Are the inverse problems of Systems Biology impossible to solve?

The answer is mostly no, and this is not as disruptive a statement as it seems to be.

I think Brenner has a point of course and he is not the only one who wonders whether the systems biology can create a holistic model of living things.  Still I wouldn't take this to mean we should stop doing systems biology research.

At 18:30 brenner illustrates the inverse problem with some examples 1) can you create a drum from only the sounds that come from the drum? (no he says). 2) can you solve the molecular structure of a molecule from a diffraction problem (no he says).

Of course we can do both of these, but the point is valid as we need to have an idea of what a drum looks like.  If we did have even a glance at a drum, this lets us build a model (cylinder of diameter d, height h and with a drum head of a tension t and material properties alpha beta, etc) from the sounds is a lot of work, but it could be done.

The problem of solving a molecular structure from diffraction intensities alone has also been solved for small molecules in the 60s I believe by so-called 'direct methods' which don't work well or proteins and larger molecules.  Still the point is that you had to have a good mathematical model of molecules and diffraction to get to direct methods, MIR, MAD and other diffraction only methods. Sorry I can't go into details here...it might bore you to death if you don't care about crystallography.

In both cases the statement is that you need to have that model - what does a molecule look like, what does an x-ray do when it encounters a crystal? In order to get there.  Which makes total sense and I agree with.

I wouldn't read too much into this though, because in practice this has never been done, yet Bragg started with just the diffraction pattern and drew in models from other fields of study.  Given the nature of the proof described, no scientific discovery has ever happened in a mathematical vacuum and systems biology will not either.

Rather I would read this talk as saying that the models we are using for action are not very good yet.  What is happening is that synthetic biology (engineering approaches), experimental observation, and intensive modeling (the 'inverse' and 'forward' approaches Brenner mentions) are all happening at once and are informing each other.

Its hard to imagine that data from inverse approaches can't be an important part of any solution to biology.  Its also looking likelier that a mathematical model alone of biology will be difficult or impossible to find also.  What is currently (IMHO) working is a framework that is both conceptual (and not entirely quantitative) as well as analytical (mathematical) and data driven.


How to preserve leaves between sampling (collection) and analysis?

You may want to see:

Mark W. Chase, Harold H. Hills; Taxon, Vol. 40, No. 2,  1991, pp. 215-220: 'Silica Gel: An Ideal Material for Field Preservation of Leaf Samples for DNA Studies'

Summarized, the process would be the following:

Place the leaves inside ziplock plastic bags;
Add ten times (minium) the weight of the leaves in silica gel;
After 12 hours (after which the degradation of the biological material is more likely), check the leaves by bending them: if they break cleanly, the leaf is dry;
Store in the ziplock bag, inside a box with an hermetic lid;
Refrigerate (if possible).

Note: Freezing by submersion in liquid nitrogen is also a viable approach, yet might be less practical


How can I produce milligram quantities of an isotope-labeled DNA oligomer?

You can also design a plasmid that has your 35mers and raise the bacteria with isotopic carbon and nitrogen C13 acetate and N15 ammonium sulfate will work with E coli in a minimal medium.

this is not cheap, but the cheapest available sources of the isotopes can be used.


Do all chromosomes have the same DNA?

No.  Not any more than each chapter of a book has the same words in the same order.

  If so, does it mean that in different cells with different functions
  some genes are expressed and some aren't?

Yes.  In general, all cells in your body have all the same DNA; what makes your retina cells function differently from your pancreatic beta cells is which genes they express.  Like if every chef in a restaurant had the same recipe book which had every recipe the restaurant can make, but the pastry chef only makes pastries.

  Also, if each chromosome has different lets say "fragment" of the
  genome, how is the genome interconnected?

The genome is not physically connected except for all the genes on a chromosome being physically connected.  But a gene product from one  chromosome might control expression of another gene by physically binding to the DNA close to it, which can affect its expression.  But most gene-gene interactions are really protein-protein interactions.  (Or in some cases, RNA interacting with RNA)


A major determiner of blood flow redirection among muscles is increased oxygen demand in the working muscles.

When a muscle works, it uses oxygen, so the partial pressure of oxygen (PO2) in the muscle falls, which signals small arteries (arterioles) to dilate, which results in increased blood flow and hence oxygen and nutrients delivery to the muscle (Skeletal Muscle Circulation, NCBI Bookshelf).

When you exercise your forearm muscles without exercising upper arm muscles, the arterioles in the forearm muscles will dilate but in the upper arm muscles will not. The blood will just flow through the large arteries of the upper arm toward the forearm, but it won't be delivered to the upper arm muscles.

A long-term effect of exercise is the formation of new capillaries in the exercised, but not in other muscles (PubMed, 2008). So, six months of exercising forearm muscles without exercising upper arm muscles will result in better circulation only in the forearm muscles.


Variations in action potential threshold and temporal coding

Hi,
For what I read, the objective of the paper is in fact to study the neural code using methods that study the membrane threshold changes (as you said). They mention both rate and temporal code in the introduction and they do give more emphasis to the temporal coding because it explains better the irregularities of the neuronal transmission.
They did find some correlations between changes in the threshold, which influences the iniciation of the action potential, and the timing and rate of the firing or the firing pattern. That means that the firing pattern influences the iniciation of the action potential even if in an indirect way (which is by influencing the membrane threshold). Saying that the pattern of firing is important it means that the timing is also important, instead of only the rate the firing. Because this is the major difference between both neural codes theory, it does support more the temporal code.


can one be infected with Naegleria fowleri by taking Steam?

N. fowleri infection can occur after nasal and sinus irrigation, swimming and other exposures to contaminated water. The infectious agent in this case is the trophozoite, not the cyst. Boiling water contaminated with this amoebae kills it, preventing infection. Though it does thrive in warm water (37 C), it doesn't survive in steam (100 C).

Despommier's Parasitic Diseases Ch. 14 discusses N. fowleri in some detail. It's also covered in Murray Medical Microbiology Ch. 82, and Cecil medicine Ch. 360. There's also useful study in The Laryngoscope on the viability of various pathogens in contaminated water after sterilization methods.


Why are cells in blood smears undetectable after absorbing moisture?

It might be helpful if you are able to post a picture of what you're seeing, however, it sounds like the blood cells are lysing.
The water you introduced to the cells through the moisture in your breath is likely creating a hypotonic environment, causing the cells to intake a lot of water and then lyse, causing their appearance to become atypical.


Because in different cells different copies of the X chromosome might be inactivated.
So, in (approximately) 50% of the cells you will have the X carrying the normal gene activated, and in the remaining 50% you will have the other.
You might start reading something here, and then go in further detail to understand. A nice article is here


molecular indicators of apoptosis: clarification needed

Although both involve DNA fragmentation, the pattern produced is very different.  During apoptosis, DNA fragmentation is done in a regular, controlled pattern, which if run on a gel produces a characteristic "ladder" pattern.  Necrosis, on the other hand, is a more stochastic process, and will produce a smear.  This details the difference rather nicely, including different ways to assay for either one in table 18.3.1 such as morphological staining or flow cytometry.

Here's a nifty image from the link.  Figure 18.3.2.  M is the marker, and in panel A, a conventional gel, lane 1 is apoptotic DNA, lane 2 is unprocessed DNA, and lane 3 is necrotic DNA.  In panel B, a pulsed-field gel, lanes 1 2 and 3 are untreated, apoptotic, and necrotic, respectively.


Before Evolution was proposed by Charles Darwin, what were the leading secular theories to explain how life developed?

There were many (more or less) non-theological theories of how life had developed before Darwin, starting at the ancient greeks. Many theories included spontaneous generation but also aspects of modification by descent of existing species (i.e. evolutionary change), but most were not that well developed and complete thought. However, one of the more complete evolutionary theories that pre-dated Darwin was Lamarckism, which claimed that individuals pass on traits that they have acquired during their life time. So the basic idea was that individuals respond and adapt to the environmental conditions they experience, and that these traits are then transferred to their offspring. This is one example of a non-theological theory that pre-dated Darwin, but I cannot really say if it was the leading one. I do know that Lamarck's ideas were relatively ignored during his own lifetime.

Darwin included some aspects of these ideas in his "Origin of Species", but challanged Lamarckism when it came to the main processes of evolution. A weak interpretation of Lamarckism has actually seen a revival after the discovery that epigenetics can be transferred from parents to offspring, see e.g. Heard & Martienssen (2014) and Szyf (2014).


What is the relationship between stroke volume of blood and ventricular end-diastolic volume?

The simplest relationship is "EDV=SV+ESV", "EF=SV/EDV" (EDV: end-diastolic volume, SV: stroke volume, ESV: end-systolic volume, EF: ejection fraction)


The difficult step will be getting samples of sap: have a look at the WP page for maple syrup for ideas about methods of tapping into the xylem of your trees.

You will then need to assay sucrose in the sample of sap. There are many commercial assay kits available (Google: sucrose assay), which rely on an enzyme, invertase, to convert the sucrose to glucose + fructose. The released glucose is then measured by a glucose oxidase assay. You would need some kind of colorimeter/spectrophotometer for quantitative results but there is a visible color change, so you could probably get a rough idea of what is going on by visual comparison with a set of glucose standards.

Supplementary
An alternative would be to measure sugar concentration by refractometry: see here and here.


What is the difference between the cellular affix -cyte and -blast?

Short answer
 - The affix -cyte means cell;
 - The affix -blast means a germ (bud) cell or a cell that produces (building) materials.

Background
Cells are denoted as -cytes. There are many of them, e.g. melanocytes in the skin and chondrocytes in the cartillage.

Germ cells are denoted as -blasts. These cells typically are precursor cells such as the lymphoblasts that are undifferentiated precursor (stem) cells situated in the bone marrow that produce leukocytes.

Blast cells may also be cells that produce materials. Your examples are of that category; odontoblasts generate dentine, the main hard tissue of the tooth; ameloblasts deposit tooth enamel, which is the hard outermost layer of the tooth forming the surface of the crown. in that sense, also progenitor cells produce something, namely new cells. Hence, blast cells are cells with a chief building function, either materials or new cells.

