Effects of HRT on transgender(M to F) physiology and athleticism.

We have two groups of people or better to say scientists and specialists that have their own ideas and theories and approvements.

People that are relay on genetic related ideas that mostly consider rule of Y chromosome on men and how some genes' rules will not be diminished only by hormone therapy or non genetically engineering methods.

Case example:

  Chloie Jonsson, 34, who transitioned more than eight years ago, is legally recognized as female in the state of California. Despite the medical community's consensus that transgender women do not have a competitive advantage over cisgender (nontrans) women, Jonsson's application to participate in CrossFit's women's division was rejected with a bizarre letter claiming she and her supporters do not understand "the human genome" and "fundamental biology." In response, Jonsson filed suit against the fitness giant.

  The letter from CrossFit general counsel Dale Saran reads:

  "We have simply ruled that based upon [Chloie] being born as a male, she will need to compete in the Men's Division. The fundamental, ineluctable fact is that a male competitor who has a sex reassignment procedure still has a genetic makeup that confers a physical and physiological advantage over women. ... Our decision has nothing to do with 'ignorance' or being bigots — it has to do with a very real understanding of the human genome, of fundamental biology, that you are either intentionally ignoring or missed in high school."
  Later, Saran disputes the statement made by Jonsson's attorney that "by all accounts, both physically and legally, Chloie Jonsson is a female."

  "This is simply wrong as a matter of human biology and if you can't see that, there really isn't much to talk about," writes Saran, citing Encyclopedia Britannica. "Chloie was born, genetically — as a matter of fact — with an X and a Y chromosome and all of the anatomy of the human race. Today, notwithstanding any hormone therapy or surgeries, Chloie still has an X and a Y chromosome."

To add some details to group one's idea, if you think of some genes and their rules in men that makes them more accurate and more muscular than women in the field of physical activities, you'll get to the point of how to control or change behaviour of these genes in the body of a man to make him woman, both muscularly and neurologically which is not possible for now because we need some very detailed and powerful calculations to know the exact equilibrium of a man genome as if he was a woman.

To change the complicated mechanism of Y chromosome on Biochemistry and behaviour of other chromosomes we have so much to learn and we need very fast computers to simulate the behaviour of molecules and new formation of mass body.

And we have other ideas by people who insist on level of hormones that has a great effect on mass of bone and muscles in men and women regardless of how their sex and genome is.

Case example:

  Eric Vilain, Director of the Center for Gender-Based Biology and Chief Medical Genetics Department of Pediatrics at UCLA, says of any perceived advantage a transgender woman may have, “Research suggests that androgen deprivation and cross-sex hormone treatment in male-to-female transsexuals reduces muscle mass; accordingly, one year of hormone therapy is an appropriate transitional time before a male-to-female student athlete competes on a women’s team."

A great article and detailed explanation by an example that helps to answer your question is here.


What kinds of animals does insular dwarfism affect and how large does an island need to be to escape it?

There are no general rules. We have just observed repetitively that organisms living on small pieces of lands tend to be particularly large (insular gigantism) or particularly small (insular dwarfism) compared to the main land counterparts.

There are several possible reasons for these changes and those reasons vary among species. Dwarfism is most definitely not always a consequence and there is no hard coded minimal island size for such change to happen or not happen.


qPCR: Accounting for different sample mass when interpreting and comparing Ct

If you are always using a relativ amount of your input yield for each sample, then you'll need to correct your Ct values for the absolute DNA yield of each sample. If you can't measure the DNA yield of each sample, then you'll just have to assume it is directly dependent on the sputum input mass. This assumption is pretty faulty though, since direct DNA measurements are much more exact and are not affected by biases from DNA extraction efficiency differences or batch effects.

Since Ct values represent a single qPCR cycle in the linear phase in which the target DNA is doubled, you need to adjust the CT values by +1 for samples with half DNA input and by -1 for samples with double input (or generally $Ct_{adjusted} = Ct - log_2(inputfactor)$ ). Of course this method of normalising assumes that the relative content of your target DNA in the sample is independent of the total sample yield (which may or may not be true; if your specific bacteria species is proliferating a lot more in one patient compared to the other this might affect both relative and absolute DNA amounts).


precursor miRNA is ~70mer RNA with a stem loop structure. It is cleaved by dicer to generate one or two mature miRNAs (from one or both the 'arms' of the stem ; called 3p and 5p which are ~22nt long). Refer to this review. (It is an old one and some facts might have changed, but the basics are there.)

Yes, there can be different precursors giving rise to same mature form. There are a few cases like that (check for entries like mir-x-y [where y can be 1,2,3,...], in miRbase).

Usually pre-miRNA is shortlived and is immediately converted to mature form. Therefore, in small RNAseq data, most miRNA reads (more than 90% [at least that's what I get]) come from mature form (pre reads would be longer [after adapter removal] and will contain sequences not retained in mature form). Most algorithms select for the mature reads.

It is difficult to determine which precursor gave rise to a certain mature miRNA, using an RNAseq data. The usual practice is to assign the average read count to each locus. E.g., for a mature form that has 3 precursors, each precursor is assigned 1/3 of the total mature reads. However, in most RNAseq experiments, the objective is to obtain the mature miRNA profile and which precursor gives rise to it becomes immaterial.


Does transcription terminate at the end of antibiotic resistance genes on the Duet expression plasmids?

Generally they do, however this is often doesn't completely stop transcription run-through.
Note that in a T-7 reaction there shouldn't be any transcription of the Amp or Kan genes as these are run off promoters that  the T7 phage RNA polymerase won't be able to transcribe off as it is extremely specific for the T7 promoter.
The solution if you are really worried is to linearize your plasmid immediately downstream of your terminator but before the AMPR gene using a restriction enzyme with a single cut. This will also give you a specific size sequence being transcribed, which is very useful if you are determining copy number in say a qPCR.


Standard notation for crossings (female, male)

For plants, seed (egg cell) parent is shown first and pollen (sperm) parent second.
The rule is mentioned in wikipedia,
http://en.wikipedia.org/wiki/Hybrid_(biology)
section : in plants.
Another mention of plant example:
https://www.rhododendron.org/v50n1p36.htm


Are there any examples of sudden leaps in evolution?

Zuk et al. (2006) document the rapid evolution of song-less crickets in a population of crickets that previously used song for courtship.

In less that 20 generations, over 90% of male crickets of the species Teleogryllus oceanicus evolved to a novel morphology ("flatwing") that rendered them unable to call to females. They hypothesize that this shift resulted from the presence of an North American invasive "acoustically orienting parasitoid fly."

Basically the flies detect calling males and parasitize them, rendering them unable to reproduce. Were it not for the presence of the parasitoid fly, the flatwing flies would likely not have survived. Non-calling individuals rely on the presence of calling males to bring females near for mating.


How is breathing involuntary if the muscles that control it are skeletal?

Breathing is controlled by both the Autonomic nervous system and the voluntary nervous system. You see this in instances where our breath rate increases in flight or fight situations glide to the secretion of Adrenaline and also when we intentionally increase the breathing rate when undergoing high levels of activity. This is due to the fact that the involuntary aspect of breathing is controlled by the medulla oblongata and the voluntary aspect s controlled by the cerebral cortex. The fact that it is controlled by skeletal muscles has nothing to do with how it is innervated. For example, Cardiac muscles are innervated by both the hearts own conducting system and by the Autonomic nervous system.
If you're wondering why the skeletal muscles dont get fatigued, it's because there is a small but significant rest period between each Breathing cycle (inhalation and exhalation). Therefore the skeletal muscles have a rest period. However if a high rate of breathing does occur for a sustained period, they will fatigue and that's why you get cramps after a marathon or a sprint.


It could not fit in a comment..
You recorded bats. You are interested in social calls. Socials calls can be recorded by your microphone but they cannot be read by standard media player because...

the standard media player are limited to certain frequencies
your speakers cannot produce such high sounds
your ears are not able to hear many of the frequencies emitted
you formatted your records in a format that cannot hold very high frequency (for reason of optimizing data compression)

You might use some program like Adobe Audition in order to easily visualize the frequencies (vs time) of your record. (It might also help you finding all harmonics or performing Fourrier analysis)

This wiki article says :

Social Calls
This is a wide subject and there is still a lot to be discovered about bat social communication and how they use social calls in roosts and when flying. Generally a bat social call is not tonal, in other words it does not consist of a musical type note. Some bat detectors do not produce an accurate recording of a bat social call. Typically bat social calls use a lower frequency range than echolocation calls, and can thus be heard further away. Sometimes a bat will make a social call while echolocating which can cause confusion.
We can see and hear how the lower frequency social calls are heard at a greater distance than the higher echolocation calls as the bat approaches and departs. Zooming in on a spectrogram, social calls are atonal and repeated rapidly about five times in each call. The social calls are interleaved between the echolocation calls. They show a ragged frequency distribution around 20 kHz. Note the FD detector divides frequencies by 10.
The echolocation calls are single "hockey stick" calls at a higher repetition rate. At this scale the hockey stick shape is not very clear, but the end frequency can be measured as 45.2 kHz. A doppler shift is recorded as the bat approaches. The frequency was measured as it passes


Enhancers and silencers are binding sequences for transcriptional activators or repressors, in which case the sequence is often located some distance upstream or downstream of the gene it regulates. See regulation of transcription for information about how these interact with their target genes (through DNA bending, mediator, etc.). A note about enhancers and silencers, though, they're not necessarily required for transcription: they help the gene attain robust up- or down-regulation of transcription.

