity, distribution, and impacts of non-native apple snails in the continental United States"3.

Egg masses of introduced and native Pomacea in the continental U.S. a. P. haustrum, b. P. diffusa, c. P. canaliculata, d. P. paludosa, e. P. insularum. Scale Bar:5 cm.
References:
1: Yang, Q. Q., Liu, S. W., He, C., & Yu, X. P. (2018). Distribution and the origin of invasive apple snails, Pomacea canaliculata and P. maculata (Gastropoda: Ampullariidae) in China. Scientific reports, 8(1), 1-8.
2: Yang, Q. Q., & Yu, X. P. (2019). A New Species of Apple Snail in the Genus Pomacea (Gastropoda: Caenogastropoda: Ampullariidae). Zoological Studies, 58(13).
3: Rawlings, T. A., Hayes, K. A., Cowie, R. H., & Collins, T. M. (2007). The identity, distribution, and impacts of non-native apple snails in the continental United States. BMC Evolutionary Biology, 7(1), 97.


It turns out that this was a question that was answered by Alan Turing in the 1950s.

Turing hypothesized there would be two morphogens, an inhibitor/ activator pair, each of which would produce a one of two phenotypes by activation or suppression of a trait.  He hypothesized that this would produce a pattern like stripes or other patterns (e.g. black and orange stripes).

This year just such inhibiting/activating pairs produce patterns like ridges in the top of the mouth of mice.

In a broad way, this seems like X-inactivation, where there is an X-inactivation center (XIC) that is inhibited or activated when the cell is created in mitosis.  XIC is still hypothetical and undiscovered, but it can create patterns and is non-random.

So I would say that this tiger stripes and X-inactivation may share Turing's mechanism, but the stripes, found in male and female tigers alike is not linked causally to X-inactivation.


Can animals like squirrels leave "gifts" or tribute for humans?

I believe a lot of these behaviours can fall under the umbrella term of reciprocity, or  reciprocal altruism.

  In evolutionary biology, reciprocal altruism is a behaviour whereby an
  organism acts in a manner that temporarily reduces its fitness while
  increasing another organism's fitness, with the expectation that the
  other organism will act in a similar manner at a later time (...) The concept is close to the strategy of "tit for tat" used in game theory.

For example, red-winged blackbird males help defend neighbor's nests. There has been some discussion around the reasons for this behaviour, but it has been observed that males reduced the amount of defense given to neighbors when neighbor males also reduced defense for their nests. Since kin selection doesn't seem to be an important factor here, this would support a tit-for-tat strategy (animals help those who previously helped them).

Some primates do this frequently too:

  A monkey will present its back to another monkey, who will pick out
  parasites; after a time the roles will be reversed. Such reciprocity
  will pay off, in evolutionary terms, as long as the costs of helping
  are less than the benefits of being helped and as long as animals will
  not gain in the long run by "cheating" – that is to say, by receiving
  favours without returning them.

The example with the crows, mentioned in the comment, can be interpreted under this light too. Those crows seem to give presents expecting something in return (albeit delayed!).

What's interesting though is that altruism, at first sight, would seem to go against reproductive success. Group Selection, however, is something Darwin was already talking about in Origin of the Species.

So, back to squirrels. I didn't find particular research about them in their relationship with humans (will keep looking), but analysing it under reciprocal altruism it could be justified that they give nuts expecting a potential future benefit for them or their group. There's much more to this complex dynamic, but reciprocity is definitely a strong candidate for explaining your kind gift-presenting squirrels.

Some quick references and materials:

The evolution of reciprocal sharing
The Gift, by Marcel Mauss (complete online book) --> From an anthropology point of view, Mauss was the first one to talk about recicprocity as economics. Absolutely recommended read.
Social semantics: altruism, cooperation, mutualism, strong
reciprocity and group selection


To go the PBPK route:

I would recommend using the organism parameters and structure from the whole body platform model by Shah and Betts.

Shah, D.K. & Betts, A.M. J Pharmacokinet Pharmacodyn (2012) 39: 67. doi:10.1007/s10928-011-9232-2

They have assigned a plasma space volume, plasma flow, blood cell space volume and blood cell flow for each organ and the total body.  The base model structure for circulation is complete if you use the equations for the blood cell space in this paper as the foundation (Eq 2 and Eq 5).

Once the model structure is complete, step 2 is to model all processes that can affect the cell in each compartment.  If the cell is adhering to a nanoparticle, a compartment equation could then be:

d[cell]/dt = (flow in - flow out)/volume + Kon x [nano] x [cell] - Koff x [cell-nano complex]

To model the interaction of the cell with the nanoparticle you will need to model both within the same structure.  A review of PBPK modelling for nanoparticles can be found here:

Physiologically Based Pharmacokinetic Modeling of Nanoparticles
Mingguang Li, Khuloud T. Al-Jamal, Kostas Kostarelos, and Joshua Reineke
ACS Nano 2010 4 (11), 6303-6317 doi: 10.1021/nn1018818

A pharmacokinetic (top-down, classical) model for nanoparticles in the circulatory system may also give insight to how to model the processes that affect nanoparticles in vivo.  This model accounts for fluid dynamics, pore size and specific nanoparticle properties.

Kirtane, A. R., Siegel, R. A. and Panyam, J. (2015), A Pharmacokinetic Model for Quantifying the Effect of Vascular Permeability on the Choice of Drug Carrier: A Framework for Personalized Nanomedicine. J. Pharm. Sci., 104: 1174–1186. doi:10.1002/jps.24302


Flagella in prokaryotets is very different from that of eukaryotes.