There are also -clast cells - cells that destroy something. Fig. 1 below gives an overview of these cells as present in the bone, namely osteoblasts (bone builders that secrete the matrix), osteocytes (osteocytes are osteoblasts that are embedded in bone; they stop secreting matrix and only maintain it) and osteoclasts (different class of cells that mediate bone resorption).

Different cells in the bone. source: University of British Columbia

Why then do not call odontoblasts odontocytes? - Because it would mean loss of information. It would be the same as calling a car and a bike both transport vehicles. Moreover, the example in Fig.1 is quite convincing, as osteocytes and osteoblasts are considered to be different cells altogether (although the former is derived from the latter).


The 15:1 phenotypic ratio resulting from the self cross suggests duplicate dominant genes without cumulative effect.
In other words, two genes with complete dominance and dominant alleles producing the same phenotype, but independently, meaning that dominance at one locus ~ dominance at the other locus ~ dominance at both loci as far as phenotype is concerned.

So, in the self cross:
AaBb x AaBb =>
9 A_B_  double dominance = dominance
3 A_bb dominance from A
3 aaB_ dominance from B
1 aabb recessive
So that's where you get your 15:1 dominant:recessive phenotypic ratio.

Now, with a testcross, you were on the right track:
AaBb x aabb =>
1 AaBb
1 Aabb
1 aaBb
1 aabb
So, comparing this to the selfing results above, you'd get 3 dominant : 1 recessive for your phenotypic ratio.


There are various factors which decide the dominance of one gene over the other. Owing to the complex biochemical pathways it is difficult to predict which gene is dominant unless we know exactly how the gene is translated to protein and how the protein interacts with the body.
These are the few answers that could help:-

What makes a gene dominant or recessive
What determines if an allele is dominant or recessive?

As for your question;

There are two genes:

D- The allele which is dominant
d-The allele which is recessive.

A recessive gene is a gene that is nonfunctional or expresses its characteristic phenotype in presence of an identical allele.

For a person to have Rh negative blood group he must inherit 'd' allele from both the parents as it is a recessive trait.And as @swbarnes2 mentioned in the comments 'd' allele is more common in European countries leading to a wide range of population possessing Rh negative blood groups.


Brainbow fluorescence labeling technique

Yellow would need the expression of red and green so that would mean the excision of the blue fluorophore. It would be one line with egfp and the other line with mKO2--- the order doesn't matter-- these represent chromosomes.


Do Gametes contain mitochondria/chloroplasts from their parent cell?

Is this DNA found in the mitochondria and chloroplasts coded for in the host's (animal's or plant's) DNA.

No, the DNA contained in these organelles it not a subset of the nuclear genome. However, part of the original genome of the prokaryote has been moved to nuclear DNA. That is why, as you cited, they "can no longer live independently."

  If not are there fully formed mitochondria and/or chloroplasts in all gametes (obviously chloroplasts only in the plant gametes) which were transferred directly from the parent who had them transferred directly from their parent and so on?

As the child organism would eventually need these organelles, and they can only be inherited, at least one of the gamete must contain them.

For the chloroplast, the general rule is that only one of the gamete provides it. For example, in gymnosperm it is the male gamete (pollen), in angiosperm, it is the female gamete (ovule). Either it is just not present in the other gamete, or a specific exclusion mechanism makes it mono-parentally inherited.

Mostly the same for the mitochondria, with the caveat that (motile) spermatozoa contain mitochondria for their metabolic functions (energy to move), but these are discarded when forming the zygote, and only the maternal mitochondria are inherited. (In plants, mostly maternal too with exceptions)

This does mean that there is a lineage of organelle on one of the parent's side, up to the most recent common ancestor (approximately, the first individual of the species). In humans, this translates to a presumed Mitochondrial Eve from which all human mitochondrial DNA descends from.

  If so are all the mitochondria and chloroplasts of one type identical in a organism? Are they almost identicle in families (of organisms not the classifictaion Family)?

Every mitochondrion of an individual organism comes from the stock of mitochondria of the zygote, through replication. They are thus very similar, except for cell specialization (giving particular morphology to the organelles), and possible mutations. Same for the chloroplast.

Mitochondria (and chloroplasts) are basic components of the eukaryotic cell, providing essential functions  which are highly conserved in a species, let alone related individuals.

However, this does not means the DNA of these organelle is the same for every individual : different sequences may give the same protein, or mutation may affect non-coding segment of the genome. This is the basis for genetic genealogy, retracing family lineage though analysis of DNA, including mitochondrial DNA.


A copy number variation (CNV) is when the number of copies of a particular gene varies from one individual to the next.
From: the NIH Glossary

Focal CNVs are regions of repeated genetic information that only span a small proportion  (<25%) of the chromosome arm (although this does not seem to be a consistent rule), and can contain few genes. CNVs greater than this are termed either 'large-scale' or 'broad'.

Here are some relevant papers I came across (no doubt there are more);
This paper is about a program (VarScan2) the authors have made to robustly detect somatic mutations and CNVs;

To identify SCNAs [somatic copy number alterations], VarScan 2 compares Q20 (base quality >=20) read depths between tumor and normal samples for contiguous regions of coverage ... Therefore, we apply a circular binary segmentation (CBS) algorithm (Seshan and Olshen 2010) to delineate segments by copy number and identify significant change-points. A subsequent joining procedure merged adjacent segments of similar copy number and classified them as either large-scale (>25% of chromosome arm) or focal events.
From: Koboldt D, et al, 2012.

I continued searching, as I wondered whether this was a standard definition, or just one used by the authors.
This paper is reporting bacterial genes that drive focal chromosomal aberrations, but do not give a great definition (as it seem quite arbitrary to me);

Many of these [chromosomal] aberrations concern large chromosomal regions, which makes it difficult to identify actual driver genes. Increased resolution has led to the detection of focal chromosomal aberrations, defined as 3 Mb or smaller in size [5–8]. Inherent to their size, focal aberrations contain a small number of genes, facilitating driver gene identification
From: Brosens R, et al, 2010.

This extract is from one of the studies referenced by the previous paper (when they mention their definition of focal CNVs). This paper is about CNVs in different tumour cells;

Primary tumors contain varying proportions of nonneoplastic cells thereby obscuring focal amplifications, defined by the increased copy number of a small region of the genome, from simple gains of whole chromosome arms.
From: Leary RJ, et al, 2008.


One Sample, Different Methylation Values

I looked into this and if the effect is real, which it sounds like it is, it may be 5-formylcytosine.

Methylcytosine oxidizes into hydroxymethylcytosine, which reacts with bisulphite exactly like you expect (identically). Hydroxymethylcytosine further oxidizes to 5-formylcytosine, which behaves like unmodified cytosine (i,e. deaminates to form U). TET enzymes mediate this behavior in vivo but I can't find any data on spontaneous methyl group oxidation or what the kinetics might be like. This paper relies on the properties of 5-formylcytosine outlined above.

You could use this paper to test if that's true. Reduction with sodium borohydride converts 5-formylcytosine back to hydroxymethylcytosine, which reads as methylated under bisulfite sequencing.


Transfer of antibodies in breast milk of humans

It is!  Here is an amazing review from 2011 that literally has all the answers.  I'm not kidding, all of them.  I would marry this review if I could.1  It also includes information on other animals.

The main takeaway is that IgA from milk is not readily absorbed by the infant body.  Secreted IgA is mainly to provide a protective coating for the mucosa while the infant is developing its own nascent immune system.  IgG passed along from the placenta (your other question) provides the main source of absorbed antibodies.  As it says in the review:

  Milk sIgA is not taken up by the infant’s intestinal mucosa. In fact, gut closure in humans occurs before birth and little immunoglobulin is absorbed intact in the intestine after birth. However, the presence of sIgA in the intestinal lumen is part of the protective function of the epithelial barrier in the intestine... Secretory IgA is considered to be the primary immunoglobulin responsible for immune protection of mucosal surfaces such as the intestine.

In terms of enzymatic activity, the digestive system will in indeed chomp up the antibodies; that's part of the reason breast feeding should continue as needed.  That's okay, because there's plenty to go around:

  Much of the immunoglobulin consumed in an immune milk can be expected to be partially or completely digested, however some portion of the immunoglobulin will remain intact or at least partially intact and capable of binding to an antigen.

It turns out that immunoglobulins are moderately resistant to digestion, at least more so than other milk proteins.  There's a section in there detailing some experiments where Ab was given to individuals:

  In adult humans consuming a bovine whey protein concentrate, approximately 59% of IgG and IgM was detected by radial immunodiffusion from effluents from the jejunum, while 19% was detected in the ileum. These estimates of digestion of immunoglobulin compare with estimates of digestion of milk proteins in adult humans which are approximately 42% complete at the end of the jejunum and 93% complete by the end of the ileum, again underscoring the relative resistance of immunoglobulins to digestion in the gastrointestinal tract.

Digestive enzymes vary as to which antibody they prefer to digest, but at least some of them will technically digest the antibody, but still leave functional Fab fragments, which are still immunologically active and useful to the infant immune system.

1: Did I mention I love this review?  I love it.


Is reverse tonotopical organisation possible?

There are indeed constraints: in principle, low-frequency sound waves travel better in viscous media (look here for a simple explanation). The idea behind that is that being sound a vibration in the medium, it causes its molecules to move. The faster the movement (that is, the higher the frequency) induced by the wave, the more the particles will disperse their energy by crashing into each other. This leads to more loss of energy for high-frequency waves compared to low-frequency ones when travelling in a medium.

Now, all of this leads to the detection of high frequencies being better at the beginning of the canal. However, here is the law that quantifies the loss of amplitude of the wave with distance. As you can see, the damping is higher for high frequencies, as well as high viscosities. However, plugging in some sensible numbers (20 kHz for very high-frequencies heard by humans, 1500 m/s for the speed of sound in endolymph, 1 centipoise for its dynamic viscosity, 1 kg/liter for density) gives a negligible loss of intensity (something like 0.0001. I'm sorry for the poor formatting, but I'm on my phone right now and I hope you will try to run the calculation yourself).

Now, a possible need for the accurate detection of even higher frequency sound waves in water for the fish in which the cochlea appeared is possible. However, I neither know if that is the case, nor if the difference would be a significant one.


What predates on cactus in the Atacama desert?