The operator, on the other hand, influences whether the promoter will do something, or nothing. If we're talking about inducible systems, the repressor is bound to the operator, blocking action to/from the promoter (an inducer will bind the repressor and keep the operator from blocking the promoter). If we're talking about a repressible system, the repressor will need a corepressor to bind the operator to abrogate transcription by blocking action to/from the promoter.


The human blood contains about 45% of erythrocytes and 54.3% of plasma by volume. The plasma contains about 92% water, while the erythrocytes, about 64% by weight.

The blood is slightly less than 80% water.

Dehydration occurs when water intake is insufficient to replace free water lost due to normal physiologic processes (like sweating, urination etc). Hyponatremia is low sodium concentration in the blood. Usually, the Sodium and water concentrations in blood are regulated independently. Hyponatremia can be caused by intake of to much water, which reduces the sodium concentration.

References: The sodium, potassium, and water contents of red blood cells of healthy human adults by L J Beilin, G J Knight, A D Munro-Faure, and J Anderson, J Clin Invest. 1966 Nov; 45(11): 1817–1825.


Darwin thought quite a bit about this. He even said "The sight of a peacock makes me sick". https://www.ncbi.nlm.nih.gov/pubmed/10824193
He added to his ideas about natural selection to include sexual selection. Traits selected by females, even when they are non-adaptive for males, will increase the males fitness (as defined by his number of offspring). There is also the idea that perhaps possessing such an outrageous and non-adaptive tail proves that you a good mate, the same way we would think that a guy who could win a sprint while carrying barbells must be superior.


How do heredity and regression to the mean work with respect to intelligence?

I think the question mainly highlight either of two misunderstandings:

misunderstanding about the definition of heritability
misunderstanding why the slope of the regression line is equal to heritability (in the narrow sense).

Definition of heritability

Please have a look at the post Why is a heritability coefficient not an index of “how genetic” something is?.

Notation

Please note that, here I use $h^2 = \frac{V_A}{V_P}$ to designate the heritability in the narrow sense, where $V_A$ is the additive genetic variance and $V_P$ is the (total) phenotypic variance. If anything of what I just said is unclear, please refer to the aforementioned post.

Without any loss of generalization, we will set our scale so that the average phenotype in any studied case is equal to zero. From this starting value, we note X (with a subscript) the contribution of a given haplotype (or allele) to deviate the phenotype of an individual. We will note $E$ (with a subscript) the contribution of a given environmental state to deviate the phenotype of an individual.

An individual phenotype

Let's consider an individual O (stands for offspring, it will makes sense later). The phenotype of this individual is given by the addition of the contribution of each haplotype and of the environment. The expected phenotype of O (called $P_O$) is therefore

$$P_O=X_m + X_p + e_O$$

, where $X_m$ is the contribution of the maternal haplotype, $X_p$ is the contribution of the paternal haplotype and $e_O$ is the contribution of the environment.

Just a note

It might be worth skipping this note and coming back to it once you understood the below calculations (but I did not want to move this note to the end).

In the above calculation, one must assume absence of epistasis and dominance effect. I am not exactly sure how this might eventually cancel out later or whether results would then differ. I would welcome a follow-up in the comments to clarify this point but it might be worth its own post. As the question refers to the heritability of intelligence (assuming this term is defined), I would like to highlight that it is unlikely that we have much understanding about the exact pattern of epistasis underlying this trait as measure of epistatic interaction are often difficult to achieve.

Phenotype of O's parent

Let's note $P_P$, the phenotype of one parent of O'. The below notation applies to the mother but calculations would be the same for the father.

$$P_P = X_m + X_m' + e_P$$

, where $X_m'$ is the haplotype of the mother that has NOT been transmitted to the offspring and $e_P$ is the contribution of the environment experienced by the parent (mother).

Covariance between $P_O$ and $P_P$

The covariance between $P_O$ and $P_P$ (noted $cov(P_O, P_P)$ is just the sum of the covariances of all contributions, that is

$$cov(P_O,P_P) = cov(X_m,X_m) + cov(X_m,X_m') + cov(X_m,e_m) + cov(X_P,X_m) +\
 cov(X_P,X_m') + cov(X_P,e_m) + cov(e_O,X_m) + cov(e_O,X_m') + cov(e_O,e_m)$$

I let you take a few minutes to think about the values of each of these covariances.... They are almost all equal to zero (are independent). There are only two covariances that (under a simple model) can potentially be different from 0; $cov(X_m,X_m)$ and $cov(e_O,e_m)$. $cov(e_O,e_m)$ is teh correlation between the environment experienced by the mother and the one experienced by the father. For simplicity, we will make the assumption that these two environments are independent and therefore $cov(e_O,e_m)=0$. The above, long and hairy equation therefore reduces to

$$cov(P_O,P_P) = cov(X_m,X_m) = var(X_m) = \frac{V_A}{2}$$

Correlation between $P_O$ and $P_P$

By definition the correlation (which is the slope of the regression line) is just the covariance divided by the total phenotypic variance. Therefore the correlation between $P_O$ and $P_P$ (noted $cor(P_O,P_P)$) is

$$cor(P_O,P_P) = \frac{V_A}{2} \frac{1}{V_P} = \frac{h^2}{2}$$

Generalization to any correlation

Following the above logic, one can show that in general the correlation between any two individual phenotypes $P_X$ and $P_Y$ is

$$cor(P_X,P_Y) = r h^2$$

, where $r$ is the coefficient of relationship. For parent-offspring $r=\frac{1}{2}$.

Particular case of mid-parent vs offspring relationship

This is just a study case to show that when consdiering a made-up phenotype such as a hypoethetical mid-parent phenotype, then the math are just a little bit more tricky. If you consider the mid-parent phenotype $P_{mid}$, then you must consider that the total phenotypic variance is half the actual phenotypic variance. The correlation therefore becomes

$$cor(P_{mid},P_O) = \frac{cov(P_{mid},P_O)}{\sqrt{\frac{V_P^2}{2}}} = \frac{h^2}{\sqrt{2}}$$

Conclusion

All of the above mean that if you plot the phenotypes of a series of individual pairs, where each pair is related by $r$, then the slope of the regression line is $r h^2$. For example, if you plot the phenotype of the mothers with their offspring, then the slope of the regression is equal to $\frac{h^2}{2}$. If $h^2=0.4$ (which is a typical value of heritability), then the mother-offspring regression will have a slope of $0.2$.


Was site-directed mutagenesis used to study the effects of sickle-cell anemia?

The cause of sickle-cell anemia to be a molecular defect was discovered in 1949 by Linus Pauling. In his experiment hemoglobin molecules were broken down to smaller fragments, which were then subjected to electrophoresis and chromatography. The results of these measurements were compared between healthy and affected samples, allowing the identification of a mutated fragment.
The amino acids in the mutated fragment were analyzed in 1956 by Vernon Ingram, identifying the single mutation. The process in a bit more detail is described on this webpage.

Site-directed mutagenesis is used primarily in research aimed at finding a gene therapy based treatment for sickle-cell disease, such an attempt is described in this publication.

Also, the technique was used on recombinant hemoglobin to create and study some properties of naturally not occurring mutations. [Link]


How does DNA determine all of our hereditary traits?

Does that mean that hereditary traits, like the shape of our nose, are determined only by the proportions in which various proteins are synthesised in various parts of our body ?

Yes, more or less!

A trait that is called heritable is a trait which variance in the population is in part at least explained by genetic variance. Most of these heritable traits, however, are also affected by environmental variation (and other sources of variance). For more information, please have a look at the post Why is a heritability coefficient not an index of how “genetic” something is?

So when you say

  [..] are determined only by the proportions in which various proteins [..]

The term "only" is a bit misleading. Other sources of variance exist that will affect the variance for this trait. However, it is a pretty good approximation to say that the heritable information is conveyed via the transmission of DNA and the phenotypic expression of this DNA is mediated via proteins.

We refer to the DNA -> RNA -> protein having some phenotypic impact relationship by the term central dogma of molecular biology. You might want to read more about it or maybe have a look at an online course such as this one from Khan academy for example. You will want to know the terms translation and transcription.

Now, in reality DNA can affect an individual's phenotype by means other than proteins (or polypeptides to keep it more general) that are synthesized from it. Indeed, many loci (locus=position on a chromosome) affect the expression of other proteins, others are translated into RNA but not transcribed into proteins (e.g. rRNA, tRNA, RNAi, ...) but yet still have an important action on a cell's physiology.


Are the arrows in this diagram of ATP synthase correct?

Yes, the arrows are correct. However, it's not immediately clear what they're trying to show.
ATP synthase
ATP synthase can act as a generator or a motor. Interactions cause rotation of the F0 subunit and the  subunit's axle has a kink in it which deforms the stationary F1 subunits (the axle can turn either way to act as a generator or a motor). Read more at PDB's ATP synthase 101.

What The Asker's Diagram is Trying to Show
The black arrows in the asker's diagram are implying the movement of ADP or ATP (generation) in and out of the catalytic site. The pink line implies the movement of the axle kink and not the transition of ADP+pi->ATP.
Let's focus on the left-hand subunit across the subfigures and it makes more sense (ADP and Pi go in, protein "closes" and ATP is formed, ATP is released). Meanwhile, the "kink" completes a full rotation.


Amino Acid requirement + intake in relation to diet + meat type

There is a difference between animals in their requirements for amino acids. For example, cats need high amounts of taurine (and can't make it) and when fed diets lacking enough can go blind. This is why vegans trying to feed vegan diets to their pets can be very bad for the pet. Animal proteins have sufficient taurine for the cat.