The main structural protein in a prokaryotic flagellum is flagellin. The flagellar motion is caused by a molecular motor similar to Mitochondrial ATP-synthase; molecular motion generated by the chemiosmotic energy.

Eukaryotic flagella or cilia are made of microtubules with dynein attached on to them and cause the movement by the energy generated by ATP hydrolysis.

See the wikipedia article. It is clear enough.


How well understood are the long-term effects of nuclear radiation?

The three major nuclear incidents I can think of are the Japanese atomic bomb attacks, the Chernobyl disaster, and Fukushima disaster. Of course other nuclear incidents have occurred, but usually give much higher doses to far fewer people.

Many studies have been done on the survivors from the atomic bomb attacks, and increased rates of cancer have been the strongest conclusion. This review article looks at those studies for both cancer and non-cancer effects. Leukemia is the most well known cancer to be caused by radiation, and excess leukemia was discovered in bomb survivors within 5 years of the attacks. Rates of most solid tumors had increased by 10 years after the attacks. However "Even 55 years after the
bombings over 40% of the Life Span Study cohort remain alive", indicating that the amount of radiation most people were exposed to wasn't enough to kill them. Here is another article on atomic bomb survivors.

The Chernobyl accident was a very different type of exposure, but many people were exposed to radioactive materials. Immediately after the disaster, the "liquidators" received high doses of radiation while cleaning up the site and building the containment structures, but very few have died from radiation exposure. While the environment around the power plant did suffer in the years after the accident, after the humans moved away the environment has greatly improved. Thyroid cancer rates increased due to Iodine-131 exposure, especially among those exposed as children, but rates were still low.
 Yellow = adults Blue = Adolescents Red = Children.

It is too soon to draw many conclusions about the Fukushima accident, but some studies (7, 8) have tried to predict the number of cancer cases that will be caused by it. In general the rates are expected to be low, with far fewer deaths than were caused by the earthquake and tsunami that caused the accident.

A few instances exposed small numbers of people to very high doses, and are interesting from a radiation safety veiwpoint. The infamous "Demon Core" killed 2 scientists in separate accidents while handling the core. The Goiania incident involved men breaking into an old hospital and stealing a radiation source without realizing what it was. They broke the source open and passed the radioactive material around because it looked cool, resulting in several deaths due to acute radiation sickness.

While radiation can be dangerous, with proper precautions we can avoid accidents and disasters. Remember that Chernobyl was a poorly designed Soviet reactor, and that Fukushima was a 50 year old plant that needed both a magnitude 9 earthquake and a 30 foot wave to disable it. Modern nuclear plants can be built safely and provide clean electricity for many decades, and if they are breeder reactors can recycle the used fuel to reduce both the amount and half-life of the material, making storage easier.


Typical firing patterns of (some) motor neurons

I can't answer the whole question, but what I do know:
An actionpotential can't have a small amplitude, the amplitude is always the same. If a neuron gets excited enough there will be an action potential, otherwise there won't.

"When the depolarization reaches about -55 mV a neuron will fire an action potential. This is the threshold. If the neuron does not reach this critical threshold level, then no action potential will fire. Also, when the threshold level is reached, an action potential of a fixed sized will always fire...for any given neuron, the size of the action potential is always the same. "
quoted from https://faculty.washington.edu/chudler/ap.html

Neurons have a maximum firing rate, a point where they cannot fire faster. (http://blog.eyewire.org/why-do-neurons-fire-at-a-maximum-of-about-200-hz/)
So to move faster your body can't fire faster. But it can fire more: more neurons fire if you want to move faster, and less neurons fire if you want to move slower: https://blogs.scientificamerican.com/scicurious-brain/when-you-run-fast-your-brain-runs-faster/

I do think your first row of spikes is kinda correct. Neurons fire as long as you move your hand/finger(s) in a certain direction, and as soon as these neurons stop firing and their complementairy neurons start firing you move your hand to the opposite direction.


It doesn't

As long as liquid water is present osmosis will never stop, the closest you can get is a point at which it happens at equal rates in both directions, called equilibrium.

Plant cells will help you understand as osmosis will create immense internal pressure as water enters the cell even though the cell cannot expand thanks to the cell wall. the amount of water inside the cell will keep rising until it reaches equilibrium, this also makes the cell more rigid.


Why are transmembrane proteins difficult to crystallise?

There are several factors that make obtaining crystal structures from membrane proteins more difficult.  In brief, nearly every stage of obtaining the structure via crystallography is more difficult.

First: protein expression.  Large amounts of pure, well-folded protein are required and this is much more difficult to achieve than it is with a soluble protein. Since membrane proteins are bound within a membrane, the mechanisms to translate the peptide into the membrane and to fold the protein in the membrane are different.  They may involved folding factors which are only available in a particular compartment of the cell (making bacteria impossible as a system of expression).  In high amounts in the cell, their hydrophobicity might tend to result in clumps of unfolded protein instead of gobs of membrane-associated protein.

Next: Purifying the protein is more difficult.  The expressing cells are usually broken open in the presence of detergent to get the proteins to float around as individual proteins in detergent micelles.   The wrong detergents might break up the membrane protein and it may lose its fold - the concentration of detergent must be carefully managed and kept at optimal levels or the micelles might break up and the protein will be ruined.