Short answer
This type of herbivory is probably from feral livestock, especially donkeys.
Long Answer
There is video footage of guanacos eating flowers off of cacti in the Atacama. For example, an image capture of a Getty Images video:

 Credit: BBC Natural History
This type of florivory has been documented in related species of cacti as well (e.g., see Gomes et al. (2016)1)
However, I could find little evidence about guanacos eating the trunk of these cacti (especially to the degree you describe).
Actual herbivory of Echinopsis cacti has been reported in multiple publications. For example, Peco et al. (2011)2 cite feral livestock as a major source of herbivory in columnar cacti in South America:

Columnar cacti are an important feature of the arid “cardonal” landscape in South America. The predominant columnar cactus in the southern zone is Echinopsis (=Trichocereus) terscheckii. At some sites, the species suffers considerable trunk damage, attributed in previous studies to feral livestock grazing (donkey and cattle).
In a previous study we found that damage intensity on Echinopsis terscheckii trunks correlated with abundance of livestock dung in their surroundings, but not with the abundance of guanaco dung (Lama guanicoe) (Malo et al., 2011; Novillo and Ojeda, 2008). Futhermore, E. terscheckii was found in summer or winter donkey diet but not in guanaco diet in the study area (Reus pers. comm.). Direct observation of donkeys feeding on columnar cacti suggests that this species is the main cause of stem damage

See this National geographic video explaining how camels and other related animals handle eating spiney cacti. (Specifically, they accomplish eating cacti through the use of hardened papillae guiding the spines down the throat vertically).

Works Cited:

 Gomes, V.G.N., Koroiva, R. and Araujo, A.C., 2016. Vertebrate florivory on the short-columnar cactus Echinopsis rhodotricha K. Schum. in the Brazilian Chaco. Plant Ecology, 217(12), pp.1481-1487.

 Peco, B., Borghi, C.E., Malo, J.E., Acebes, P., Almirón, M. and Campos, C.M., 2011. Effects of bark damage by feral herbivores on columnar cactus Echinopsis (= Trichocereus) terscheckii reproductive output. Journal of arid environments, 75(11), pp.981-985.


Determine similarity in percentages between species A and B, A and C, and B and C

Step number one is correct, but note that there are several similarity (or alternatively distance) measures. What you choose is the simplest and most intuitive one and it a good one without any other assumption or explanation given.
Step number two is also correct, if the similarity is a good proxy for when the last common ancestor between two species is in time, which in this case should be.


Can I use PCR buffer instead of cDNA synthesis buffer?

This page has the recipe for 10X M-MuLV RT buffer:

500 mM Tris-HCl
750 mM KCl
30 mM MgCl2
100 mM DTT
pH 8.3

If you have the basic reagents, I suggest making that.


What do bloodsucking animals actually feed on?

Lets find out how much calories are there in the blood. I am using this site for main reference, but will also add more references where needed. But before that, we should know that one donation of blood is about 1 pint (or 450 ml) blood1. But here, I calculate with volume 500 ml.

First calculate calories for plasma. Blood is denser than water by six percent2, so multiply that 500 ml donation times 1.06 to get to grams (because calorie content will be calculated from grams). Multiply that by 55/100 for men or 60/100 for women to get to grams of plasma. Now, multiply that by .07, because plasma is only 7% protein3, to get to grams of protein. Finally, multiply that result by four to get protein calories. Here, considering 55/100, I get 81.62 calories.
Now for sugar in plasma. Normal fasting blood sugar is around 0.09 grams per 100 ml of plasma (more familiarly expressed as 90 mg/dl4). Multiply the amount in grams time 2.75 for men or 3.00 for women, i.e., equal to how many hundreds of mls of plasma there are in 500 ml of blood, and then times four to get to calories. Result should be 1 calorie.
For plasma calories from fat, use 0.5 grams per 100 ml5 of plasma, times hundreds of mls of plasma, times nine - for calories from grams of fat - to get to calories.  Result is roughly 12 calories.
Next comes calories from red blood cells. RBCs are mostly water and protein, the protein almost entirely hemoglobin. Hemoglobin does not conform to the rule of four calories per gram because the heme portion of the molecule is not metabolized for energy. Use average hemoglobin values of 160 g/L for men or 140 g/L for women6, multiplied by 0.5 to get to the blood donation volume of 500 ml, multiplied by 0.96 to correct for using only the non-caloric heme portion of the hemoglobin molecules, then multiplied by four to get to calories. Hemoglobin is only 90% of the dry weight of RBCs7. Multiply one-tenth the amount of the hemoglobin weight in 500 ml times six (see below for why six) and add that to red blood cell calories. I get 353.28 here.
Finally, estimate calories for the other types of cells. Of the 500 ml blood donation, roughly one percent will be white blood cells and platelets8. Figure five grams, times one-third to get to dry weight, times six, to get to an estimated 10 calories. The "times six" is because some of the dry weight is protein or carbohydrates, which both have four calories per gram, and some is fat, which is 9 calories per gram.

Add everything up. The total should be approximately 425 calories for women and 460 for men in 500 ml blood i.e. even 10 ml of a man's blood contains about 9.2 kcal (there's no definite answer about how much blood a leech drinks at a time). Now, as you say in your question that a leech requires about 0.714 kcal, it means that a leech can survive for almost 13 days by sucking just 10 ml of a man's blood (if they have to metabolize everything present in blood (except, of course, water)), which justifies your statement.


Why are haploid cancer cells not killed by immune system?

Now that I did some research on this, it seems to be a very rare condition of acute lymphoblastic leukemia (ALL), see this article:"Chromosomes and causation of human cancer and leukemia. XLVII. severe hypodiploidy and chromosome conglomerations in ALL.".
This article ("Origin of near-haploidy in malignant hematopoietic cells.") hypothesizes that this might happen through gradual chromosome loss during cancer formation and that in the end one clone with a lower than normal number of chromosomes.

This seems connected to a much worse outcome of the cancer than for hyperdiploidies (more chromosomes than normal). See the "Atlas of Genetics and Cytogenetics in Oncology and Haematology".
They also define why haploid (or near haploid means: Less than thirty chromosomes, down to 23 have been observed). This is not the normal haploidy found in germ cells. Se also "Isolation and Characterization of a Near-Haploid Human Cell Line".

Since these chromosomal changes occur inside the nucleus I think this is mostly invisible to the immune system - so there is probably no difference how these cells escape the immune system compared to other cancer cells. I think its possible that due to the chromosomal loss some proteins which control apoptosis are lost, so the cells escape this fate as well.
Regarding the immune question, you can either start with the following articles or simply go over to Pubmed and choose some articles. In this field there is a lot of research going on.

Does the immune system see tumor as foreign or self?
The tumor microenvironment and its role in promoting tumor growth
Tumor Evasion from T Cell Surveillance

If there are access problems, let me know.


If body temperature is 37°C (98.6°F), why are most people more comfortable at around 21°C (70°F)?

This is due to the fact that skin is the interface where heat is lost.

Our body due to constant functioning, produces heat constantly as a by-product (due to exothermic reaction of ATP break mainly). The excess heat needs to be conducted away from the body, or it will cause a decrease in the body metabolism to prevent temperature rise.

Heat is lost mainly through the skin by:

Sweating - Through evaporation
Radiation - As heat waves (IR rays - That's why IR camera captures people at night)
Conduction - Directly through objects that touch skin
Convection - Through air circulation

When the ambient temperature rises, the heat lost through radiation, conduction, and convection drastically decreases. And often when the temperature is high, there is a accompanying rise in the relative humidity which decreases the heat loss through sweating (as the amount of water vapor is high in the atmosphere, the sweat does not evaporate, so no heat is lost).

So the heat which is not lost is felt as the "hot sensation". It relieves by stopping any activity, seeking shade or a cool place, etc... all of which increases the heat lost or decreases the heat produced.

You have to note that the temperature of skin is lower than the body temperature.

The Skin temperature is lower than the core body temperature for two reasons:

The skin acts as a medium through which the external temperature is measured - as such the skin temperature is at equilibrium with the external temperature. The brain regulates the core-body temperature in response to temperature measured through skin. If a person is exposed suddenly to cold environment, skin looses much of its heat in the form of radiation (radiation is direclty proportional to the temperature difference) this will cause perception of cold and the body starts shivering even though no actual heat loss has occured from the core body thermal load (only skin looses heat, not the body core). The brain anticipates that the core will loose its heat when exposed to such low temperature for prolonged periods and starts the warming mechanism before the actual cooling occurs such that the cooling is either prevented or minimized. This is called Anticipatory control and the temperature of skin being close to the ambient temperature within physiological limits is needed for this.
Skin is the medium (almost the only medium) through which the excessive heat produced by the body core during activity is expelled. The skin temperature is lower so that a constant gradient can be created between the body core and body surface to maintain the flow of heat. (Heat losses through urine and feces is minimal)

For more details see this question. All the answers in this question are good and will increase your understanding of what actually happens.


How does genetical variability works on bacteria?

The question is based on the false assumption that sexual reproduction creates genetic variance. If we neglect epistasis, then on average segregation and recombination do not increase genetic variance within the population.

All 3 of the following processes present in some bacteria lineages do increase the amount of genetic variance:

conjugation
transduction
transformation

You should have a look at the wikipedia articles.


I would recommend using a Bray-Curtis dissimilarity matrix since it accounts for abundances and can handle the so called double zero problem. I'm on my commute now and so must return to this for a complete answer later


It's pretty clearly an Araneid of some kind, based on the large, globular abdomen, the eye arrangement at the front of the 'head', and the characteristic defensive posture when out of the orbweb.  All known orbweavers are completely harmless to both cats and humans, so nothing to worry about!
Unfortunately, I'm not familiar enough with central European spiders to tell you exactly what it might be, but I can assure you that it is not the only problem biter in your area - one of the Black Widows.  I include a photo I found of a common orbweaver in Europe (the Cross Spider) which was also caught out of its web, and in a similar position (although clearly not having been attacked by a cat..).  Whether yours is normally a plain white species, or yours is a leucistic (all-white or partially-white) variation of a normally darker and patterned species, I have no idea.  As I say, I'm not familiar enough with European spiders to be confident about something like that.