However, the meat of a cat or dog is just as a complete source of protein for humans as any other meat. All essential amino acids are there in sufficient ratios. Suggesting otherwise by her father suggests some confusion between the dietary needs of cat vs. the nutritional value of the cat to another predator.

Your second question is easily answered by looking up essential amino acids.  Wiki is plenty sufficient to get the gist Wiki Link. In short, most plants don't contain the full complement of amino acids that humans require (and can't make on their own). So to get this full complement, it requires eating multiple plant products that together contain the required amino acids.

From Harvard School of Public Health

  Protein is built from building blocks called amino acids. Our bodies make amino acids in two different ways: Either from scratch, or by modifying others. A few amino acids (known as the essential amino acids) must come from food.

  Animal sources of protein tend to deliver all the amino acids we need.
  Other protein sources, such as fruits, vegetables, grains, nuts and seeds, lack one or more essential amino acids.

  Vegetarians need to be aware of this. People who don’t eat meat, fish, poultry, eggs, or dairy products need to eat a variety of protein-containing foods each day in order to get all the amino acids needed to make new protein.


DNA-DNA cross-linking with formaldehyde?

The fact that there is no inter-strand cross-linking between different double strands might be just because the cross-linker cannot bridge the distance between amines of different bases on different double strands.

The formaldehyde based linking of nucleobases has been described by Chaw et al. (1980) where formaldehyde bridged a gap of app. 3 angstroms (2x 1.3 A for N-C bond).

Even if you take the most condensed form of DNA as in nucleosomes (see X-ray model of nucleosome with bound DNA) you still have at least 20 angstroms between the bases of different double strands.
At the same time there are only 3 angstroms between the nucleobases of the same double strand, agreeing well with the length of a methyl-bridge.


Measurement of glucose concentration in the human brain

It is possible by using 13C NMR Spectroscopy.

It has been done after infusing enriched D-[1-13C]glucose in six healthy children. The results showed that at euglycemia glucose concentration is about 1 micromol/ml.

Source: Gruetter R, Novotny EJ, Boulware SD, Rothman DL, Mason GF, Shulman GI, Shulman RG, Tamborlane WV. Direct measurement of brain glucose concentrations in humans by 13C NMR spectroscopy. Proc. Natl. Acad. Sci. U.S.A. 1992 Feb 1;89(3):1109-12. PubMed PMID: 1736294.


Are phylogenetic tree construction algorithms any different than general clustering algorithms?

One difference is that phylogenetic tree construction algorithms will typically try to jointly estimate the tree and the transition parameters.  A general clustering algorithm might assume that a difference in one feature would make the same contribution to 'distance' between clusters as a difference in another feature. In phylogenetic tree construction, it is explicit that not all differences between taxa represent the same evolutionary distance between taxa, and the parameters governing the distribution of distance/difference may be jointly estimated with the tree.


Valid XHTML http://nar.oxfordjournals.org/content/29/17/e88/F1.large.jpg.
Figure 1. Schematic presentation of the tetra-primer ARMS-PCR method. The single nucleotide polymorphism used here as an example is a G→A substitution, but the method can be used to type other types of single base substitutions. Two allele-specific amplicons are generated using two pairs of primers, one pair (indicated by pink and red arrows, respectively) producing an amplicon representing the G allele and the other pair (indicated by indigo and blue arrows, respectively) producing an amplicon representing the A allele. Allele specificity is conferred by a mismatch between the 3′-terminal base of an inner primer and the template. To enhance allelic specificity, a second deliberate mismatch (indicated by an asterisk) at position –2 from the 3′-terminus is also incorporated in the inner primers. The primers are 26 nt or longer, so as to minimize the difference in stability of primers annealed to the target and non-target alleles, ensuring that allele specificity results from differences in extension rate, rather than hybridisation rate. By positioning the two outer primers at different distances from the polymorphic nucleotide, the two allele-specific amplicons differ in length, allowing them to be discriminated by gel electrophoresis. (http://nar.oxfordjournals.org/content/29/17/e88/F1.expansion)


If higher levels of atmospheric oxygen can lead to larger animals, can it also lead to larger plants?

Oxygen is good for animals because our basic metabolism is this:

  High energy carbon molecules + O2 → energy + H2O + CO2

Plants do that too at night, but during the day, they mostly do this:

  High energy photons + H2O + CO2 → High energy carbon molecules + O2

Rubisco, one of the most important enzymes in photosynthesis, can bind to O2, leading to less efficient photorespiration, instead of photosyntheis.  Rubisco is often a bottleneck in photosynthesis, in large part for that reason.  So high oxygen isn't helpful to plants.  In fact, C4 plants and CAM plants have evolved more complicated physiology to minimize the effect of O2.


Benign tumors can absolutely have mechanisms available to them to commit to and carry out apoptosis.  An example of this would be benign prostatic hyperplasia, in which the balance of apoptotic and proliferating cells is offset, but apoptosis is still occurring, simply at a lower comparative rate than the proliferation.
Benign tumors can therefore be caused either by excessive proliferation or inadequate cell death; evidently, a complete failure of programmed cell death in many tissues would result in a tumor, benign or no.

Source:

Kyprianou N, Tu H, Jacobs SC. Apoptotic versus proliferative activities in human benign prostatic hyperplasia.  Hum Pathol. 1996 Jul. 27(7): 668-75.


what is the function of satellite in a chromosome?

There are at least 2 SAT chromosomes in each diploid nucleus. They
  play a vital role in the formation of the nucleolus after cell
  division is completed.

  In humans, chromosomes number 13, 14, 15, 21 and 22 are examples of
  SAT chromosomes.

cuted from http://en.wikipedia.org/wiki/Satellite_chromosome


What is the result of modifying the reagents in the Sanger method?

If by one of the dideoxynucleotides, you mean one of ddATP, ddCTP, ddGTP, or ddTTP was omitted from the process, then the sequencing would only be able to terminate for the other three dideoxynucleotides. And you would not be able to get the full sequence, and only nucleotides of whatever three you had.

The function of ddNTPs (the dideoxnucleotides) is to stop the elongation of DNA and to subsequently be read by either fluorescence or radioactivity.

Source: https://en.wikipedia.org/wiki/Sanger_sequencing


Are there any studies of epigenetic difference between twins during their lifespan?

I would think there have to be, though do you mean collecting samples on a regular basis and plotting out the difference at each point? Or do you simply mean the total accumulated change. If it is the latter, the answer is certainly "yes". You have probably seen the Nova documentary "Ghost in Your Genes" (The US, not BBC one). In it they show comparison of accumulated epigenetic change between a pair of identical twin Spanish women. I'm guessing you are more looking at measuring this change on a regular basis and looking for points of rapid divergence.... I don't know if this has been done for individuals, but it appears that it has been done for sample sets (see the same documentary). They discuss accumulated genetic change in younger twins vs older ones...


Problems with analysis of small RNAseq data - Adapter trimming

I would first recommend you ask this question biostar as the subject matter you are inquiring about is much more relevant there.

That having been said, you have another option which is to use an aligner that soft clips 3' ends of reads specifically to account for adapter (or polyA, or whatever) contamination that might have flew under your radar.

STAR is such an aligner. If you search their mailing list archives for "clip", you should find several posts related to your question.


Apparently, microbiologist use this term to describe the process of culturing microorganisms from soil. You make a 'slurry' which has both growth media and the soil (which would fall under the english definition of a slurry) and incubate it waiting for growth. Media(Liquid) + soil = Slurry


Why do I see an inverted image of an object when I close my eyes?

I think it is because of light adaptation. The rods that are perceiving strong light, downregulate their response. But when the light is suddenly withdrawn then the rods that are adapted to perceive bright light cannot immediately sense dim light.

There are two forms of adaptation- fast and slow. The fast one is Ca²⁺ dependent- decrease in Ca causes cGMP to increase which in turn depolarizes the cell. Calcium modulates this process by other means also. This article suggests that slow adpatation is  because of an allosteric binding of cGMP on transducin-phosphodiesterase complex, which stabilizes this transition state and delays the signaling.

Adaptation can also happen because of photobleaching of rhodopsin.

I don't know how an image "remains" in the eye for a while. I believe it is because of asymmetric slow light adaptation between different spatially distributed rods(some rods take a while to readapt to dim conditions).

Similar effect you can feel with colour vision also. You keep staring at green for a while, then when you see something else it appears reddish.


What motivates children to start walking?

You might be interested in Alison Gopnik's book "The Gardener and the Carpenter", where she gives thoughts on how children develop and learn. Children are very disinhibited in their behavior, and this is generally considered to be a consequence of their prefrontal cortex being immature, but she proposes that this is not a bug but a feature. That there is a tradeoff in any algorithm between "exploiting" the possibility space (incrementally improving your solution until it's as good as it can be) and "exploring" the possibility space (casting a wide net to find totally different solutions that might be even better). If you just "exploit" you are liable to stay stuck in local maxima; if you just "explore" you're never going to find a good solution because your search is too random and the possibility space is too large to examine every possibility. Good optimizing algorithms have alternations between the phases, with "explore" phases to look at many different areas of the possibility spaces, and "exploit" phases to optimize the most promising candidates. Gopnik's argument is that children are the "explore" phase of human development, and that is why they are disinhibited: they are motivated to try many different things for the sake of it, with no specific objective in mind or much thought to the consequences. (and in this view, an important job of parents is to make sure the consequences won't be fatal).
This might answer some of your question of babies thinking about "pros and cons". It might be more realistic to see them as thinking only in terms of "pros". Not, "if I do this this will be the consequences, if I do that those will be the consequences, what should I do given the consequences I want", but "what happens if I try this? And that? And that? And that? And that?"
Another factor that wasn't mentioned in the comments is imitation; children like to imitate others around them and odds are they see adults walking all the time.
In terms of walking though I'd expect instinct to play the major role. Not that walking would be hardwired per se, but there are probably movements and reflexes that babies are hardwired to try, and once they get to a physical maturity where walking is possible the odds are that they will try those movements, and find the results interesting at least, profitable at best.