Crystallizing the protein is quite a bit more difficult too.  Membrane proteins in detergent micelles which may or may not be charged themselves look like oily blobs with hopefully a domain or two of folded proteins sticking out of them.  Compared to a soluble protein with a nice ordered surface in every direction instead of a detergent micelle which might undergo a phase change at high concentration or by the addition of a salt or change in pH, membrane proteins take a task that might take thousands of trials and adds new dimensions to worry about.

The proteins are 2D-like, but the crystals still have to be 3D for crystallography to work usually.  Protein crystals are small, but those derived from membrane proteins - which tend to organize into planes like the membranes they inhabit - are often thin, which can make them too delicate and small to get a good set of data even from synchrotron beams.  As a result, the crystals are commonly too small or thin to use at first, requiring extensive optimization after the first crystal are found.

In a few cases some membrane proteins have been solved with 2D crystals using electron microscopy on crystalline arrays of porins and rhodopsins in membranes. That was a ton of work but they were the first membrane protein structures by years and years.

Not to make all this sound impossible - once you have crystals, they can usually be improved; there are good starting points to crystallization and purification with detergents.  It's just that a process which can already take quite a bit of time (years) and can sometimes end in frustration takes even longer and is less certain with a membrane protein.


Yes, these include:

neurons
melanocytes
Merkel cells

In all cases, as you suggested, their function is to extend the surface area of the parent cell. In the case of neurons, the role of dendrites, which receive the vast majority of synapses, is to maximise the number of synapses the cell receives from different pre-synaptic partners (Chklovskii et al. 2002, Chklovksii 2004). In melanocytes, they are used to transfer melanin to keratinocytes. In Merkel cells, they are again used in order to form synapse-like connections with neurons (Mihara et al. 1979).

The word originates from the Greek δένδρον, which means 'tree'. Dendritic structures are found throughout in nature, including in...trees, where presumably they are used to maximise exposure to sunlight. Theoretical studies on the formation of dendritic arborisations in neurons indicate that they are governed by at least these factors: i) repulsion between dendrites (Wen et al. 2009), ii) minimisation of dendritic volume used (Tamori 1993), possibly through resource competition (Graham and van Ooyen 2004). It is an intuitively attractive idea to think that similar processes govern dendrite-like formation in the other biological systems described above as well.

References
- Chklovskii, D. B., Schikorski, T., & Stevens, C. F. (2002). Wiring Optimization in Cortical Circuits. Neuron, 34(3), 341–347. https://doi.org/10.1016/S0896-6273(02)00679-7
- Chklovskii, D. B. (2004). Synaptic Connectivity and Neuronal Morphology: Two Sides of the Same Coin, Neuron, 43(5), 609-617. https://doi.org/10.1016/j.neuron.2004.08.012
- Graham, B. P., & van Ooyen, A. (2004). Transport limited effects in a model of dendritic branching. Journal of Theoretical Biology, 230(3), 421–432. https://doi.org/10.1016/j.jtbi.2004.06.007
- Mihara M., Hashimoto K., Ueda K., Kumakiri M. (1979). The Specialized Junctions between Merkel Cell and Neurite: An Electron Microscopic Study, Journal of Investigative Dermatology, 73(5), 325-334. https://doi.org/10.1111/1523-1747.ep12550322.
- Tamori, Y. (1993). Theory of dendritic morphology. Physical Review E, 48(4), 3124–3129. https://doi.org/10.1103/PhysRevE.48.3124
- Wen, Q., Stepanyants, A., Elston, G. N., Grosberg, A. Y., & Chklovskii, D. B. (2009). Maximization of the connectivity repertoire as a statistical principle governing the shapes of dendritic arbors. Proceedings of the National Academy of Sciences, 106(30), 12536–12541. https://doi.org/10.1073/pnas.0901530106


What is the general term for tree-dwelling animals?

You answered your own question - arboreal.

Another term that is somewhat related is scansorial, describing animals that climb trees. For example, black bears and raccoons are scansorial, though they aren't really arboreal. Conversely, there are probably some arboreal birds that aren't really great climbers; they simply fly or glide between branches.


Why do dragonflies have these special little spots on their wings?

Pterostigma is what those spots are. Wikipedia article is at https://en.wikipedia.org/wiki/Pterostigma.
I read the summary of the technical article below.
The pterostigma are heavier than the rest if the wing, and so the insect can glide faster without a destabilising flutter beginning.
The author also believes that the pterostigma contribute to more efficient active flight.
Technical details at:
Norberg, R. Åke. "The pterostigma of insect wings an inertial regulator of wing pitch". Journal of Comparative Physiology A. 81 (1): 9–22.
doi:10.1007/BF00693547.


Altruism in viscous (asexual) populations

The $sR$ that your looking at is the average relatedness of the next generation.  This assumes that the new immigrants into the the population are completely unrelated. So if the population is completely viscous ($s=1$) the average relatedness of the next generation equals that of the current generation.  On the other hand, if the population is not viscous ($s=0$) the next generation would be entirely unrelated because it would only be made up of unrelated immigrants.

The $s(b-c)$ is the number if individuals that are displaced by new offspring.  Again if all of the new generation sticks around ($s=1$) then the number of displaced individuals equals the number of new individuals.  And if all new progeny leave ($s=0$), there are no displaced individuals.


Which method of gene amplification for toehold switches?