When you just want to list the components of the brain, that is to say what the brain consists of from the gross anatomy perspective, you can say that the main parts of the brain are:

cerebrum
cerebellum
brainstem

You can also say that the parts of the brain are some smaller, but anatomically well defined components, such as the pineal gland and pituitary gland.

When you intend to describe the functions of anatomically well defined brain areas, you can say that the brain structures are cerebral lobes, thalamus, hypothalamus, hypocampus, amygdala, putamen, corpus callosum, cyngulate gyrus, etc.

A part is "a portion or division of a whole that is separate or distinct; piece. A structure is "mode of building, construction, or organization; arrangement of parts, elements, or constituents." So, it's not about what "it is," but about how you look at it. A thalamus is a part of brain and is a structure made of several nuclei...

You can see these terms used very differently in various texts, but a short overview of brain anatomy by Mayfield clinic use them in the same way as I did. These terms are not a part of any official classification in neurology.


Errors in division occur all the time and can show up in any dividing cell; this is, of course, important for cancer biology.  If one of my cells replicates oddly right now it likely won't matter since it's only one out of trillions, but if that happened at a very early age in development it could be present in many if not all of my cells.  Identical twins indeed come from the same egg-sperm fusion event but they develop separately from a very early state.  It's trivial to imagine a minor replication error in DNA at an early cell stage that results in different genotypes between so-called identical twins.  Besides, we've known for years that identical twins can have major epigenetic differences, so this isn't particularly ground-breaking.

  If we assume that identical twins are exactly identical, then if we make a clone of a twin, will all three be exactly identical?

Depends on your definition of "clone" but how identical is identical?  If you mean exact, then probably not; at the very least they will have different numbers of cells, for example, not to even mention CNV or epigenetics.  If you want some SciFi cloning thing then, well, join the club.


How HIV Affects and Its Treatment using Combination Therapy

a) HIV uses a certain receptor that's expressed widely on T helper cells. As this is homework I suggest looking at the wikipedia article to look this up for yourself. It is under tropism.

b) You mentioned mutation. That's very true but this question is excluding people with that mutation called the delta 32 mutation. Thus HIV can infect these people, but what happens to any virus in the context of infection? How does the human body deal with viral infections. Is there any variation that would account for why some people can be resistant to HIV and others not be?

c) Yes! Well done :) You're thinking along the right lines. Look up the drug on wikipedia and look up it's mechanism.

d) i) Yeah exactly that. But more than that. There's optimal HIV which in the absence of drugs does the best job at infecting. If we give a drug then HIV has to mutate away from optimal HIV to stay alive, but it's weaker. Give multiple drugs and it can't mutate away from all of them because if it did it would be so far from optimal it would be a rubbish virus.

ii) 1) It could affect the HIV binding receptor protein or the protein with which it binds on the host cell. So both! Logic would dictate we would use self receptor blockade because at least they're more conserved but I'm sure both are probably used. Enzymes and receptors are both proteins.

2 + 3) Look up the lifecycle of HIV

e) Theoretically possible. He might not take the drugs. If he takes the drugs unlikely because the virus basically becomes undetectable. Look this up, it should be on wikipedia again.


That is a flour beetle, the two most common and likely types are the confused flour beetle and red flour beetle but to identify look at the antennae. I'd suggest it is the confused flour beetle because the antenna go from thin to fat quite gradually, though the pictures may not be good enough for that to be certain.

Other commonly used names are tribolium (the genus name) or flour weevil. They are also used in labs as a model organism, groups in my last two labs have used them. They are a pest and you should probably get rid of them.

  "Both types of beetles are often found not only in infested grains,
  but in crevices in pantries and cabinet, as well. Damage to food is
  caused somewhat by the beetles' feeding, but also by their dead
  bodies, fecal pellets, and foul-smelling secretions. In addition to
  creating a foul odor, the beetles' presence encourages the growth of
  mold." - Wiki.


You can use much longer primers (up to 70bp or so), such that they span the repetitive region you want to change and some more specific sequence to anchor the primer (assuming your vector allows). If the multiple sites you want to change are within range of one another, you can order primers with 2 or more mutagenised sites - though expect your efficiency to drop. Your other option would be to do multiple rounds of mutagenesis, altering one position at a time.

I would then simply try these primers on a gradient PCR using a good enzyme like NEB's Q5. Trying to find a temperature for the correct size band will likely be key.

The real problem you're going to have though probably isn't the cloning, it'll be proving it. Homopolymer stretches are a real problem for sequencing, and the longer they get the worse it is. Automated sequencers find it difficult to tell between, for instance, 29 Adenines, and 30 adenines in a row. When your sequencing results are returned, if your sequencing is off by a base or two, it will be pretty much impossible to tell if your sequencing was wrong, or your construct was.


Same target receptor different mechanism of action?

Not necessarily!

Biased agonism

It's reasonable to start with an expectation that agonists at the same receptor have the same effect, but that's not necessarily true due to biased agonism. Biased agonism occurs when binding of different agonists to the same receptor results in different downstream activation of second-messenger systems.

Psychedelics and serotonin receptors

A particular example I am familiar with (besides the Jarpe paper) involves the 5HT2a serotonin receptor. This receptor is a shared molecular target of several psychedelic drugs: LSD, psilocybin/psilocin, DMT and others. However, this receptor exhibits biased agonism (Berg et al 1998).

In fact, it seems like agonists at the 5HT2a receptor neatly segregate into those with psychedelic effects (eg: LSD/psilocybin) and without (eg: lisuride/ergotamine, also serotonin itself) based on the different downstream molecular signalling pathways that they trigger, despite binding to the same general site on the same receptor.

Other considerations

Drugs' mechanisms of action can also depend on concentration and on all the other possible targets for those drugs. Pharmaceuticals are often small molecule drugs and while they may have preference for certain receptors, they are rarely (probably never) purely specific.

For example, the NSAID class of anti-inflammatories all work through inhibition of cyclooxygenase enzymes, but they differ in their relative specificity for COX-1 and COX-2. If you are looking at two drugs that have the same effect on COX-2, but don't compare their effects at COX-1, you might be surprised to find they have different results.

For another class, SSRIs used as antidepressants also have effects on other monoamine transporters (dopamine and norepinephrine) but vary in how specific they are.

Berg, K. A., Maayani, S., Goldfarb, J., Scaramellini, C., Leff, P., & Clarke, W. P. (1998). Effector pathway-dependent relative efficacy at serotonin type 2A and 2C receptors: evidence for agonist-directed trafficking of receptor stimulus. Molecular pharmacology, 54(1), 94-104.

González-Maeso, J., Weisstaub, N. V., Zhou, M., Chan, P., Ivic, L., Ang, R., ... & Sealfon, S. C. (2007). Hallucinogens recruit specific cortical 5-HT2A receptor-mediated signaling pathways to affect behavior. Neuron, 53(3), 439-452.

Jarpe, M. B., Knall, C., Mitchell, F. M., Buhl, A. M., Duzic, E., & Johnson, G. L. (1998). [D-Arg1, D-Phe5, D-Trp7, 9, Leu11] Substance P acts as a biased agonist toward neuropeptide and chemokine receptors. Journal of Biological Chemistry, 273(5), 3097-3104.


Your estimation of the sizes of the fragments for pC508 are incorrect.

Look at the size of the plasmid at the center of the circle.The size of your fragments has to add up to that number. So if you were sure that one fragment was 1000bp, then the other fragment would need to be 6300bp.

You should also notice that fragment sizes for EcoR1 and HindIII digests should not be the same size.

You also need to say something about the type of DNA you have in the pBR322 lanes. Is it linear, circular, supercoiled?

For question 2, your explanation for pBR322 is okay, you should still mention the type of DNA you have in those lanes.

You need to explain not only where PSTI cut but also the size of the fragments that it produces.

A place where a restriction enzyme cuts is called the restrictions site, so instead of saying cuts in one place, or two places, you should say at a single restriction site, etc.


The information carried by nerve signals

Neural info is contained in spike trains, mainly in terms of spike frequency and related parameters. These spike trains in individual neurons can be measured by techniques like patch clamp and Ca2+ imaging. These techniques are all pretty sophisticated and computer assisted for sure.

However, by recording of action potentials in e.g. the optic nerve, we cannot  possibly know what the person is seeing. Nonetheless, by cleverly mapping responses of conglomerates of neurons we can make estimates of what the information carried in the nerve fibers mean. For example:

Mapping the responses of an ensemble of place neurons in the hippocampus has been successfully used to predict where a mouse is exactly located in a maze (Guger et al., 2011);
Gross potentials measures with EEG can be used to move artificial limbs, as shown in physically handicapped people. In essence, by mapping out the responses of motor areas in the brain, it can be predicted where a person is thinking their limb is moving.

Reference
- Guger et al., Front Neurosci (2011); 5 85


What volume of elution buffer for plasmid-containing filter paper?

The answer to this is... some.
You only need a tiny amount of plasmid DNA to transform bacteria like DH5$\alpha$, typically in the 1-10 ng range, but much less, as low as about 10 pg (10 picograms) may still work. If you can get even 0.2 ul of the liquid out of that tube, try using that in the transformation.
Things you can try;

remove the paper, spin the tube down and see if you can recover even a tiny amount of liquid.
Add a bit more liquid - another 30 ul will be fine
Snap the tube lid closed on the paper to hold it in place, then spin the liquid out of the paper - this is quite difficult to do.

Note - even with 10% DNA recovery (very low for this method), with 30 ul you will still have 100 ng of DNA, or about 3.3 ng/ul.


Do mutagens ever increase the "rate of evolution"?

Do mutagens ever increase the “rate of evolution”? [..] By "rate of evolution", I'm informally referring to either the amount of time or the number of generations that pass before some beneficial mutation occurs and is selected for

This is a very unusual definition of "rate of evolution" but I'm happy to consider it if you want.

If more mutations happen per generation, then it takes less time for a beneficial mutation to happen. So yes!