How does natural selection explain sexual display?

Short answer
Survival does not get your genes into the gene pool, reproduction does.
thus reproduction based selective pressures can be stronger than survival based ones. there are plenty of organisms that die during or right after mating because of this.
Consider an example In species A finding a mate is fairly rare, it may only happen a few times in an organisms life. if individual X is guaranteed to mate and reproduce when they find a mate but will die after mating, and individual Y will not die after mating but only has a low chance to mate then the genes from X will spread much faster than the genes for Y, because mating is already a rare event, but X genes spread every time while Y genes will also only spread once or often not at all, and will also take much longer.
Or to put it another way, a chicken is just an eggs way of making another egg, the survival of the chicken is only useful as much as it facilitates reproduction.
Any mutation  that happens to make you better at attracting a mate will spread, how it does so is basically irrelevant as long as it works, loud noises, bright colors, eye spots anything that draws the females attention works. studies on several bird species have shown even the colored bands used to identify birds for study effect their mating chance is they are right colors. Animals often already have a variety of biases for their attention hijacking them is an easy way to improve your chances of mating.  Of course once a way evolves that reliably improves mating chances preference for that becomes favorable as well which can lead to a run away selection feedback loops AKA Fisherian runaway
https://link.springer.com/article/10.1007/BF00172135


Stabilizing forces between the protein sequences?

Proteins often undergo conformational changes. The activation energy required to undergo a conformational change in a protein with only covalent interactions would be much higher compared to that of a protein with weaker bonding forces. An example of a conformational change seen in enzymes is the change in conformation during allosteric regulation, in which an effector molecule binds a site on the enzyme distant from the enzymes active site. The binding of the effector molecule induces a conformational change that exposes the active site of the enzyme. Another example of conformational change is the change in conformation seen in Toll-Like-Receptors (TLRs). Additionally, many proteins change their conformation in response to pH. These changes would likely not occur if the protein only contained covalent bonds, and the ability of proteins to undergo such changes makes them responsive to the environment, as well as allowing them to carry out their enzymatic actions, if such actions exist for that particular protein.

Here is the wiki on allosteric regulation https://en.wikipedia.org/wiki/Allosteric_regulation

Here is a figure on conformational changes in TLRs http://www.nature.com/ni/journal/v8/n7/fig_tab/ni0707-675_F1.html

And here is the wiki on activation energy, a concept used in chemistry (see section on catalysis and Gibbs free energy) https://en.wikipedia.org/wiki/Activation_energy


How much does hearing deteriorate with age?

Hearing sensitivity deteriorates with age, which is called age-related hearing loss, or presbyacusis. Presbyacusis is characterized by elevated hearing thresholds. Especially the high frequencies are affected by age, but eventually even the low frequencies may deteriorate substantially. Hearing sensitivity is typically expressed in an audiogram, which depicts the hearing threshold as a function of acoustic frequency. To express hearing loss as a function of age, however, it is more convenient to plot the threshold at various frequencies as a function of age (Fig. 1).

Fig. 1. Hearing thresholds at various frequencies plotted as a function of age. source: Handbook For Acoustic Ecology.

Exposure to loud sounds may be detrimental to hearing, referred to as noise-induced hearing loss. Typically this results in a loss of sensitivity at the moderate frequencies (3k to 4k); a mid-frequency dip (Fig. 2). Old age will add a high-frequency hearing loss on top of that.

Fig. 2. Typical audiogram associated with noise-induced hearing loss. source: American Hearing Research Foundation

The brain will not adapt to elevated thresholds. A threshold represents the minimal intensity level a sensory system can detect. Elevated hearing thresholds due to old age and noise-induced hearing loss are caused by sensori-neural hearing loss, meaning the hair cells in the inner ear (the cochlea) are dying. The brain can never detect a signal that is not transmitted via the auditory nerve and can hence never compensate for elevated thresholds. In turn, when thresholds are elevated substantially, a person suffering from such a hearing impairment may ask you several times kindly to repeat what you were saying, but a little louder. Then, when you start screaming after the third time, the hearing-impaired person returns the dreaded "You don't have to scream at me!". That is because the brain does not adapt to the elevated thresholds; once the sound is transmitted by the degenerated cochlea, it is transmitted at that loudness and perceived at that loudness by the brain. Moreover, a process of recruitment can occur in the hearing impaired, where the perceived loudness is exaggerated. Recruitment may occur at the hair cell level, but it is a not well characterized phenomenon.


What's the difference between Phage DNA and Recombinant DNA

Phage DNA is the DNA in a bacteriophage.

Recombinant DNA is synthetically combined DNA used in genetic engineering.

In your case, since the phage's DNA is used as a vector, the phage DNA is the recombinant DNA, but that does not mean every phage's DNA is recombinant, since phages occur naturally. The point is, the phage DNA was altered to become recombinant DNA.


Why is there such in interest in antibiotics against Pseudomonas?

Indeed Pseudomonas is a very peculiar (and concerning) genus in clinical microbiology, specially P. aeruginosa. The reason why you keep finding emphasis on antibiotics that have pseudomonal activity is because this organism is the model of bacterial antibiotic resistance. It is often considered more deathly than other important multi-resistant bacteria such as S. aureus, Acinetobacter or Enterobacter.

P. aeruginosa is responsible for multi-resistant nosocomial diseases (a basic definition of nosocomial is an infection acquired inside a hospital) that have really high mortality rates. It is not uncommon to see hospital antibiogram results for this bacteria informing about resistance for all the commmonly used classes of antibiotics for Pseudomonas infections including 3rd and 4th generation cephalosporins, fluoroquinolones and carbapenems.

Reference: Evolution of Pseudomonas aeruginosa Antimicrobial Resistance and Fitness under Low and High Mutation Rates

There are LOADS of articles and info to read about P. aeruginosa antibiotic resistance, but I like this one since it tries to explain how the problem appeared from a genomic point of view.


The human organism knows what we have to eat?

Assuming you mean organism, not organisation, it's not entirely false that cravings can be driven by deficiencies. In the case of the eating disorder pica, where a person eats non-food items like dirt and clay, can be caused by iron deficiency (Source). However, that article also suggests the possibility that pica causes iron deficiency by causing the person to eat items that lower iron absorption. So, my answer to your question is, maybe.


I'd like to challenge your question.
What is a sense?
Are you looking for a complex organ that integrates with the central nervous system? Or just any part of your body that can be used to determine the property of something in the outside world? For example, you can use your toenails to test whether a hot plate is of sufficient temperature to melt dead keratinous biomaterial, like your nails. This would count as an integrated sense for a specific physical chemistry.
Or do you think a sense is a thing that detects a singular property of the world? For example, do you discriminate proprioception from gravity sensing, even though it may be performed by the same organ? Historically, each classic sense is limited to one property, but this I think is outdated. For example, skin is not only capable of performing touch and texture detecting ("tactile" sense), but also heat, pain, and other things like sensing noxious poisons such as bee stings.
Also, do senses have to detect stimuli in the external world? Plenty of sensing goes on internally, both in interstitial spaces and fluids in your body, on the surface of cells, as well as within cells, and the variety of cellular and sub-cellular equipment is hugely various. Should light receptive cells only count as 'vision' or 'light receptive' when they are found in the eye, or can light-sensitive cells found deep within the body can also be classified as part of the visual sense? There are many animals and tissues in biology where light-sensitive receptors are not exclusively found in eyes.
These are only 3 things you did not consider. There are many other questions you must answer along these lines to have a clear, at least temporarily operational definition that can be used to make distinctions to answer what things can count as a separate, countable sense.
Just as a proof of concept, I can list more than five senses off the top of my head to show you that the "five senses" concept is woefully outdated in my view, and I'm sure some others would agree. I will pick some weird examples just to demonstrate the complications that the above questions illustrate.
Chemosensory systems
(considered a sense for chemistry? or a collection of senses?)

Olfaction (smell, as carried out by neurons in the nasal epithelium; e.g. smell of vanilla, and smell of bad food)
Gustation (taste, as carried out by neurons on the tongue; e.g. salt, sugar)
Antigen chemosensing (chemical sensing, as carried out by, for instance, immune antigen receptors on B cells)
Hormonal signaling chemosensing (chemical sensing of hormones such as insulin, as carried out for instance by myocytes)
Starch sensing? (amylase in saliva can be used as a test for digestable starch)

Visual system, at the retina?

Visible light (sensing electromagnetic radiation on the order of a few hundred nanometers in wavelength)
Internal methanol sensing (the visual system as a sensor for methanol, which disproportionately affects myelin surrounding the optic nerve)
Pressure sensing (see phosphenes)

The vestibular system

Gravity sensing
Balance
Coordination
Motion sensor
Head position sensor
Spatial orientation

Skin

thermosensation (touching a hot kettle!)
Nociception (pain sensing)
allergen sensing
sensor for gamma rays, X-rays and UV light (indicated by radiation burns, development of skin cancer, sunburns, etc.)

Bones and muscles?