Option 2 is your simplest and easiest. It should give you unlimited plasmid to work from. Note that ordering pre-made sequences of this size isn't particularly cheap and might take a few weeks to get to your destination.
It may be easier (quicker + cheaper) to find a plasmid with the luciferase CDS and terminator already built in. You could then amplify this with primers incorporating your promoter and riboswitch sequences and some restriction enzyme sites to generate a product that looks like this:
RE1-ara-riboswitch-luciferase-RE2
You can then clone this into a(nother) plasmid cut with RE1 and RE2.
Another option is that if you have a plasmid with a luciferase gene in it already and a multiple cloning site (MCS) you can order complementary primers (note single-stranded DNA, anything less than about 150 bases is fine) containing the araC and riboswitch sequences flanked by two restriction sites, you then anneal the two primers, digest off the ends and ligate. You just have to be careful with making sure that everything is in-frame. I don't know anything about riboswitches though so frame may not matter so much.
As you have limited time I suggest buying chemically competent cells for heat-shock transformation (if you don't have some already); make sure you don't get electro-competent ones, as these will only work with an electroporator.  Also get a commercial mini-prep kit (e.g. Qiagen plasmid mini-prep). These are easy to use and reliable.
I think in option 1 you have something a bit odd going on - why would you digest your plasmid then re-ligate it, when it is already in the form that you are going to use?
I am not quite sure why in options 3 and 4 that you think that these are any different in terms of the end result to option 2.


Is DNA from more parents (than two) better for the fitness of the offspring?

There are very many details to address in this question. I will try to keep it brief and keep the scope of your question in mind, which is rather narrow. I also think your friend is over-simplifying and misleading you, assuming he is honest about the explanation he gave you.

We are talking about sexual reproduction, correct? Firstly, with 3+ parents:

it's not obvious that you will have "more diversity" in the DNA, nor that
"more diverse" DNA will be a cause for increased fitness.
Additionally, it would take a whole lot of machinery and evolutionary happenstance at the cellular and molecular levels to recombine DNA from 3 or more parents to make a stable, recombined genome, and this itself may introduce more problems than solutions.
More so, you're implying that a sexual organism that requires mating between 3 or more individuals will be fitter than an organism born of fewer parents. This is subject to whether the gain in fitness of having more genetic parents will outweight the cost of maintaining such a system. This would certainly be dependent on the environment, the population, and all the nasty little details of life, such as how mate choice would work, whether a backup for 2-individual mating would exist, etc.

Remember that fitness is a probability of obtaining a number of offspring rather than the number of offspring. I think it is self-evident that the requirement for more parents, rather than less, lowers the probability (i.e. fitness).

This is quite a hypothetical discussion. In nature, for all its ever-experimenting and ever-diverging forms of life in the last 4 billion years, we find no organisms with more than 2 sexual parents. Take this as a sign that the natural occurrence of this kind of system is probably not favorable to survival and reproduction.

And I realize we could discuss this topic on many fronts (I have a few more ideas that I omit here), it's a rich question to digest.


Is it possible to distinguish between coding and template strands from the sequence?

I don't know about your specific example (perhaps look for triplets that code start codons?), but machine learning has been used to predict promoters from sequence information (from promoter regions, you get downstream initiation of transcription of DNA to RNA). You would probably need more sequence to predict a promoter with more certainty. Cites: https://en.m.wikipedia.org/wiki/Promoter_(genetics) and https://academic.oup.com/bioinformatics/article-abstract/35/16/2730/5270663


Broadly speaking there are two classes of cell in an organism:

Somatic cells

These are by far the most numerous in your body, and are the differentiated cells including everything from retinal cells to liver cells to neurons.

Stem cells and germ cells

Stem cells reside in tissues and replenish the somatic cells as they are damaged or removed, or as the organ grows,
Germ cells - in particular oocytes in women's ovaries - are pools of immature eggs that are generated when a women is still a foetus in her own mothers womb!

The difference between these two types that relates to your question is that somatic cells have a limited replicative lifespan - a limit to the number of times they can divide - because their telomeres (caps to the ends of chromosomes) erode during cell division, whereas stem cells are able express the enzyme telomerase which extends the telomeres and allows cells limitless replicative potential (excluding other factors). Replenishing telomeres is a major step in cancer progression [1].

Embryonic cells have 'complete' telomeres when they are fertilised and begin to proliferate into a new organism. Interestingly the telomere length of the germ cells is not at all related to fertility [2], suggesting to me that telomerase is expressed for a while post-fertilisation, so the length prior to fertilisation is not important.

Dolly was produced by a process called Somatic Cell Nuclear Transferase, where the nucleus from a somatic cell from an adult organism is transplated into an embryo with its nucleus removed [3]. A study found that she had consistently shorter telomeres corresponding to the fact that the original donor was 6-years old already [4]

You might also be interested in my answers to these questions

Are human bodies programmed to die?
Cell proliferation limit and senescence of embryonic stem cells and fibroblasts
Do trees age on a microscopic level?
Difference In Telomeres Between A Thale Cress Plant And A Methuselah Tree

Shay, 2001, Human Molecular Genetics. Telomerase and cancer. http://hmg.oxfordjournals.org/content/10/7/677.full
Turner, 2013, Mol Hum reprod. Telomere lengths in human pronuclei, oocytes and spermatozoa. http://www.ncbi.nlm.nih.gov/pubmed/23519357
http://learn.genetics.utah.edu/content/cloning/whatiscloning/
Shiels, 1999. Cloning. Analysis of telomere length in Dolly, a sheep derived by nuclear transfer. http://www.ncbi.nlm.nih.gov/pubmed/16218837


Can a chicken's lard become liquid depending on its diet?