By rate of evolution, some people may like to refer to the rate at which neutral mutations fix (fixation=reaching a frequency of 1 in the population). If $\mu$ is the mutation rate, then $2N\mu$ mutations are produced each generation (assuming diploidy), and a fraction $\frac{1}{2N}$ of them fix (as they are neutral), this means that the rate of fixation is $\frac{2N\mu}{2N} = \mu$. So, again increasing the mutation rate increases the rate of fixation of neutral mutations. It is actually true also for deleterious and beneficial mutations but the computation is a little more complicated.

Note however, that there is a point after which the mutation rate is so high, that your population might be drawn to exctinction. This is called a mutational meltdown. Mutational meltdown is unlikely to happen unless the population size is already small to start with and/or the mutation rate is really really high.


There is indeed a positive correlation between gastric reflux disease and esophageal cancer, and also between stomach ulcerations and stomach cancer. There are more than one possible mechanisms for these correlations to arise, but what you are proposing is definitely a prime suspect.

http://www.webmd.com/heartburn-gerd/news/20130523/chronic-heartburn-may-raise-odds-for-throat-cancer-study

http://www.ncbi.nlm.nih.gov/pubmed/10658066


Roles of creatine and bilirubin in foetus circulation

Creatine is an important energy source for body, especially for the muscles, so it is no wonder you can finde it there. I don't think it has a special role besides that. See the Wikipedia article for more information.

For bilirubin this is different, this substance is a breakdown product of the heme metabolism (basically hemoglobine). It is not water soluble and needs to be conjugated to a carrier protein (albumin). In this way it is transported to the liver, where the glucuronyltransferase conjugates it to glucuronic acid. This step makes the bilirubin water soluble and it can be excreted from the body.

Newborns have a higher bilirubin level, since their glucuronyltransferase activity is at about 0.1% of that of adults. This can lead to the typical newborn jaundice. For more details about bilirubin, see here.


Why is gastric lavage considered to be helpful only if a patient comes to a hospital within 1 hour of a toxic ingestion?

Gastric lavage only washes out ("lavages") the stomach ("gastrium"). Gastric emptying time is generally ~60-120 min, probably on the lower end of that for ingested liquids. After that amount of time, most of the toxic substance will be beyond the level of the pyloric sphincter (i.e. in the duodenum) and not accessible to lavage.

The second question is not possible to answer without some information about what specific toxic ingestion you are interested in knowing about.


Why is the human ear most sensitive to 4000 Hz tones?

The frequency-selectivity of loudness perception was first shown in the 1930s, when Fletcher and Munson published a set of curves showing the ear's sensitivity to loudness compared to frequency. These equal-loudness curves, as shown in the question above, are now known as Fletcher-Munson equal-loudness contours.

One straightforward physical explanation is the fact that sounds with frequencies around 4 kHz are amplified in the middle ear canal through the process of resonance. In effect, they are perceived 10 to 20 dB louder than other audible frequencies. The pinna also affect resonance and hence the outer and middle ear together join forces to create humps and bumps in the equal-loudness curves.

The evolutionary reason why 4 kHz, and not, e.g. 0.5 or 8 kHz, is difficult to pinpoint. First I can clarify some misconceptions in the question, before getting back to the question proper:

Firstly, you mention that the "characteristic frequency" of a human voice is between 80 and 250 Hz. You are referring to the fundamental frequency; the characteristic frequency is a measure used in electrophysiology to determine the frequency-specificity of inner-ear neural structures.
Secondly, the fundamental frequency does not determine the frequency-selectivity of speech understanding. A useful picture is given below in Fig. 1, which shows which frequencies convey which speech components.

Fig 1. Frequency dependence of speech components. source: The Essential Guide to Hearing Loss

It becomes aparent from Fig. 1 that consonants (f, s, h etc.) are higher pitched than vowels (a, o, u etc.). Arguably, consonants convey most of the word information. Indeed, speech understanding is generally less affected by removing the vowels than by removing the consonants. One may deduce from all this that high-frequency hearing (say 2 - 8 kHz) is most important to understanding speech.

And then, to get back to your evolutionary motivation behind the Fletcher-Munson equal-loudness contours, it may, purely hypothetically be so, that our ancestors with a middle-ear resonance around 4 kHz were advantaged over those that had resonances elsewhere in the audible frequency range, if any, because of an enhanced perception of the spoken word. But this is entirely and purely speculative and remains an unreferenced statement for which I do not wish to be held repsonsible in any way :-)


What does "~mitochondrial DNA ~bp linear DNA" means?

Well, Mitochondrial DNA CAN be linear (in some organism), see the wikipedia page on this

  In most multicellular organisms, the mtDNA - or mitogenome - is
  organized as a circular, covalently closed, double-stranded DNA. But
  in many unicellular (e.g. the ciliate Tetrahymena or the green alga
  Chlamydomonas reinhardtii) and in rare cases also in multicellular
  organisms (e.g. in some species of Cnidaria) the mtDNA is found as
  linearly organized DNA. Most of these linear mtDNAs possess telomerase
  independent telomeres (i.e. the ends of the linear DNA) with different
  modes of replication, which have made them interesting objects of
  research, as many of these unicellular organisms with linear mtDNA are
  known pathogens.[19]

  For human mitochondrial DNA (and probably for that of metazoans in
  general), 100-10,000 separate copies of mtDNA are usually present per
  cell (egg and sperm cells are exceptions). In mammals, each
  double-stranded circular mtDNA molecule consists of 15,000-17,000[20]
  base pairs. The two strands of mtDNA are differentiated by their
  nucleotide content, with a guanine-rich strand referred to as the
  heavy strand (or H-strand) and a cytosine-rich strand referred to as
  the light strand (or L-strand). The heavy strand encodes 28 genes, and
  the light strand encodes 9 genes for a total of 37 genes. Of the 37
  genes, 13 are for proteins (polypeptides), 22 are for transfer RNA
  (tRNA) and two are for the small and large subunits of ribosomal RNA
  (rRNA). This pattern is also seen among most metazoans, although in
  some cases one or more of the 37 genes is absent and the mtDNA size
  range is greater. Even greater variation in mtDNA gene content and
  size exists among fungi and plants, although there appears to be a
  core subset of genes that are present in all eukaryotes (except for
  the few that have no mitochondria at all). Some plant species have
  enormous mtDNAs (as many as 2,500,000 base pairs per mtDNA molecule)
  but, surprisingly, even those huge mtDNAs contain the same number and
  kinds of genes as related plants with much smaller mtDNAs.[21]

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

In the case of your sequence, it only means that it has been entered in NCBI as a linear piece of DNA (it is usually the case when you sequence only a piece of a circular DNA for example)
It does not mean that within the organism it is linear !

I hope this answers your question !


Reconstituting genomes of archaic tribes of humans

The answer is basically 'No.'.

Too much mixing has happened since then. Fortunately, in most of the world we had scientists 2000 years ago describing facial features, and in part of the world (i.e. China) we had scientists describing facial features 4000 years ago.

We do occasionally recover viable DNA samples from both 2000 and 4000 year old corpses, also actual corpses that still retain significant vestiges of their facial features, but expecting to recover even general facial features over hundreds of generations from present DNA is quite frankly unrealistic.

The good news is that human facial features aren't actually super variable; humans are just super good at spotting small differences (which comes with the territory as social animals). The bad news is that as a modern reader of latin or chinese texts on phylogeny (if you can find them, which I won't guarantee) the subtle differences in what they mean when they describe a nose as, let's say hooked, will probably be lost on you, or me, or any of us.

Your best chance is probably sequencing corpses from the relevant era and matching them up with phylogenisists' descriptions to form an idea of what they were talking about; and you might end up with a general sense of what people looked like.

I expect it will lead to severely underwhelming results, but I suppose it's worth a shot.


@Colombo explains one reason that I think is obvious. However, there has been some research done on this.

One other reason is because it would provide an evolutionary advantage in environments where calories are scarce. Also, sugar actually acts like a pain reliever. Studies show that giving sugar to babies and children during surgery act like a pain reliever.

The sweet tooth could be controlled by hormones secreted from the growing bones. Some common hormones like insulin also affect sensory centers in the brain. This explains why the sweet tooth goes away as an adult.

Reference

NPR -http://www.npr.org/sections/thesalt/2011/09/26/140753048/kids-sugar-cravings-might-be-biological


Can brain damage caused by physical injury affect the social behaviour of a person?

Socialization is a cognitive and executive brain based function that requires higher level thinking mechanisms usually dependent on the prefrontal coretex. A lot of social cues we obtain from our environment when we are young can shape our brains during its developmental growth (infancy-post puberty) and cause our brains to develop social habits and access specific social functions.

A great text book example of altered social behavior due to brain injury is Phineas Gage. He had a metal rod shot through the prefrontal cortex and it caused a severe change in his behavior. He no longer cared about social cues and people often referred to his behavior as becoming "rude" and "out of context." There are many subtle aspects of behavior that are regulated by brain functions and there are many books on the topic.

Source: Wikipedia page on Phineas Gage and
Pyschopharmacology, book by:  Meyer and Quenzer
DSM-5, text book on clinical psychology

Further Reading on Phineas Gage
- What were the symptoms of Phineas Gage after suffering his brain injury?


Why is chromatin not condensed during interphase but is in prophase

Here's an image that explains the cell cycle:

And here's one that explains Mitosis as a subcategory of the cell cycle:

Chromosomes condense on the metaphase plate before they are pulled apart by kinetochore microtubules in a Tug-of-war. Chromosome condensation is not yet fully understood, but nucleosome structure is hypothesized to play a role. This is a very good question and is definitely not too broad.


Which bacteria takes the longest to double?

There is no answer to your question

The doubling time of a bacterium is dependent on the conditions: primarily on the temperature and the availability of nutrients, but other factors can apply. Because of this, the doubling time of any particular bacterial strain cannot be considered in the abstract, thus to give a single number  we can consider the optimum doubling time for a strain instead - i.e. how fast it will double under the perfect (for it) temperature and nutritional conditions. For the E. coli strain you worked with, this is likely 37 degrees and in a rich media such as Lysogeny Broth. But for the staggeringly vast array of bacteria out there, we simply don't know what the optimum conditions are much less have actually measured growth under them. In fact, there are many bacteria which are known about, but currently uncultured so we haven't even begun to understand their growth dynamics.