Kinesthetic and bodily proprioception

Brain/mind/mental/social senses?

mental pain
boredom
mental or spiritual distress
sense of self and other, including friendship, power, place in social hierarchy, reputation, companionship
motivation and love (oxytocin, dopamine, etc. in limbic systems and other neural correlates)

I'm sure some would agree, and some would disagree about the specific cases I provide. Thus the definition of senses, or sensing, seems to be opinion-based or at the very least very sensitive to an agreed-upon operational definition, for which there is none.


Why isn't hearing the same as tasting? How do we feel and differentiate external stimuli?

The problem you are seeking an answer to is referred to as the hard problem of consciousness, the term originally coined by David Chalmers, or more generally the mind-body problem.

Just how "hard" this problem is seems a bit unclear; some people argue it isn't truly "hard" at all, but they make these claims in support of their own particular views of the nature of consciousness. Since not everyone agrees with them, it seems like to at least some extent the "hard problem" description is appropriate.

There certainly are quantum explanations, and you will find proponents like Stuart Hameroff, but most neuroscientists consider his theories to be crank science since he hasn't provided any evidence of his theories, only hand-waving explanations of how they could be plausible.

There are also metaphysical explanations, going back to the dualism of Rene Descartes. The problem with these metaphysical theories is that they aren't scientifically disprovable, and the more we learn about the brain the more of its functions can be explained physically. Dualism is ultimately a religious or philosophical stance rather than a scientific one.

There are several neuroscientific theories of consciousness, including integrated information theory(IIT) and global workspace theory(GWT). For IIT, consciousness occurs through the integration of information in a causal structure like the structure of a brain. GWT proposes that consciousness occurs through the transmission of information through particular central brain structures. In both, the qualia that are experienced occur through the neural substrates of either the processing or the information carried. Hearing and tasting are different because they involve different groups of neurons and synapses; you don't typically taste a sound because the parts of the brain that process taste are not getting direct auditory information.

However, that doesn't mean that senses are completely disconnected: it is possible to form relationships between senses by association, like how both written and spoken language evoke the same meanings, or how certain colors seem to be associated with "hot" versus "cold" temperature.

As far as what it means to experience things how others do, I'd recommend Nagel's What Is It Like To Be a Bat? which argues that subjective aspects of consciousness cannot be completely understood, but that there are objective features that can be understood. So, although you cannot know that others taste or feel music in subjectively the same way as you, you can objectively understand that other people can taste sweet and sour, can hear music in a similar frequency range, etc.


TCGA data, and bioinformatics design questions for SNP/ mirna analysis

You can take a look at this tutorial to understand TCGA MAF files. And you can find a list of TCGA MAF files containing mutations mapped to genes and miRNA at https://www.synapse.org/#!Search:syn1710680


Chiral (a)symmetry of curly hair (and fur)

Microscopic chirality is not at all necessary to explain curly hair (or other objects).  All that is required is flexibility. Once hair gets long enough, it collides with itself, and is pushed off to one side or another, forming a chiral curl.

For some anecdotal evidence against microscopic chirality, find someone with large diameter hanging curls in their hair. Those seem to often curl straight back on to themselves. A more compelling anecdote is that curled objects, including hair and telephone cords (if anyone still remembers those) can be pulled through themselves and chirally inverted. Sometimes there will be some resistance, but that could be the keratin or plastic or whatever having set in its shape over time, rather than being preferentially formed that way.

These are obviously both anecdotal though, and the idea that there is some slight chiral preference isn't ruled out. I'm not even opposed to the fundamental idea of transitive chirality through several orders of superhelicity (look at DNA), but it just hasn't been my empirical experience. As Ryan points out, if it were a strong effect, all hair would curl the same way, and straight hair wouldn't exist at all.

Just to provide a bit of data, this paper demonstrates that hair curvature is based on the distribution of 4 different cell types in a follicle. The keratin (and many other proteins associated with) intermediate fibrils were associated with curvature, but only to the extend that their compositions were different in the 4 cell types. But the curvature was based on the distribution of the cells themselves.  Chirality wasn't specifically studied in the paper, but I think (given that they were staring at individual fibers with an electron microscope) that they would have noticed it had it existed.

Cortical cell types and intermediate filament arrangements correlate with fiber curvature in Japanese human hair
http://www.sciencedirect.com/science/article/pii/S1047847708002980

  Naturally straight and curved human scalp hairs were examined using fluorescence and electron microscopy techniques to determine morphological and ultrastructural features contributing to single fiber curvature. The study excluded cuticle and medulla, which lack known bilateral structural asymmetry and therefore potential to form curved fibers. The cortex contained four classifiable cell types, two of which were always present in much greater abundance than the remaining two types. In straight hair, these cell types were arranged annularly and evenly within the cortex, implying that the averaging of differing structural features would maintain a straight fiber conformation. In curved fibers, the cell types were bilaterally distributed approximately perpendicular to fiber curvature direction with one dominant cell type predominantly located closest to the convex fiber side and the other, closest to the concave side. Electron tomography confirmed that the dominant cell type closest to the convex fiber side contained discrete macrofibrils composed of helically arranged intermediate filaments, while the dominant cell type closest to the concave side contained larger fused macrofibrils composed of intermediate filament arrangements varying from helical to hexagonal arrays approximately parallel to the longitudinal fiber axis. These findings concur with the current hypothesis of hair curvature formation and behavior.


Can foxes move their ears independently?

Yes, they can. Here are a couple pics I found of foxes moving their ears independently:

This is something all canids can do (1)(2) Btw, I can move my ears independantly. It's all in the finding the right muscles.


Why are triacylglycerols broken down before being absorbed?

Your question does not have a clear answer yet, as stated in Metabolic regulation: a human perspective / Keith N. Frayn. – 3rd ed (2010) on page 39.

  There is still debate about how fatty acids cross cell membranes.

On that page they claim that a simple diffusion transport is possible through a 'flip-flop' mechanism, where the fatty acid inserts itself in the membrane and then experiences a reversal movement. The kinetics of the process seem to be in agreement with the observed utilization rates.

Also, it is claimed that there is growing evidence specific fatty acid transporters like FAT and FATP (fatty acid translocase and transport protein) play a key role in the process. They might join forces with the fatty acyl-CoA synthase, consuming ATP. ATP consumption activates them, i. e provides energy, for the acyl-CoA formation (not in order to move against gradient). The activated state would enable them to both move into the cell and regenerate a triacylglycerol.

Why do these (triacylglycerols) have to be broken down in order to be absorbed?

I would say that the hydrolyzed products (fatty acid and glycerol) are more readily internalized because their structure is simpler. Fatty acids can perform the flip flop mechanism, but whole triacylglycerols might not (I am not sure). There is a fatty acid binding protein that may help maintain the fatty acid importation gradient too.

What is the driving force for reformation once absorbed?

It is the secretion of chylomicrons loaded with regenerated triacylglycerols. Since they are secreted, they don't pile up inside the enterocyte (intestine cell) and the equilibrium in the synthesis route (the monoacylglycerol esterification pathway) favors the production of triacylglycerols.

Remarkably, not all fatty acids are reesterified, those of short length (< 14 carbons) are not compatible with the acyl-CoA synthase and enter the plasma in a free state. That happens when digesting dairy products.


Can humans perceive sounds above 20 kHz?

Yes, we can. By means of bone conduction we can hear up to 50 kHz, and values up to 150 kHz have been reported in the young (Pumphrey, 1950). However, it is indeed generally agreed that 20 kHz is the upper acoustical hearing limit through air conduction. The reason for this is debated, but the transfer function of the ossicle chain in the middle ear is a suspected culprit in setting the upper frequency limit to 20 kHz (Hemila et al., 1995).

Hence, using normal speakers or headphones 20 kHz is a very reasonable absolute upper limit. Note that the Nyquist criterium necessitates higher sampling rates (at least 40 kHz), so your statement of using 50k-60k sound cards is correct. If you decide on using bone conduction aids, you might start to think on using higher sampling rates still.

Here is an example of a commercially available bone conduction head set (AfterShockz):

These devices have the potential to increase the upper limit because they bypass the middle ear and hence circumvent the limiting transfer function of the middle ear. They induce vibrations onto the temporal bone, that travel via the bone directly to the inner ear. See the following picture from The High Tech Society:

As a side note: when you grow older the hearing sensitivities at high frequencies  are severely reduced, and even the 6 kHz range is severely affected in the elderly (picture from John Perr's website):

Disclaimer: I haven't looked into the capabilities in terms of upper frequency limits of bone conduction head sets. I am just talking theoretical limits.

References
- Pumphrey, Nature 1950; 166:571
- Hemila et al., Hear Res 1995; 85:31-44


What species is this fast-moving spider?

Pawelek;

Unfortunately, I'm not very experienced at European spiders, but I suspect you're looking in the wrong place.  First of all, this appears to be an adult male spider (large ball-like structures at the ends of the pedipalps, in front of the 'face'), so the body pattern is probably going to be a bit different from the one you see on the females.  Male patterns are often an afterthought in identification references, unfortunately.

Secondly, this doesn't look much like a Pholcid to me - I'm getting more of a Linyphiid impression, from the shape of the abdomen, the visible patterns on cephalothorax and abdomen, and the filmy sheet it's hanging under.
I wish I could be of more help than this - but perhaps Ed Nieuwenhuys can help.  Here's a link to his site; if you look down toward the bottom, there's a contact link you could send him a photo and this question:

https://ednieuw.home.xs4all.nl/Spiders/spidhome.htm


Question about microaerophilic parasite tolerance for oxygen

Short answer: 50-60 µM O2 is ok; 80 µM is toxic.

Giardia lamblia (aka intestinalis) is a microaerophilic intestinal parasite.