Without going into the biochemical details of fatty acid digestion, mobilization, and synthesis, the brief answer is that the animal regulates its own fatty acid composition to within a specified range regardless of its food. Lipid metabolism does not differ from the metabolism of other compounds, in that it is a highly regulated, enzyme-mediated process, which ultimately is genetically determined.

It must be stressed that a heterotroph assimilates its food, not as complete macromolecules, but as their base components. For example, the starch-fed chickens you described would digest the starch down completely to glucose, which would then be converted in the liver to fatty acids. These fatty acids would be, of course, those that the chicken had the enzymes to synthesize, which are consequently mostly saturated fatty acids of a certain length that happen to solidify when cooled.


RE: Fasting gastric pH vs Normal gastric pH

Food only partially buffers the pH of stomach contents and acid is not the only esophageal irritant present in the stomach.

The goal, therefore, is to have as little as possible present in the stomach when lying down (supine) to reduce risk of gastro-esophageal reflux (GER) through the lower esophageal sphincter (LES) into the esophagus. Avoiding meals just before bed, especially fatty meals (which delay gastric emptying), may help in this regard perhaps by avoiding supine position while there is a low pH layer, formed in response to the meal, lying atop the stomach contents.

Weight loss and smoking cessation are frequently recommended to reduce GER symptoms, with some evidence to support this advice. Use of tobacco or alcohol may relax the LES and tends to be associated with GER symptoms, though trials of counseling to reduce their impact have not significantly reduced those symptoms (and another study).


Is there a schema for how human behavior is genetically determined?

We can only observe correlations

Let's just talk about statistics. You can see a correlation between two things only if there is variation for these two things. It therefore, make no sense to look at a single trait that has no variance and ask "is it genetically coded?". The only thing that makes sense is to understand what variables explain the observed variance for the trait of interest. Here, in your question, you are interested in behavioural traits. This answer stands for behavioural traits as it stands for any other phenotypic traits.

What variables could explain variance in a given trait?

To make it easy, let's consider only two variables, genetics and environment. In reality, one should consider other variables such as epigenetic for example. The total variance in phenotype that you observe is the result of the addition of the variance of this phenotype that is due to genetics variance ($V_G$) and the variance of this phenotype that is due to environmental variance ($V_E$) and their covariance ($COV_{GE}$). In other words:

$$V_P≈V_E+V_G+COV_{GE}$$

It is very common to express the phenotypic variance as being the sum of the genetic and environmental variances (and some others such as epigenetic variance). However, you are free to make this partitioning as you feel it useful for you.

Let's investigate those variables a bit further

Of course, $V_E$ and $V_G$ can be further decoupled into a sum of variances (and covariances). And you are free to do the decoupling exactly as you want to. For example $V_E$ could be defined as the sum of the phenotypic variance that is due to variance in temperature ($V_T$), the phenotypic variance that is due to variance in water availability ($V_W$) and the phenotypic variance that is due to variance in the culture of the parents ($V_P$) (and all the covariance). $V_E = V_T + V_W + V_P + ... $

Similarly, the genetic variance $V_G$ can be further decoupled. It is standard to decouple this variance in dominance vs additive effects (relating to the genetic architecture underlying the trait) but this won't be of great help to you. How about talking about variance in the genes affecting brain morphology $V_B$ and variance in the genes affecting hormones concentration $V_H$ and their covariance (epistasis and pleiotropy) $V_G = V_B + V_H + ...$.

Common schema

To my knowledge there is no common schema in how to partition those variances for the specific study of the mechanistic of behaviour. I don't really understand what is the partitioning that you're suggesting in your post but I am hoping that this answer can help you to think further and eventually come up with a satisfying schema.


Can connections between neurons be weakened?

Short answer
Yes, neural connections can be weakened.

Background
Chemical connections between neurons (synapses) can certainly be strengthened or weakened, dependent on their input. Single synapses can undergo long term potentiation (LTP) or long term depression (LTD). As a typical example there are hippocampal neurons. High-frequency (tetanic) electrical stimulation in hippocampal neurons can result in long-term potentiation (strengthening) of synaptic connections in the hippocampus Moreover, when a synapse receives synchronous input from multiple incoming axons they can potentiate each other's responses (Purves et al, 2001). In contrast, low-frequency stimulation and  prolonged inactivity of synapses in the hippocampus can weaken them (Bear & Abraham, 1996).

The connection between learning, let alone good and bad as you ask for in your question, is far from clear. However, LTP and LTD do provide plausible mechanisms that could underpin these processes at the cellular level (Purves et al, 2001).

References
- Bear & Abraham, Ann Rev Neurosci (1996); 19: 437-62
- Purves et al., eds. Neuroscience, 2nd ed., Sunderland (MA): Sinauer Associates; 2001


Sex differences in response to food deprivation

There are very few studies about the gender-based differences in response to food deprivation in humans (or at least I didn't find many such reports).

In one of the papers, Sodersten et al conducted a research on 30 (17 women and 13 men) high school-aged subjects. After a short-term fast (skipping 2 successive meals), males consumed much more food while women actually ate less, when compared with their respective baseline quantity of meal. They suggested an inherent difficulty for women to compensate a period of fasting by increasing their food intake. They, thus, concluded that fasting might be more risky for women than men as this may start them down a self-sustaining pattern of reduced calorie intake. You can see the reference from Yamada's Textbook of Gastroenterology.