So even the simplified question of longest optimal doubling time cannot be answered because we don't have the data for so, so many bacteria. The question of the maximum time between divisions is even less clear: there are bacteria that live under conditions of extreme nutritional limitation that can take thousands of years to double, and strains that can exist as spores for at least 100,000 years and maybe even tens of millions. Do we consider their doubling time to be a 100,000 years? 25 million years? Without specifying the conditions under which the doubling takes place, the question is poorly defined.


Do animals feel emotions, or display empathy?

The answer to the question "Do scientists agree whether animals feel emotions, or display empathy?" is No. However, there are some animals that certainly do not have emotions or empathy (for example animals that have no substantial nervous system, like sponges), and some animals that certainly do have emotions. The only disagreement is in the middle and where to draw the boundaries. In reality, drawing such boundaries is probably not all that productive, coming down to semantic rather than biological argument.

As a citation for the disagreement, see the two answers and the comments here already.

The difficulty in assessing a statement like this is largely one of operational definition: you need to define what an emotion is, and depending on that definition you will get entirely different answers. You will also get different answers depending on your philosophical approach to questions like these and what the essence of experience is. I would also point out that emotion and empathy are vastly different levels of cognitive ability according to typical definitions of the two.

However, I will say that there are a lot of recent findings of higher cognitive abilities in non-human animals than previously thought. Rodents have long been used as generic models of mammalian nervous systems, including emotional processes. Mirror neurons in non-human primates respond to the behaviors and movements of conspecifics, which is an important aspect of both social learning and potentially empathy. Self-recognition is an important aspect of theory of mind, and has been observed in several species of different types. Mourning behaviors have been observed in various animals in response to death of conspecifics. There can be some disagreement of the interpretation of these findings, but I'll include some references here so readers can do some of their own research and find if they are convinced.

Note that these works study particular animal abilities in particular contexts, rather than making blanket judgments about "all animals" or anything like that. This is typically how science works, incrementally based on the results of individual experiments.

References

Gallese, V., & Goldman, A. (1998). Mirror neurons and the simulation theory of mind-reading. Trends in cognitive sciences, 2(12), 493-501.

Lane, R. D., & Nadel, L. (Eds.). (1999). Cognitive neuroscience of emotion. Oxford University Press.

Mulcahy, N. J., & Call, J. (2006). Apes save tools for future use. Science, 312(5776), 1038-1040.

Plotnik, J. M., De Waal, F. B., & Reiss, D. (2006). Self-recognition in an Asian elephant. Proceedings of the National Academy of Sciences, 103(45), 17053-17057.

Prior, H., Schwarz, A., & Güntürkün, O. (2008). Mirror-induced behavior in the magpie (Pica pica): evidence of self-recognition. PLoS biology, 6(8), e202.

Rajala, A. Z., Reininger, K. R., Lancaster, K. M., & Populin, L. C. (2010). Rhesus monkeys (Macaca mulatta) do recognize themselves in the mirror: implications for the evolution of self-recognition. PloS one, 5(9), e12865.

Roth, G., & Dicke, U. (2005). Evolution of the brain and intelligence. Trends in cognitive sciences, 9(5), 250-257.


How can I re-format my DNA motifs' position weight matrices?

So what you need is basically your data expressed as counts instead of proportions. Even if you do not have the matrix of counts as raw data, these proportions only needs to be multiplied by the total number of binding sites used in the study (e.g. the number of sequences that have been analysed) to get the counts (since proportion = count/total number of binding sites). You should have that information somewhere.

@hello_there_andy: indeed there was this missing piece of information available to me, it came in the form of a variable called nsites which equates to the total number of DNA sites that the PWM was generated from.


Short answer
Six legs allow for locomotion, while maintaining a supportive tripod at all times.

Background
There are several million species of insects, all on 6 legs. This implies that any change in this number is promptly selected against. It is generally agreed that insects were derived from many-legged ancestors, e.g. centipedes.

One explanation is the tripod gait that results from having six appendages. This hypothesis, formulated more than 6 decades ago (Lanham, 1951), reasons that a reduction of the number of legs during evolution did not go further than 6, because locomotion of a small animal encased in a rigid exoskeleton is not effective with less than 3 pairs of legs. Insects generally walk by lifting the two outer legs on one side and the middle on the other side, sweeping them forward and placing them down together. Hence, insects support their rigid structures with a tripod at all times. Tripods are among the most stable configurations, and they never wobble (why on earth do tables have 4 legs?). Figure 1 shows an illustration of insect locomotion (Lanham, 1951).

Fig. 1. Insects' locomotion resembles a double tripod. Insects have a cyclic gait which consists of two phases, the stance phase and the swing phase. The stance phase is the power stroke, it pushes the body forwards in the direction of travel while the leg remains on the ground. Three legs are used is this phase by forming a tripod with the front leg and the hind leg on one side of the body and the middle leg on the other side. This formation is why this gait is known as the tripod gait. Source: Insect robotics.

Larger animals can afford to have less legs, because their vestibular systems have more time to maintain balance and adjust gait during locomotion. Because insects are so small, their strides are so quick that the nervous system may not be fast enough to deal with gait control. Instead, insects rely on the tripod gait to prevent any imbalance, rather than adjusting it. In addition, the exoskeleton effectively restricts small bodily movements to control balance. Larger animals such as mammals make small adjustments in their gait constantly to maintain balance. An insect has less opportunities to do so, because of their rigid exoskeleton (Lanham, 1951).

Reference
- Lanham, Science (1951); 113(2946): 663


Human anti animal antibodies issues in blood testing

You do not need to be exposed directly to animals to get human anti-mouse (or human anti-animal) antibodies; you can also be exposed to animal products in various ways.

  Circulating anti-animal antibodies can arise from iatrogenic and noniatrogenic causes. The former is the result of the normal response of the human immune system to an administered “foreign” protein antigen. Currently available diagnostic and pharmaceutical agents derived from an animal source are extensive and range from rodent immunoglobulins to hormones isolated from fish. In addition, some recombinant proteins are affinity purified on immobilized monoclonal mouse antibody columns, and the possibility exists for some of the mouse monoclonal antibody to detach and copurify with the protein

You can also get anti-animal antibodies from blood transfusions:

  Blood transfusion is also associated with an increased incidence of anti-animal antibodies. A study of 2829 participants in a population health survey revealed that 14.4% of the participants who had been transfused were anti-animal positive, compared with 10.4% of the participants who had never received a blood transfusion. This difference was presumably attributable to infusion of preexisting human anti-animal antibody or as a result of infusion of a foreign antigen present in the unit of blood

or through vaccination:

  Vaccination against infectious diseases is another route by which animal protein antigens may be inadvertently presented to the immune system and trigger antibody formation. In the US, chick embryo or egg cultures are frequently used in vaccine production, and residual chicken protein may be present in vaccines, whereas in Europe, some vaccines contain rabbit serum, e.g., rubella vaccine in France, and multimicrobial vaccine (Bruschettini vaccine) in Italy

or "unconventional therapies":

  The administration of unconventional therapies is also a route to immunization with animal protein. For example, a patient developed anti-rabbit antibodies following injections of “antireticulocytoxique”, which is a lyophilized serum obtained from rabbits injected with homogenates of human bone marrow and spleen and is intended as a tonic to improve senescence and to reduce fatigue and debilitation

Other routes:

  Noniatrogenic causes of anti-animal antibodies include maternal transfer across the placenta to the unborn child (37)(38), animal husbandry or the keeping of animals as pets (39), and the transfer of dietary antigens across the gut wall in conditions such as celiac disease (40)(41). Anti-animal antibodies are also more common in multiparous females (36), and a high incidence of human anti-animal antibodies has also been observed in association with certain disease states, e.g., idiopathic cardiomyopathy

All quotes from Human Anti-Animal Antibody Interferences in Immunological Assays, by Larry J. Kricka (1999).


What is the difference between embryology and developmental biology?

It's a simple sub-set relationship, embryology is a sub-set of developmental (it's a "specialty"). Embryology is only concerned with the embryo - developmental is a larger group, concerned with developments that may occur in other stages of life. Such as the development of secondary sexual characteristics in humans - a developmental thing, but not embryonic.

These are not purely objective definitions and the dividing lines are not well defined. Labels for various scientific fields are only generally applicable, and they are very flexible. For example, many Chemists also do a lot of physics. Many Biologists do a lot of Chemistry. Many Embryology studies dip into developmental stuff. These divisions are not always clear.

Embryology is a part of Developmental Biology in the same way that Biology is part of "Science" - simple sub-set relationship. If you don't understand sub-sets very clearly, you'll want to study up on that relationship - it's very important in ALL sciences, so you can understand things like "All squirrels are animals, but not all animals are squirells"

This statement would be reasonable - "All Embrology is Developmental Biology, but some Developmental Biology is NOT Embryology"


Meaning of some unit of measurement of kinase activity

It is not a specific unit of kinase activity, rather a general approach taken for following reactions where there is no change of colour. The abbreviation cpm stands for counts per minute and is a measure of radioactivity.
In this particular example a radioactive phosphate has been incorporated in the ATP of the protein kinase assay. If the protein kinase is active with the substrate, the phosphate will be transferred from the ATP to the substrate peptide/protein. If the sample mix is loaded on a SDS-PAGE gel, a scintillation counter can be used to measure the radioactivity of each band and one will be able to  show how active the protein kinase has been in phosphorylating it's substrate.


Are there any anatomy books focusing on etymology?

Though a little bit outdated looking this from the university of Sydney is pretty good and searchable.
I find it pretty useful for aiding memorisation or just a quick entertaining read.

Arnold's Glossary of Anatomy - The University of Sydney


What is the difference between a response element and a enhancer?

Enhancers specifically bind transcription factors in an effort to obtain robust rates of transcription, in a very general fashion and may be upstream or downstream of a promoter. Remember that you don't need to receive a signal to produce housekeeping genes, regulated by general transcription factors, because they're always needed (in part). A response element can enhance or repress transcription depending on the stimulus.

Vitamin D response element (VDRE) is a fair example: In response to your extracellular calcitriol or 1,25(OH)2D, the vitamin D receptor will complex with a number of proteins that bind at the VDRE, controlling transcription of various vitamin D-controlled gene targets.