According to:

  Lloyd et al. (2000) The microaerophilic flagellate Giardia intestinalis: oxygen and its reaction products collapse membrane potential and cause cytotoxicity. Microbiology 146: 3109 - 3118

Giardia colonises the upper intestine, and the oxygen concentration there has been measured at 60 µM. At oxygen concentrations up to 50 µM the organism can scavenge oxygen; above 80 µM oxygen inhibits the oxygen-scavenging process. In this paper the authors used 10% air (equivalent to 25 µM oxygen) to characterise  oxygen toxicity.

The source of oxygen sensitivity was investigated by:

  Li and Wang (2006) A likely molecular basis of the susceptibility of Giardia lamblia towards oxygen Molecular Microbiology 59: 202 - 211

These authors propose that the enzyme DT-diaphorase, previously suggested as a component of the oxygen detoxification system promotes the formation of reactive oxygen species which lead to death. Thus they found that overproduction increased sensitivity to oxygen, whereas a knock-down decreased sensitivity. This work does not, however, use controlled microaerophilic conditions.


How is Pseudomonas aeruginosa diagnosed?

Well, the answer is actually a Wikipedia search away. But from the 7th edition of the book Microbiología Médica and Todar's Online book of Bacteriology:

Nutriotional needs. Simple. Part of why Pseudomonas spp. grows everywhere is that it can metabolize a wide array of carbon and nitrogen-containing compounds. Blood agar and McConkey are enough for its growth.
Colonies. They generally show a mucoid appearence and are flat.
Respiration. Practically an obligate aerobe. Usually oxidizes glucose, but it is capable of anaerobic respiration as well, using nitrates or arginine as electron donors. The cytochrome oxidase assay is positive, unlike Enterobacteriaceae and Stenotrophomonas.
Pigmentation. P. aeruginosa synthesizes pyoverdin (fluorescent and green) and pyocyanin (blue and water-soluble). Pyocyanin is produced when the presence of iron in the media is low, however, and not all strains synthesize it.
Temperature. Its optimal temperature is 37ºC, but its survival range is quite wide, from as low as 4ºC to as high as 42ºC.
Antibiotic resistance. And to many antibiotics. The presence of beta-lactamases makes P. aeruginosa withstand penicillin, carbapenems and cephalosporins.
Odor. Cultures emit a pleasant aroma that most associate with grapes or soap.

Wikipedia does show a nice battery of tests that identify P. aeruginosa, but if I were you I would compare them to other sources.

Positive: oxidase, citrate, motility, gelatin hydrolysis, acid production (from glucose and mannitol), nitrate reduction, lipase, pigmentation (green or blue), catalase and beta-hemolysis.
Negative: Gram staining, indole production, methyl red staining, Voges-Proskaeur (?), hydrogen sulfide production, urea hydrolysis, phenylalanine deaminase, lysine decarboxylase, acid production (from lactose, maltose and sucrose) and DNAse.


Traceability of a mature tree to its original seed via DNA

As the embryo of a seed typically contains many cells, it should in theory be possible to obtain DNA from a seed without disrupting it (there may be pragmatic issues with protocol, depending on the particulars of the seed).
If you have the DNA and each seed has been produced by a separate fertilization event, then each seeds DNA would be unique and it should certainly be possible to identify an individual genetically, just like it is with animals.
Not all seeds are genetically distinct however. For example, many plants will also produce seeds asexually under appropriate conditions, a process known as apomixis. If the seeds are being produced asexually, then your only hope would be to identify different mutations in different seeds, which is a much fainter signal and likely to fail for your intended purpose.


Multiplex PCR, shorter amplicon inhibiting longer amplicon?

It turns out that the $T_m$ was in fact the issue, or rather, that the computation algorithm overestimated the $T_m$ of the primer pair for the longer amplicon (or underestimated that of the shorter one). At any rate, it seems that at 60°C the shorter amplicon primers hijack the polymerization mechanism.

Setting the annealing phase temperature to 55°C solved my issue, and now I consistently get better results:


Human sleep cycles and dream times, what influences the timing and intensity? Sleep history included

I'm interested in learning what influences the desire to go to bed at
  a particular time? What influences the getting out of bed times?

It is the circadian rhythm. Circadian rhythm is mediated by the suprachiasmatic nucleus of hypothalamus, which gets afferent nerves from optic nerve. So, the circadian rhythm is mediated by light. Initiation of the NREM Stage 1 sleep is controlled by the lateral preoptic nucleus, which is another area in the hypothalamus, so it is mainly the absence of light which starts sleep.

  I'm also interested in any insight as to what's causing me to wake up
  at certain times and report dreams.

Sleep is not equal to absence of consciousness, it is just an diminished state of consciousness. Sleep consist of mainly 4 stages, NREM-1, NREM-2, NREM-3 and REM. Every stage, the "depth" of sleep, or the level of the decrease in your consciousness changes. REM is the stage in which dreaming most frequently occurs, and also it is the sleep stage where your consciousness is highest, so you are more likely to awake because of the stimulus coming from the environment.


I will just show the statistics of last attempt to mimic the brain process.

In 2011 fastest computer in Japan was launched:

K computer OR SPARC64 VIIIfx 2.0GHz

Features:

Manufacturer:    Fujitsu
Cores:   705,024
Linpack Performance (Rmax)   10,510 TFlop/s
Theoretical Peak (Rpeak) 11,280.4 TFlop/s
Power:   12,659.89 kW
Memory:  1,410,048 GB (16GB RAM per CPU)
Processor:   SPARC64 VIIIfx 8C 2GHz (88,128 CPUs, 8-core each)
Operating System:    Linux

It's currently world's 4th fastest supercomputer.

Source: Top 500 Supercoputers

Image Source: http://wondergressive.com/wp-content/uploads/2014/01/WG-k-computer.jpg

Now,

  An 83,000-Processor Supercomputer Can Only Match 1% of Your Brain

  ...The most accurate simulation of the human brain to date has been
  carried out in a Japanese supercomputer, with a single second’s worth
  of activity from just one per cent of the complex organ taking one of
  the world’s most powerful supercomputers 40 minutes to calculate.
  Researchers used the K computer in Japan, currently the fourth most
  powerful in the world, to simulate human brain activity. The computer
  has 705,024 processor cores and 1.4 million GB of RAM, but still took
  40 minutes to crunch the data for just one second of brain activity...

  Source: http://gizmodo.com/an-83-000-processor-supercomputer-only-matched-one-perc-1045026757

Human Brain:

  Do we have brain to spare?

  by David A. Drachman, MD

  Within the liter and a half of human brain, stereologic studies
  estimate that there are approximately 20 billion neocortical neurons,
  with an average of 7,000 synaptic connections each.1 The cerebral
  cortex has about 0.15 quadrillion synapses—or about a trillion
  synapses per cubic centimeter of cortex. The white matter of the brain
  contains approximately 150,000 to 180,000 km of myelinated nerve
  fibers at age 20, connecting all these neuronal elements. Despite the
  monumental number of components in the brain, Szentagothai estimated
  that each neuron is able to contact any other neuron with no more than
  six interneuronal connections—“six degrees of separation.”

Image Source: http://www.nature.com/polopoly_fs/7.2933.1329907514!/image/far-to-go.jpg_gen/derivatives/fullsize/far-to-go.jpg

Why Brain beats Supercomputer?

  Why is it so hard for computers to reproduce what your grey matter
  does as a matter of course? Volume. The human brain consists of about
  200 billion nerve cells (neurons) that are linked together by
  trillions of connections called synapses. As the tiny electrical
  impulses shoot across each neuron, they have to travel through these
  synapses, each of which contains about 1000 different switches that
  route that electrical impulse. In total, one human brain could contain
  hundreds of trillions of these neural pathways. It's like a Choose
  Your Own Adventure book that stretches from here to Jupiter.


Antimalarials, fever, age (of the RBC), other drugs, and a host of other things increase oxidative stress in RBCs (which results in the production of H2O2.)

The line you point out as a problem is a bit confusing, but it is entirely correct. It helps to keep in mind that 'glutathione' exists in two forms in the cell: glutathione disulfide (GSSG) and glutathione (GSH). GSH is the reduced form. So a reduction in GSH (the reduced form) does lead to an increase of H2O2.

Another way to say it is that in the absence of G6PD, the amount of reduced glutathione is decreased.

Glucose is used by RBC's as food, and G6PD is needed to metabolize it. G6PD reduces a molecule of NADP to NADPH + H+, which then reduces glutathione disulfide into GSH (reduced glutathione). That molecule is used in the reduction of H2O2 to H2O.

If there is a deficiency of G6PH, there will not be enough NADPH to reduce GSSG, leading to decreased levels of GSH; H2O2 levels rise, and oxidative damage to proteins in the RBC occurs.

  Glutathione metabolism consists, in large part, of its oxidation to the disulfide and recycling to the reduced form by the co-enzyme nicotinamide adenine dinucleotide phosphate (NADPH) by mediation of glutathione reductase (Figure 1⇓). Reduced glutathione is important in the detoxification of free radicals. In normal cells, NADPH is regenerated by G6PD during oxidative stress. Impairment of this step prevents reduced glutathione recycling, exposing the cell to oxidative damage. Alternative pathways to G6PD-dependent NADPH production exist in most human cells but not in erythrocytes, and the lack of protein synthetic machinery deprives the erythrocyte of the opportunity to replace enzyme that has been lost. For these reasons, these cells are uniquely vulnerable to oxidative stress in G6PD deficiency.

These damaged proteins bind to the red cell membrane, which is then processed in the spleen; the spleen removes the damaged part of the RBC membrane. A few passes of this, and the RBC can no longer maintain the integrity of its cell membrane, and it breaks up (hemolysis).