In another study, Soeters et al, 2007 showed that after a period of fasting for 38 hours, women had low plasma glucose levels than men, although they have higher amount of free fatty acids in plasma. They suggest that women are somehow protected from free fatty acid-induced insulin resistance, probably because they prevent myocellular accumulation of ceramide.

A yet another study, by Wu et al, 2011, touches upon the point that the relation between kilojoules consumed and kilojoules utilized is different in men and women. They also state that women consume less kilojoules per kilogram lean mass and store more fats in their body, especially during gestation period, as compared to men (I'm obviously not comparing the gestation period). This finding can, in a way, support the observations by Sodersten et al (see first paragraph).

If you want a more detailed report, you can have a look at this report from United Nations University (old website) by Sara R. Millman and Laurie F. DeRose. They discuss in detail why and how women and children are considered the vulnerable groups in times of long-term food deprivation since they are more likely to express hunger and have more serious probable consequences of hunger in times of food scarcity.

If you can expand your terms a little bit, there are (comparatively) many such studies on rats and other animals. For example, Sarookhani et al, 2014 measure the effects of food deprivation on formalin-induced nociceptive behaviors and $\beta$-endorphin and testosterone concentration in rats. You can find many such studies quite easily. However, I'll keep searching and adding more related studies on humans here.


This is not a hornet, this a wasp. See the yellow dots on the thorax ? They are typical of the Vespula genus. So is the yellow and black stripe pattern on the abdomen. Those wasps are smaller than hornets (1-2 cm for wasps, 3-4 cm for hornets). Picture from Wikipedia:

There are two common Vespula species in France  (V. vulgaris and V. germanica), but to identify yours, we would need a better view of the head and abdomen.

On the image below, you can compare it to the two hornet species you can find in France (source). The first one is a bee, the second one is a wasp (Vespula), the third one is the invasive "Asian hornet" (Vespa velutina) and the fourth one is the native "European hornet" (Vespa crabro).

So no extermination needed ;) You can find more information (in French) on how to recognize these species on the Natural History Museum website.

Sources:

Le Rucher des Plaisirs - French beekeeper website
Natural History Museum - hornet and wasp identification in France
Same source in English
Wikipedia page


Is there any format for official Physiological/Medicine answers?

Given the highly variable nature of such processes and systems, it's unlikely that a common standard is feasible or sensible. In medical questions, a bottom-up order like in your example usually makes sense, starting with the most specific known cause and deriving from there until you arrive at the symptoms. Treatments can branch off or into the order at the point where they apply logically.

If your exam instructions ask for flow text, your question is alreay unnecessary - but if you believe you have the choice, use a note format that is appropriate by common sense. You are essentially creating a diagram, and like any diagram you have to ensure that it is self-contained and comprehensive.

You can shorten the amount of time it takes to write sentences by reducing the literary quality. Of course a well-written text is more pleasing to read and mark, but the main emphasis in your grading will usually be content, meaning that you can afford to form sentences of repetitive structures or lacking logical connection if it is difficult to figure out quickly whether there is one or how to express it etc.


What will happen to a neuron if I suddenly remove the pump but not the leaky Na+ and K+ channels?

Both Na+ and K+ will move according to the electrochemical gradient. Given that K+ leaky channels are ever present, the cell is already around its K+ equilibrium. If you introduce leaky Na+ channel and remove the pumps, eventually the cell will be nothing more than a passive membrane and it will adopt the same concentrations of ions as the extracellular space, i.e., Na+ will pour in along its electrochemical gradient, after which K+ (formerly already at equilibrium) will start pouring out alongside its chemical gradient, due to the reduced electrical gradient because of Na+ coming in.


Can a woman possessing 1 mutated allele show attenuated color-vision deficiency?

Short answer
Skewed X-inactivation may lead to phenotypic manifestation of X-linked color blindness.

Background
What an interesting question!

In a study by Jorgensen et al. (1992) two female identical twins that were heterozygotes for X-linked deuteranomaly were investigated. Phenotypically, deuteranomaly refers to anomalous trichromacy, i.e., reduced perception of a color. Note that deuteranopes are totally color blind. Deuteronomaly in the twins was associated with a defective gene derived from their father. Interestingly, while monozygotic twins are genetically identical, one of the twins was phenotypically deuteranomalous, while the other had normal color vision.

Analysis of skin cells of the color vision-defective twin revealed that almost all skin cells had the paternal abnormal X chromosome active, explaining her color-vision defect. In contrast, skin cells from her sister with normal color vision had predominantly the maternal X chromosome active. Hence, deuteranomaly in one of the twins could be explained by an extremely skewed X inactivation.

As pointed out by @mdperry, extreme skewed X-inactivation is rare, and most heterzygous females for color blindness (carriers) are indeed asymptomatic (Jordan & Mollon, 1993). Regarding your second question, all gene mutations leading to color blindness are recessive (NIH).

References
- Jordan & Mollon, Vis Res (1993); 33(1): 1495-1508
- Jorgensen et al. Am J Hum Genet (1992); 51: 291-8


Why aren't the brains of most advanced life forms in the middle of their bodies?

Because the head is where most of the sensory organs are, and once the brain started developing there it was basically impossible to move it. There is so much relying on its placement, that if it was moved many nerves would no longer be directed to the right place, as there are myoskeletal constraints around it. Basically most of an animals form around the central nervous system and moving major basal organ complexes just doesn't happen in evolution. Moving the brain would be impossible once you got to things like vertebrates.