  Vitamin D activity is mediated through binding of 1,25(OH)2D3 to the vitamin D receptor (VDR), which can regulate transcription of other genes involved in cell regulation, growth, and immunity. VDR modulates the expression of genes by forming a heterodimer complex with retinoid-X-receptors (RXR).

Source: http://www.wikipathways.org/index.php/Pathway:WP1531

And just as well, other promoters such as that for pro-parathyroid hormone contain VDRE sequences that suppress it's transcription (ref).


How can histidine be classified both as positively charged and hydrophobic?

As @wysiwig stated, Histidine is not hydrophobic. Depending on the pH different parts of the molecule can carry charges, see the image below (from here):

The nitrogen atoms can be protonated in an acidic environment, the carboxylgroup will loose it proton in a basic environment. All these forms are transferred into each other, when the pH changes.


Does anyone know of a study supporting predictions #2 or #9 of the Extended Evolutionary Synthesis?

There is no debate

The so-called Extended Evolutionary Synthesis (EES) is just a new term for a whole lot of knowledge that roughly speaking everyone acknowledge to be true. EES is really just an extension but does not say anything that conflict with previous theory. There is no conflict and no contradiction.

The only debate stand upon whether or not our current understanding of evolutionary processes deserve a new name or shall we just stick with what we call the modern synthesis.

Shall we use the term ESS?

I talked about this renaming with about 20 evolutionary biologists and all of them consider such renaming useless. However, by the end of the day, they all mainly did not care much.

My personal opinion about the renaming

IMO, one reason such naming is silly is that there has not been a major work that have completely and suddenly changed our understanding. We just keep discovering more and more as we always did. All the new things we discover we just used to integrate it what we already called modern synthesis. Those advocating for a renaming define the modern synthesis not as most people do (that is everything we know about evolution so far) but as the set of knowledge that existed in 1950.

It is funny that even the discovery of DNA did not bring about a renaming of our theory of evolution as we only considered that it added up to our current understanding. I doubt that the emergence of new fields (such as niche construction and its heritability or developmental noise) would be in any way sufficiently revolutionary to cause a renaming. And I say so even though I also work in the field of mutational and developmental noise.

Unclarity

The points listed in the link are rather unclear and it is therefore impossible to comment on them. Take the #2 you are interested in

  heritable variation will be unbiased

The term variation has no strict definition. The term variance is clearly defined. However, a variance in itself cannot be biased, only the distribution it comes from can. So, this simple sentence mainly makes no sense (to me at least). If it does make sense to those who wrote this list, then, OP, you will need to provide explanations from other source or ask for its meaning before asking for its validity.

Further reading

This paper will offer you opinions from both sides. As implicit from the above, one side (namely, the "counterpoint" side as referred to in the paper) seems to me to represent the vast majority of evolutionary biologists.

Addressing your comments

  Thank you for the clarification. I think by "heritable variation," the authors mean mutation. You feel it's still true that they are unbiased?

"mutation" is not a variable, it does not follow a distribution. It cannot be bias or unbias.

Mutational effect on fitness is a variable and follows some distribution which is most definitely biased (deleterious mutations are much more common than beneficial mutations; usually modelled with a double gamma distribution; see here).

Mutational effect on the phenotype is a variable and follows some distribution. It may well be biased indeed. The distribution of mutational effects on the phenotype were mainly unconsidered by evolutionary biologists who contributed to place the first bricks in the modern synthesis (Fisher, Wright, Haldane, Muller, etc...).

These "early" evolutionary biologist never made predictions about the distribution of mutational effects on the phenotype that would contradict today's predictions. They just had little understanding and did not talk about it much.

Again, in your question you are opposing EES with Modern Synthesis as if they were to be opposed. But by doing so, you need to clearly define Modern Synthesis. By default, one just consider the Modern Synthesis to include all the knowledge we have in evolutionary biology and therefore by definition, elements like niche construction, biased mutational effects of phenotype and other field of knowledge that one might want to specifically associate to EES only.

  Do you still feel it's true that natural selection is the only source of the evolution of adaptation?

This question depends only on the definition of adaptation. If, for example, you consider a lineage being poorly adaptive becoming adaptive as the environment changes to match their phenotype (and not the other way around) to be an adaptation, then typically nobody would have never thought that only natural selection would cause adaptation. I would personally be happy to call that an adaptation.

The question is not a question of evolutionary process but only a question of the definition of adaptation.

Note, as an extra source of confusion, when talking about adaptation one may refer to the changes yielding to higher fitness (whether the change is genetic or not is up to you) and/or to the resulting state of having a high fitness.

  For example, if there is an epigenetic modification that is transgenerationally stable and adaptive, is it an adaptation?

Again, it depends upon what you call adaptation. I would be happy to call that an adaptation.

  the discovery of DNA would not cause a reconceptualization of the modern synthesis because it was consistent with it.

Everything from the EES is consistent with the modern synthesis. Most of it are just add-up subjects that brought little consideration before. Some of it might break some simplified generalization that may have been done before though. Many does affect our view of the grandeur and complexity of evolutionary process but none is contradicting what we previously thought.

  what you mean by "becoming more adaptive as the environment changes." Would you give an example?

Imagine a population is perfectly adapted to live at an environment where the temperature is 18˚C. The current temperature is 15˚C though. Let's imagine a case where the population does not change much through time (eventually due to a lack of genetic variance to select from, eventually due to a low mutational variance or a recent bottleneck) but the environment is getting warmer and after some time the environment is at 18˚C. The population is now perfectly adapted.


How does anger relate to blood pressure?

Anger is a common emotion in most animals and it is highly related to stress. At time of anger body usually releases stress hormones and  the body's way to respond to stress is by sympathetic nervous system activation which results in the fight-or-flight response.

Anger is an emotional response related to one's psychological interpretation of having been threatened. Often it indicates when one's basic boundaries are violated. Sheila Videbeck describes anger as a normal emotion that involves a strong uncomfortable and emotional response to a perceived provocation.
Anger may have physical correlates such as increased heart rate, blood pressure, and levels of adrenaline and noradrenaline. Some view anger as an emotion which triggers part of the fight or flight brain response.
http://en.wikipedia.org/wiki/Anger

Stress and anger trigger the release of stress hormone Cortisol in the body. Mild releases of Cortisol can give the body a sudden burst of energy,it also may increase the heart rate to 180 times a minute and  blood pressure from 120 over 80 to 220 over 130.
Anger is processed in hypothalamus and amygdala,the roles of two peptide hormones, corticotropin-releasing hormone (CRH) is responsible for the production of Cortisol (Primary stress hormone) and  arginine-vassopressin (AVP) produces Vasopressin, which triggers blood pressure by increases reabsorption of water by the kidneys, this results in contraction of blood vessels which raises blood pressure.

The human stress response involves a complex signaling pathway among neurons and somatic cells. While our understanding of the chemical interactions underlying the stress response has increased vastly in recent years, much remains poorly understood. The roles of two peptide hormones, corticotropin-releasing hormone (CRH) and arginine-vassopressin (AVP), have been widely studied. Stimulated by an environmental stressor, neurons in the hypothalamus secrete CRH and AVP.
CRH, a short polypeptide, is transported to the anterior pituitary, where it stimulates the secretion of corticotropin (4). Consequently, corticotropin stimulates increased production of corticosteroids including cortisol, the primary actor directly impacting the stress response (5). Vasopressin, a small hormone molecule, increases reabsorption of water by the kidneys and induces vasoconstriction, the contraction of blood vessels, thereby raising blood pressure.
http://dujs.dartmouth.edu/fall-2010/the-physiology-of-stress-cortisol-and-the-hypothalamic-pituitary-adrenal-axis#.VH7k8cnQoX0


Why can we eat salty food, but can't stomach salty water?

Seawater is many times more salty than the "pinch" of salt that is often recommended to add to cooked dishes.
According to the USGS

the concentration of salt in seawater (salinity) is about 35 parts per thousand. In other words, about 35 of 1,000 (3.5%) of the weight of seawater comes from the dissolved salts

To translate that to a typical glass of water: seawater is equivalent to adding a bit more than an entire tablespoon (17.5 mL) of salt to a 16oz (~500 mL) glass!
By the way, 1 tablespoon of salt is about 7100 mg. To put that into perspective, you'd have to consume almost two entire 8-cut pizzas (using Domino's as a reference) or more than 7 McDonald BigMac cheeseburgers to consume that same amount of salt.
In fact, consuming 7,100 mg of salt would more than triple the recommended amount for daily intake. According to the FDA:

Americans eat on average about 3,400 mg of sodium per day. However, the Dietary Guidelines for Americans recommends limiting sodium intake to less than 2,300 mg per day—that’s equal to about 1 teaspoon of salt!


The first is a male Theridiid, probably Parasteatoda tepidariorum (see below)

https://bugguide.net/node/view/1320395/bgimage.

The second is one of the "flower spiders" in the Misumena/Misumenops/Misumenoides/etc. group of Crab Spiders.  It would take a better photo to get closer than that, since this is a young female and isn't showing the color marks that make it easier to ID.  There's a hint of patterning on the abdomen, but it isn't clear enough to ring any bells with me.  In a comment below, I'll include a link to the Bug Guide page for these spiders so you can look at it - the relatively useful marks for field observation are the greenish bands (if any) on the sides of the cephalothorax, the 'mask' (if any) over the eyes, and the pattern (if any) on the abdomen.  Also, the reddish 'racing stripes' on the sides of the abdomen of fully adult females can be helpful in working out which spider it is.  I suspect that for most of us, most of the time, "Flower Spider" is going to be good enough.


Why are proteins always made in N to C direction?

Nice question! As you already know, DNA is always shown in 5'$\rightarrow$3' direction because it is always synthesized in this direction (amino acids are joined by CO-NH peptide bond). So, a polypeptide looks like this (source):

In fact, if you just look at the polypeptide in the reverse direction, you could view it in C terminus to N terminus direction. But we don't do so because that is not the conventional direction of the polypeptide's biosynthesis.