Glucose-6-Phosphate Dehydrogenase Deficiency and Antimalarial Drug Development


Initial guess based on mouthparts, coloration and small size:

Neuropteran larva. Possibly a green lacewing (family Chrysopidae).

See:

 Source: Bugguide.net

 Source: Cedar Creek Ecosystem Science Reserve

According to here, green lacewings are found in Arizona deserts.

I will update in the morning with more detail...


Can oxygen diffuse out through the lungs?

Yes.  Blood will continue to circulate (as long as you're alive and your heart is beating), so will eventually come in contact with your lungs.  Once there, the gasses (O2, CO2) will cross out into the lung and be exhaled.  All diffusion is driven down a concentration gradient.


What causes people to feel sleepy due to recycled air?

Carbon dioxide is not the only waste product which is exhaled. NASA scientist Wolverton goes into detail in his book, "How to Grow Fresh Air".  We exhale 70% of the body's waste products in gaseous forms.  Breathing these in repeatedly and at ever-higher concentrations causes a whole host of health problems, starting with, you guessed it, an inability to stay alert and sustain full brain function.


Ammonia smell after physical exercise? What is the explanation?

There are two explanations which come to mind answering your question:

I asked if you eat a lot of protein, because the amount of protein which some body builders consume leads to renal failure. And one sign of renal failure is the smell of ammonia. It's a quite common problem. But I don't think this applies to you. Your protein intake shouldn't exceed 2g per kg of body weight per day, some body builder eat up 4g per kg.

Ammonia is normally linked to your protein metabolism, which is higher during and after sport. The smell of Ammonia can occur when your carbohydrate reservoir is depleted and the body is mainly using protein as fuel. This effect also occurs when fasting or in patients with diabetes.

Try to keep your blood sugar level raised during exercise by eating something, like a banana, powerbars (also known as high energy bar) or directly dextrose. Or eat more long-chain carbohydrates. And this always depending the form of sport you are practicing. Just like the pasta party prior to marathons.


Nice find. It's a common basilisk or jesus christ lizard, distributed throughout central america, they grow to 27 inches and can run on water, the male is bigger than the female:

https://travel.mongabay.com/colombia/images/colombia_1513.html


Causes of the stochastic behaviour of voltage-gated ion channels

The fluctuations arise form thermal energy and can be described by the Eyring equation


I see big fuzzy bands around 100bp as well. They're most likely RNA contamination. To get rid of them, digest your RT-PCR products with RNAse-H. But if you just need to visualize your band of interest, and the fuzzy bands aren't getting in the way, it shouldn't be a problem.

I usually input anywhere from 1-2 ug of RNA into my RT-PCR reaction using the Invitrogen Superscript III kit for a total volume of 20 ul. After the reaction, I use 1/10 the volume of that (2 ul) for downstream (PCR) applications. This usually gives me nice results.

To optimize RT-PCR for detection of a specific target, consider using gene specific primers (make sure to use only anti-sense primers) in your RT-PCR instead of oligo-dT or random hexamers. This enriches your target when you use them for downstream applications. When you use GSPs though, make sure to run a parallel reaction with control (i.e. beta actin) primers to prove that your RT-PCR reaction is working.


Choosing appropriate statistical test for ordinal data

You can use ordinal multinomial regression (also known as ordered logit) if the response is ordered. These methods are basically extensions of logistic regressions, but using e.g. a cumulative logit instead of the logit. However, there are a number of different assumptions you need to consider. For instance, are you going to use a proportional-odds assumption (which is commonly used), which means that there is an equal probability of going from e.g. class 1 -> 2 and class 5 -> 6? You can also evaluate the proportional odds assumption using plots or a score test. If the response cannot be ordered, there are multinomial nominal methods that you can use, and you can also evaluate the results from an ordered analysis by comparing the predictions with ones from a multinomial nominal analysis. I have used these kinds of methods for the analysis is Red list classifications, which are clearly ordered but cannot simply be transformed into a numerical response (similar to your situation).

The book Analysis of Ordinal Categorical Data (Agresti. 2010) is a really good starting point.

In R you can look at the packages polr and vgam for ways to perform different types of analyses on ordinal data. The author of the book above has also published some examples for categorical data analysis in R, using the packages I mentioned: Examples of Using R for Modeling Ordinal Data. In SAS similar analyses can be done using Proc Genmod and Proc Logistic.


How do poiklotherms survive at different temperatures even though enzymes work at specific temperature?

Instead of viewing poikilotherms as having the same temperature as the environment, view them as lacking an internal thermoregulatory system. Poikilotherms indeed suffer from not having the ability to regulate their internal temperature.

Homeothermy is ecologically advantageous, allowing optimal functioning at a range of temperature. Poikilotherms, therefore, are more restricted in their habitat range, have to depend on external mechanisms for maintaining temperature (eg: Hibernation, Shade-loving lizards, burrowing in desert animals) or simply die due to environmental change (eg: poikilothermic fish are the earliest to die from a thermal runoff into a water body).


Temporal kinetics does not refer to the kinetics of kinase phosphorylation reactions and, since it is not standard terminology, you likely wouldn’t find its meaning in any textbook.
The authors of the paper quoted in the question use the phrase temporal kinetics to describe the phosphorylation state of a proteome-wide selection of kinase substrates (ie phosphorylation sites in proteins) over time. The general idea is that since one kinase can phosphorylate many substrates, clustering substrates based on their temporal kinetics (ie the times at which they become phosphorylated or dephosphorylated) can help identify the kinase and signaling pathway involved.
Fig 6B in the paper (shown below), for example, illustrates how 3,178 phosphorylation sites can be clustered based on the time-course of their phosphorylation and/or dephosphorylation after treatment of mouse adipocytes with insulin. As discussed in the paper, each cluster can be associated with one or more kinases based on known kinase-substrate interactions.


What determined the evolution of different faces in humans?

Given the prevalance of myopia in humans I would have thought that facial recognition was secondary to other indicators such as gait recognition which is also unique to individuals though can be copied to an extent. Voice and shape are also used to identify people.

Being able to recognise individuals would allow the formation of groups, allow for structures of trust, reciprocal altruism to develop as well as punishing transgressors. Repeat interactions with other people require some kind of identification, but I dunno if facial recognition is the only/primary one.


which exact mechanism triggers the first cell differentiation after n divisions?

The first differentiation in human embryogenesis is from early blastomeres into trophoblast, which forms the outer layer of the blastocyst, and inner cell mass (ICM). It may be unsurprising then that cells on the inside of the 8-16 cell stage morula
differentiate into ICM whereas those on the outside differentiate into trophoblast. However it is currently unclear whether this is a causal relationship (the inside-outside model) or whether blastocyst patterning is set-up earlier in cleavage (such as in the apicobasal polarity model) or if it is some combination of the two.

You were correct in imagining that tissue patterning is determined by chemical substances: a very broad class called morphogens. Cells don't necessarily count how many times they have divided but cell division can certainly affect morphogen concentration and localisation. I suppose in some sense you could describe this as a clock. I wouldn't though, especially because mammalian cleavage is asynchronous.

One line of studies showed that a transcription factor called Tead4 specifies trophoblast$^{ref}$. It was then shown that Tead4 can be regulated by cell-cell contact (mediated by Hippo signalling) $^{ref}$. They hypothesised that the magnitude of cell-cell contact could provide a mechanism by which Tead4 localisation could be controlled in presumptive trophoblast and ICM. This could explain why the cells have different fates because inner cells are completely surrounded (more cell junctions) whereas outer cells are largely exposed to the medium. Note that I only provided that as an example of a possible mechanism. It is not confirmed and, as with any model, the real picture is incredibly more complex and likely involves many factors.

I'm reluctant to go into too much detail on this because you're asking about a complex process that is still under active study and I'm unclear as to how much information you actually want. A book could be written on this subject alone, and many review papers have been published. Here's a recent one:

Development: Do Mouse Embryos Play Dice?

I suggest you read that and then if you have further, more specific questions, we can try and answer them for you.


Why is there a distinction between an *allergic* and an *immune* response?

The trouble is, you can't live without being exposed to all sorts of non-self particles. Some of those particles signal an actual threat to your health (proteins associated with a disease causing virus), some are nearly harmless (bee stings), some are completely harmless (grass pollen or cat dander), and some are potentially valuable as part of a food substance (seafood or peanuts). Ideally you'd like your immune system to respond to the harmful ones, and ignore the harmless or useful ones. An allergy is defined as an unneccesary immune response to a harmless (or nearly harmless) substance.
You do want your immune system to deactivate venom from a bee sting, but you don't want it to react so strongly that as a side effect your throat swells up and you can't breathe. Most people breath in grass pollen every day of their live with no ill effects, so those folks who have an allergy to grass pollen are being made miserable by their immune system to no good purpose.
Ideally the immune system mounts a full response only when the presence of particular non-self particles is associated with other signals indicating that something "bad" is happening which merits an immune response. However, the process by which the immune system is regulated is incredibly complex, involving feedback loops from hundreds of different chemical pathways and dozens of different cell types. The process is imperfect. Sometimes it goes wrong, and the immune system mounts an aggressive response to a harmless foreign substance or even worse part of your own body.


During a large forest fire, what is the evacuation behavior of birds?