Smaller CPU only work in systems with lots of redundancy which is not an animal thing. Centralizing processing has it's own advantage because parts of the brain have to communicate with other parts a lot. You would basically have to have almost an entire other brain, which defeats any advantage.

Lastly, there really is not much of an advantage in moving the brain into the chest cavity, as for most animals the brain is small enough to be just as safe in the head as anywhere else.

That said, there are animals with a brain in their midsection; they are called cephalopods.


Is it possible to be (briefly) aware you had been decapitated?

According to this, in rats it takes about 17 seconds after decapitation for the EEG to become iso-electric. But there is no known correlation between EEG and consciousness. Also at 50-80 seconds after decapitation, EEG being iso-electric, a very slow, late wave appears on the EEG record.

The same article concludes that it takes about 3-4 seconds after decapitation for the animal to lose conscience and perceive no stress and pain.

Also, dr. Harold Hilman states in An unnatural way to die article from october 1983 issue of New Scientist, page 277 that:

  Consciousness is probably lost within 2-3 seconds, due to a rapid fall of intracranial perfusion of blood.


Are there known life forms that are able to transform mechanical energy into chemical energy?

There are no known life forms that use mechanical energy as a primary form of metabolic energy (i.e., for generic cellular functions). Many life forms are sensitive to mechanical disruption in some way, so they do utilize mechanical energy, but in a very limited fashion (@David's answer touches on this), and of course many organisms have life cycles that somehow depend on mechanical transportation (seed/spore dispersal, traveling on the wind or ocean currents, etc).

I think the main physical problem is that mechanical energy just isn't available to biological cells in a form that can be converted to substantial chemical energy. They are small, and tend to have other great benefits for being small.

To use an ocean wave as an example, there is very little or no perceptible movement for a cell in that wave, besides an apparent increase and decrease in the force of gravity. The top and bottom of the cell are moving together with the flow of water, so there is no differential to operate on.

An E. coli weighs about 1 picogram. If it could capture all of the energy from falling from 1km in the air on earth, assuming no uncaptured aerodynamic drag, that would be about 10-11 joules.

If there are ~3000 kJ/mol of energy available from burning glucose, that means about 5 × 10-21 joules per molecule of glucose, so about 20 billion glucose molecules, which sounds like a lot but it is only 1 femtogram, 0.1% the weight of the cell.

Also note: in @David's answer he makes a very good point that in a way, using mechanical force to open a channel is indeed a form of energy usage and therefore a proof of concept that this could happen. To put that process in the same ballpark, this source (originally mentioned by @GerardoFurtado) gives the work necessary to open one of these channels at around 8 × 10-22 joules. The open latency for those channels is under 50 microseconds, but that still greatly limits the number of possible cycles per unit time. Chemical energy is just substantially more dense than mechanical energy is: that's why gunpowder superceded catapults (and even the trebuchet..).


Why do humans grow taller than their ancestors?

A likely misunderstanding of yours

Now we almost don't fight with other species

Misunderstanding about selection
As you will go through this course, you will understand why this sentence makes little sense. A change in allele frequency via natural selection is caused by a fitness differential among genotypes within a population. The existence of a competitor species would eventually affect this fitness differential but there is no need for a competitor for having a selection pressure.
I think you are having the view that selection is a process that allows a species to be better at coping with a competitor but this is wrong. Selection will increase the frequency of individuals having high fitness in the population. The resulting population may well not be a better competitor.
False opinion that we are not competing with other species
Also, about nearly 50,000 people are dying every day from infectious disease (UN press release). So, we are definitely still "fighting" with other species. Adaptation to malaria in humans is a famous case study (see this answer and its links).
Also, according to reuters (who fail to link to their source), the worldwide cost of pests in agriculture is estimated to about 540 billions USD per year! So yep... competition there is.
What selection pressures are there on human height?
Review paper recommendation
Stulp and Barrett 2016 is a review paper on the evolution of height in humans that you might want to have a look to have a clearer picture than what I will give here. It is easy to read. I highly recommend having a look at it.
They cite a lot of papers. I won't cite them again below but I will just attempt to make a vague summary of the parts which I think will interest you the most.
What selection pressures are there on human height?
The question appears to not be that easy to answer. In humans, height is highly heritable and there is a lot of variance in height among populations. It is likely that different selection pressures may have acted on different populations.
There are a diversity of selection patterns
In short, selection pressures on height include intra and intersexual selection. Taller adults seem to have a reduced mortality rate. Taller women have a lower risk of complications when giving birth. However, in both men and women, the correlation between height and number of offspring varies a lot from study to study (and likely from population to population). In the USA for example, men having the highest number of offspring are of intermediate height (balancing selection).
It appears that epigenetic variation also have an important impact on height Simeone and Alberti 2014 and there might have a sex-driven intra-locus conflict on height (Gilks et al. 2014; Stulp and Barrett 2016)
There is evidence of current selection on height
We have a fair number of evidence that height was and is still under selection in humans but we think that the exact pattern of selection pressures acting on it is quite complex. Note that there is evidence that height is still under selection today.


Harvest honey without damaging brood cells

In domesticated bee hives, this is usually accomplished by excluding the queen from a section of hive frames (by the size of the entrance hole), so that these frames only contain honey and no eggs/larvae.
For instance, this can be achieved using a queen excluder.


Do miRNA and antisense RNA do essentially the same thing?