Tracing the Roots: To know why there is no "reverse" peptide bond (NH-CO), we first need to know how peptide bonds are formed in polypeptides. Polypeptides are formed in ribosome, and the process of formation of peptide bond occurs in the peptidyl transferase complex of ribosome. Since ribosome is a ribozyme, this reaction is also catalyzed by the catalytic sites of RNA (i.e. 2'-OH) instead of proteins. See the image below for the mechanism (from Marina V. Rodina):

As visible from the diagram, nitrogen (in -NH2) from acceptor tRNA (A site) attacks the ester linkage at the peptidyl tRNA (P site). Carboxylic carbon cannot attack the nitrogen (for "reverse" bond formation) because it is already in ester linkage. One might ask then "if the nitrogen was joined to tRNA at P-site, the carboxylic carbon could have attacked on amino acid at A-site. Why is amino acid not joined to tRNA by the amine nitrogen?" To know why it is so, lets go a step further and see how tRNAs are charged i.e. how aminoacyl tRNA synthetase works. Aminoacyl tRNA synthetase charges tRNA in a two-step reaction. For displaying mechanism, I will take the example of histidyl-tRNA synthetase (diagrams from Proteopedia):

amino acid + ATP → aminoacyl-AMP + PPi

→
aminoacyl-AMP + tRNA → aminoacyl-tRNA + AMP

As is clearly visible now, whether amine nitrogen or carboxylic carbon will attach to phosphate of ATP is decided in the first step. See the image again:

You might ask that since nitrogen (in -NH2) also has a lone pair of electrons, it could also make a nucleophilic attack on the phosphate group, similar to the oxygen (in -COOH). Why doesn't this happen then? This cannot be accounted for by saying that the amine nitrogen is far away from the reaction site (look at the diagram again, and pay attention to how close the carboxylic carbon and amine nitrogen are. If we could move the amino acid even a little bit, this reaction could easily occur). Well, here's the twist: the optimum pH of this reaction lies near pH 6 i.e. in the acidic pH range (Lui et al, 1978). Now, as we know, under acidic pH, -NH2 exists in the protonated form i.e. -NH3+. In this condition, nitrogen lacks lone pair and thus cannot attack phosphate on ATP. Thus, it is not possible to attach amino acid to AMP via -NH2 group and, thus, form a "reverse" peptide bond. I hope this depth of the answer would be enough to satisfy your curiosity :)


IgA-s in an immune system vaccined intramuscularly against Hepatisis A

Antibodies are produced after exposure to cognate antigen.

Remember that B cells start off expressing membrane IgM and/or IgD. IgA requires class switching recombination at the B-cell receptor locus to the IgA isotype. Further differentiation of the B cells to antibody-secreting plasma cells results in soluble IgA production and immunologic memory to the antigen. Whether you'll get IgA, IgE or IgG antibodies against the vaccine will largely depend on the signals they get in the muscle, however (Figure 1). I think IgG is largely a result, since the tissue antiviral response is often interferon gamma (Figure 2).

The importance of intramuscular vaccination is outlined here, just in case it wasn't apparent.

Figure 1. Activated helper T cells that can recognize the same antigen mediate the class switch by providing co-stimulatory signals and cytokines. Source

Figure 2. Class-switching continued. Source: Parham, The Immune System, 4th Ed.


Can a neuron make a synapse onto itself?

A synapse from a neuron unto itself is called an Autapse. Not a whole lot is known about them. Tamas et al. (1) give a summary:

  Van der Loos and Glaser (1972)proposed the word “autapse” to describe
  a transmitter release site made by the axon of a neuron and its own
  somatodendritic domain. In addition to their original Golgi study in
  rabbit neocortex predicting the existence of autapses, possible
  autaptic contacts have been described in dog (Shkol’nik-Yarros, 1971)
  and rat (Peters and Proskauer, 1980; Preston et al., 1980) cerebral
  cortex, monkey neostriatum (DiFiglia et al., 1976), and cat spinal
  cord (Scheibel and Scheibel, 1971). (...)
  Although autapses formed in cell cultures have been used extensively
  to study the physiology of synaptic mechanisms (Segal, 1991; Pan et
  al., 1993;Shi and Rayport, 1994), few proposals have been made for the
  functional significance of inhibitory autaptic innervation in
  vivo(neostriatum, Park et al., 1980; Aplysia buccal ganglia,White and
  Gardner, 1981).


Is the immune system suppressed during sleep?

During stress glucocorticoids, which are steroid hormones produced by adrenal glands (such as cortisol and corticosterone), are released into the blood-stream. These hormones have anti-inflammatory effects. You may say that they suppress the immune system.

The circadian rhythm, which controls the sleep-wake cycle, also controls glucocorticoid secretion, thereby reinforcing the sleep-wake responses [1]. Sleep deprivation is a form of stress and it causes an elevation in the levels of glucocorticoids. The effect of sleep deprivation could be replicated by adrenectomy (surgical removal of adrenal glands); there is a transcriptional downregulation of several neuroprotective genes [2]. Via glucocorticoid mediated signalling, sleep deprivation also results in inhibition of adult neurogenesis in the hippocampus [3].

Another study says that cytokine (TNFα and IL6) secretion by immune-system cells, are inherently affected by circadian rhythm via a glucocorticoid independent mechanism [4].

Overall, sleep is inversely correlated with reduced inflammation because both the processes are under the control of the circadian clock. Sleep deprivation, as a form of stress, is also correlated with glucocorticoid secretion. It should be understood that sleep doesn't necessarily inhibit glucocorticoid secretion and it would be incorrect to say that reduced inflammatory effects are because of sleep.


What is the intracellular chloride concentration in rat T-cells or thymocytes

Felber and Brand 1982 estimate the intracellular T-cell chloride concentration to be about 30 mmol, which seems to me to be on the high end for intracellular chloride in mammalian cells (though my experience is mostly with neurons, I'm not as confident of intracellular chloride concentrations in other cell types; for a neuron I'd expect <10mmol). Still, that leaves a big anion gap for your SID estimate.
I think it is more likely that your SID estimate is simply wrong. The number you report sounds like an extracellular SID; Kowalchuk et al 1988 suggest intracellular SID is about 4X extracellular for muscle, which sounds about right for your situation as well.
Most of the intracellular anion contribution is provided by negatively charged proteins, amino acids, lactate, etc, rather than strong ions like chloride. Many of these are nearly completely deprotonated at physiological pH, though (for a typical amino acid the first pKa is ~2).

Felber, S. M., & Brand, M. D. (1982). Factors determining the plasma-membrane potential of lymphocytes. Biochemical Journal, 204(2), 577-585.
Kowalchuk, J. M., Heigenhauser, G. J., Lindinger, M. I., Sutton, J. R., & Jones, N. L. (1988). Factors influencing hydrogen ion concentration in muscle after intense exercise. Journal of Applied Physiology, 65(5), 2080-2089.


Can galls be formed from mutualistic relationships?

From what I know of ant-Acacia mutualisms, I've never heard of an ant gall in an Acacia. The link in your question also never mentions a gall. You've likely confused either domatia or Beltian bodies as a gall. Both differ greatly from galls in that domatia or Beltian bodies are created by the plant and not by the insect.

Domatia are small plant-made chambers that house mutualistic insects (though are often invaded by non-mutualists).

Beltian bodies are a type of food body (or plant-made structures containing nutritional substances (often high in protein) that attract a mutualist species of ants in Acacia).

See here or here for more info about galls.

To answer your overarching question of whether there are mutualistic galls, I would have to say no. I do not know of any instances of which this is the case. Further, galls are inherently parasitic (not mutualistic). Even if the swollen cells do not interfere with normal plant function (e.g., as is common in Solidago spp.)1, the parasitic insect (or other arthropod) is still required to chew its way out of the gall. Last I checked, chewing on your host's tissues is never very mutualistic.

 1: Crutsinger, G.M., Habenicht, M.N., Classen, A.T., Schweitzer, J.A. and Sanders, N.J., 2008. Galling by Rhopalomyia solidaginis alters Solidago altissima architecture and litter nutrient dynamics in an old-field ecosystem. Plant and soil, 303(1-2), pp.95-103.


When is wing growth in the bat complete and how soon can bats fly after wing growth is complete?

The ability of the forelimbs in bats (as well as in other tetrapods) to grow depends on the proliferation activity and ossification of cartilage in growing zones of the bones. Adult bats do not grow (as is the rule for mammals) and wing parameters (wing span and area) show growth curves with more or less pronounced plateau, which asymptotically leans to "adult" values. (This reflects progressive ossification of the cartilage.) As one could intuitively expect, variability in wing relative parameters decreases with age, meaning that juveniles before their first flights show more diversity in wing shapes than flying juveniles and those, in turn, approach gradually the narrow variability of these parameters of the adults.
Juvenile bats start performing their first short flights even before weaning. The main requirement for the flight ability per se is a certain threshold value of wing loading. Sustained flights start roughly half-way to maturity and correlate with the emergence of the above mentioned plateau on the growth curves. The flight abilities improve together with aerodynamic characteristics of the wing: duration of flight increases, beat frequency decreases, but beat power increases etc.

Some references:

Jones (1967)
Buchler (1980)
Hughes et al (1995)
Isaac, Marimuthu (1997)


Why does the gravity of Earth appear in this formula estimating speed?

Units
G is going to be different depending on what units you use, the original formula was derived using FEET not meters. As it stands the formula works both with metric and imperial units. With your change this would not be true. Paleontology is often uses both units so a formula that is not unit dependent is preferable.


"Next generation" brain scanners, can they detect CTE?

I do not know the details of the innovation, but it's based on MEG. MEG is a complementary technique similar to EEG, sesitive to magnetic fields instead of electrical fields (hence the 'M' in place of the 'E'). It is used to read population brain activity in real time, and is less useful as a tool to assess structural changes. MEG is currently mainly used for research purpose, and I don't see this innovation changing that. CTE could manifest in longer conduction delays or disruption of communication, but given that MEG can only access certain areas of the brain, it is probably not going to be very useful in general. I can imagine it being useful for some very specific CTE cases.


How does one calculate how to dilute a solution to working strength?

Since its 6x (6 times concentrated), you have to dilute it 1:6, so you add 1ul of 6x dye for every 5ul of reaction.

5 +1=6ul final volume

6ul final volume / 6x concentrated = 1x working concentration

Now the dye is diluted down to a 1x(working) strength.