Antisense simply means that a sequence is the complement of another. miRNAs are naturally occurring antisense RNAs yes. The "difference" is that antisense RNA is often used for sequences developed in the lab and used for processes such as RNAi.

miRNAs, on the other hand, are encoded by the genome and are used by the cell for regulating gene expression. They do this through the RISC complex, just like artificial antisense RNAs such as siRNAs.

Basically, antisense is the general term, and can be applied to any sequence whose complement exists in the genome. miRNAs are a particular class of antisense RNAs.


Very introductory online source of information in evolutionary biology

At least online, I think the single best introductory evolution resource is the Evolution 101 tutorial at UC Berkeley's Understanding Evolution project. The site has been designed by some of the top evolutionary biologists and evolution educators in the country, and does a very good job presenting a basic overview of how evolution works.


We really don't know - we can't really ask the chicken. At least, it's unlikely it's as painful as it can be with humans.

The reason human birth is (or can be) very painful is that the human baby's head has to fit through the woman's pelvis. Since splitting from chimpanzees, human heads have gotten bigger, while the pelvis has gotten more narrow due to adapting to walking on two legs. While chimpanzees give birth in an average of around 2 hours, humans can take over a day to do so, and the baby being too big can lead to maternal and natal death.

Back to chickens, while there are different sizes of eggs,  the larger eggs come from larger chicken breeds. If it does hurt them, at least it takes a lot less time - only a few minutes. From personal experience, the hens do not appear traumatized even seconds afterwards and just go about their day as soon as the egg is out.


How good is the reproducibility of preclinical models?

The Cochrane Collaboration has a great deal of this type of analysis. One of my favourite features of a Cochrane Review is the routine use of Funnel Plots, where there are sufficient data to produce them. Sensible interpretation of funnel plots can give some fairly strong hints about the reproducibility of published literature.

Funnel plots show datapoints of individual published studies which investigated the effectiveness of a technique when used for a specific purpose. The datapoints are plotted by estimated effect size (on the x axis) and an assessment of the quality of the trial, incorporating things like sample size and experimental design (on the y axis). A study with a small sample size and/or poor design (low on the y axis) would be expected to provide a relatively inaccurate estimate of the method's true effect size. As sample sizes increase and experimental methodology gets better (travelling up the y axis), you expect the studies to zero in on the true effect size, giving a pyramid or 'funnel' shape to the overall plot.

The reproducibility of trials affects where the points are in the pyramid in a couple of ways.

If there were a bunch of studies which looked for an effect of the method, and didn't find one, they might not be published because null results are considered boring by journal editors - the so-called 'file-drawer effect'. This would show up in a funnel plot as a pyramid that has a suspiciously low number of datapoints on the side of the pyramid that is close to the zero effect-size. The 'missing' datapoints are an indicator that this technique probably did not always reproduce an effect size as strong as the published effect sizes.

The other way that funnel plots can inform on the reproducibility of published studies is simply by looking at the width of the base of the pyramid. If it's wide, then with the experimental design methods of the studies at the bottom, the results aren't highly reproducible - different studies give very different results when looking at the same question.

It's a big job to synthesise this into a global assessment of 'the reproducibility of pre-clinical trials', but if you're interested, I'd recommend you spend some time trawling the Cochrane Library to get a hang of the sorts of variance you're dealing with.


Connectivity Relation between axon terminal synapses and dendrites

Synapses are pretty much one-to-one
Here's some EM pictures of synapses, from Wikimedia commons:

You should gather from these images that these are super organized structures. There's a dense, dense gathering of cellular machinery at the synapse that creates a dark electron-dense region shown by the arrows. There's no room for more than one cell to be directly involved in this area, it's one membrane closely coupled with another membrane. It's as if you put the palms of your two hands together.
Some neuromodulators (and sometimes traditional neurotransmitters) are not released synaptically, though, and are just dumped into the extracellular space from where they diffuse in to the cleft or bind outside the synaptic region.
There can be multiple connections between two given cells
Though a synapse is a one-to-one connection, axons make multiple synaptic contacts as do dendrites. Though this can mean that cells receive and send input to 1000s of different cells, it's also very common for there to be multiple individual synapses between two specific cells.
For some examples, Tamas et al 1997 looked at synapses made from inhibitory interneurons to excitatory cells in visual cortex:

All presynaptic cells established multiple synaptic junctions on their postsynaptic
target cells. A basket cell innervated a pyramidal cell via fifteen release sites; the numbers of synapses formed by three dendrite-targeting cells on pyramidal cells were seventeen and eight respectively, and three on a spiny stellate cell; the interaction between a double bouquet cell and a postsynaptic pyramidal cell was mediated by ten synaptic junctions.

Note in this paragraph they are literally talking about 5 specific pairs of cells, where they trace both cells in EM. This is an exhausting process. The presynaptic cells were one basket cell, three dendrite-targeting cells, and one double bouquet cell. The post-synaptic cells were all pyramidal cells except one was a spiny stellate cell. In the five pairs they found 15, 17, 8, 3, and 10 connections. Of course they could have missed some, too.

Tamas, G., Buhl, E. H., & Somogyi, P. (1997). Fast IPSPs elicited via multiple synaptic release sites by different types of GABAergic neurone in the cat visual cortex. The Journal of physiology, 500(3), 715-738.


where i can download reference MSU7 rice genome?

You can find this on the phytozome website. You will have to make a free JGI account to access it


Does anyone know what marsupial this is?

I've been told it is the marsupial 'Myrmecobius fasciatus' commonly known as the numbat.

http://en.wikipedia.org/wiki/Numbat