The exact behaviour of birds during a wildfire is unclear and there is little scientific evidence on their exact behaviour. Anecdotal notes from eye witness observations indicate that healthy birds fly away from the affected area before they are in danger. Birds that are unable to fly or move out of danger from the fire such as chicks in nest and indisposed birds are likely to die. Different species are likely to react differently to fire, species that flock normally will probably flock together as they fly and species that are more solitary are not likely to flock. Most fires happen in late summer and fall, just after the breeding season for most birds and during their migration, meaning they can escape the area. If the fire is very widespread, the birds may not be able to find appropriate shelter and food and would likely die as a result.

Wildfires are a natural phenomenon and birds have evolved to adapt strategies to deal with them. Some birds benefit from wildfires as they are a normal part of ecological succession.

  Ecological succession is the gradual process by which ecosystems
  change and develop over time in response to a disturbance or
  colonization of new habitat.

Fire essentially creates a new habitat in which not all the same birds will use. Blue Jays prefer forests, but if a wildfire burns a forest, it will likely become a shrubby field afterwards and may take years to regrow into a forest. The Blue Jays will not likely return in large numbers until the habitat is a forest again.

A remarkable bird that is dependent on forest fires is the Kirtland’s Warbler. They breed in Jack Pine forests that are a certain height, once the forests mature; the habitat is no longer suitable. The jack pines themselves only release their seeds from cones in hot fires as they are serotinous and only open when exposed to intense heat, greater than or equal to 50 °C, the typical case is in a fire. The wildfires then create a succession cycle to always have suitable habitat for the Kirtland’s Warbler. Fire suppression of forests by humans has been listed as one of the reasons that led to large declines of this species.

Additional reading:

How Wildfires affects Birds?

Jack Pine Information


Degenerate primer design for DIG in situ hybridization

If the gene is supposed to be well conserved then you can use the sequence from the related species.

For protein coding genes target the ISH probe to the coding region which is more likely to be conserved.

What you can also do subsequently is to:

amplify the CDS
do 3' and 5' RACE
Clone in a plasmid (do a blunt end or TA cloning)
Sequence the insert
Design exact primers

  are there any other good databases for gene sequences?

EMBL and DDBJ


Why can't diamine oxidase be supplemented?

The article nowhere mentions diamine oxidase(DAO) cannot be suplemented.
DAO supplementation
The link clearly supports DAO can be used. Though Triptans like sumatriptans are used because of cost.
Note: Research is of 2018, so not your fault.


It  is a jumping spider. Could be Genus Epocilla sp. .

Jumping spiders have their posterior lateral eyes placed high up the cephalothorax and the rest three pairs in a typical arrangement as observed in your specimen.

An image of Epocilla sp. from Wikipedia.

Your specimen more closely resembles the E. calcarata .


What does the term 'glycogen mobilisation' mean?

I think the key to understanding mobilization in this context is in the second sentence:

[Glycogen] can be broken down to yield glucose molecules when energy is needed.

The authors are using mobilize in a figurative sense to suggest that glycogen can be quickly and efficiently metabolized to suit the energy needs of the body, like an army may be mobilized to fight a war.  See definition #2 on Wiktionary:

mobilize (verb)
2. (transitive) To assemble troops and their equipment in a coordinated fashion so as to be ready for war.


Do fish break a water molecule to absorb oxygen?

The answer to this, I reckon, is that they don't.

They use molecular oxygen (O2) dissolved in the water for respiration, where it acts as a terminal electron acceptor, just as we use molecular oxygen in the air for respiration. We can speak of the water as being oxygenated.

Water is split in photosynthesis, where reducing equivalents from water are used to reduce NADP+ (giving NADPH).

One of the great discoveries of biology, IMO, is that the oxygen formed in green-plant photosynthesis comes from water, not CO2.

Tricarboxylic Acid Cycle (Krebs Cycle) Rant

Despite claims to the contrary, most infamously by Racker (1976, pp 28 - 29) and Wieser (1980), but also by Madeira (1988) and Mego (1986) for example, water is not split in the tricarboxylic acid cycle (Krebs Cycle). Banfalvi (1991) also sails pretty close to the wind on this one.

That is, reducing equivalents from water are not passed down the respiratory chain, or in any way used to make ATP, or are in any way a 'source' of free energy.  Such claims, IMO, are nonsense.

The definitive answers to the Wieser (1980) paper are given by Atkinson (1981) and Herreros & Garcia-Sancho (1981). Both of these articles are models of clarity, and categorically refute the claims of Wieser (1980).  Nevertheless, as shown by the references above, the controversy surfaces periodically.

The only sources of reducing equivalents in the TCA cycle are carbon compounds, and the only electrons passed down the respiratory chain are those 'held' in C-H and C-C bonds (Herreros & Garcia-Sancho, 1981).  An ionization is neither an oxidation nor a reduction (see Atkinson, 1981) and neither is a hydration. Adding water to (say) a double bond does not make the compound any more oxidized or reduced.  As far as oxygen and electrons are concerned, and to generalize from a biological point of view, what is has it holds - except in photosynthesis.

As you may have guessed, the splitting of the water in the TCA cycle is a pet rant of mine.  Thanks for the opportunity of airing my views!

Edit 3

Found this one when searching Google (Brière et al, 2006).  In an invited review for the American Journal of Physiology (Cell Physiology) at that!

  Finally, TCA cycle should also be considered as a water-splitting process generating oxygen for acetyl-CoA oxidation [they quote Wieser]

So now the TCA cycle is producing oxygen from water.  Wonders will never cease!

(end edit)

(end rant)

Edit 2

As rwst and Alan Boyd have drawn attention to, the concentration of dissolved oxygen in water is all important, and varies with (for example) temperature.

In air-saturated buffer at 25oC the concentration of oxygen (O2 molecules) is about 0.24 mM (0.24 μmoles/ml, or about 0.474 μg-atoms of oxygen per ml). [Chappell (1964)]. This figure decreases with increasing temperature.

Great question, BTW.

References

(Apologies for the incomplete Atkinson and Herreros & Garcia-Sancho references. I have a photocopy of these papers but have been unable to trace the full source. They are both in the 'Letters to the Editor' section of the February 1981 edition of Trends in Biochemical Sciences. They do not appear to be in Pubmed, or anywhere else on-line.  Has anyone ever seen these references quoted, or can provide me with a full source?.  I'll update if I find anything)

Atkinson, D.E. (1981) TCA Cycle Confusion.  Trends in Biochemical Sciences (February 1981 edition; full ref to follow)
Banfalvi,G. (1991)  Conversion of Oxidative Energy to Reductive Power in the Citrate Cycle. Biochemical Education, 19, 24 - 26  [see here] (pdf apparently free to all)
Brière, J.J., Favier, J, Gimenez-Roqueplo, A.P. & Rustin, P (2006) Tricarboxylic acid cycle dysfunction as a cause of human diseases and tumor formation.  Am J Physiol Cell Physiol, 291, C1114-20. [Pubmed]  [pdf]
Chappell (1964) The oxidation of citrate, isocitrate and cis-aconitate by isolated mitochondria. Biochem J., 90, 225-237.[pubmed]  [pdf]
Herreros, B. & Garcia-Sancho, J. (1981) TCA Cycle Confusion.  Trends in Biochemical Sciences (February 1981 edition; full ref to follow)
Madeira, V.M.C. (1988) Stoichiometry of Reducing Equivalents and Splitting
of Water in the Citric Acid Cycle.  Biochemical Education 16, 94 - 96 [pdf] (apparently free to all.)
Mego, J.L. (1986)  The Role of Water in Glycolysis Biochemical Education,  14, 130 - 131. (see here)
Racker, E. (1976) A New Look at Mechanisms in Bioenergetics.  Academic Press, New York.
Wieser (1980) Textbook Errrors: The splitting of water by the tricarboxylic acid cycle.  Textbook error or textbook omission? Trends in Biochemical Sciences, 5 (Issue 11), 284. [see here].  [pdf], apparently free to all.

Edit 4

I have not been able to locate the exact reference for the incomplete Atkinson and Herreros & Garcia-Sancho references cited above but, in response to this great question, I have put a copy of a very bad scanned version here

Another great reference to this controversy which I should have quoted is the
following:

Losada, Manuel
. (1978) Energy-Transducing Redox Systems and the Mechanism of Oxidative Phosphorylation. Bioelectrochemistry and Bioenergetics, 5, 296-310 [Science Direct].

The following is the relevant section, for those who do not have access:

A more complete version of the Racker reference quoted above by Losada (1978):

However, pyruvate has only 4 hydrogens to donate to 2 oxygens and with a P:O ratio of 3 should therefore yield only 6 molecules of ATP (Table 1.2). Where are the other 6 hydrogens coming from so that 15 ATP can be formed? The answer to this question gives us what I think is the key to the puzzle why nature has designed the complex acrobatic scheme of the Krebs cycle. Its major purpose I believe is to increase the energy yield by catalyzing cleavage of water.

There are three steps at which water enter the Krebs cycle. - one at the transformation of fumarate to malate an the other two somewhat more indirectly during the utilization of acetyl-CoA and succinyl-CoA. In the course of the Krebs cycle the hydrogens of these water molecules are separated from oxygen and are donated to DPN or to a flavoprotein (e.g., succinate dehydrogenase) and then transported via the oxidation chain of mitochondria as electrons and protons as we shall discuss later.

[Racker, E. (1976).  A New Look at Mechanisms of Bioenergetics, pp 5-6, Academic Press].

IMO, the last sentence of this quote is complete rubbish. (For DPN, read NAD. DPN, or diphospo-pyridine-nucleotide (or something close), is an old name for NAD)


Why is the  microbial ecosystem of the gut so susceptible to disruption by pathogens?

There are two types of food poisoning:

Alimentary intoxication

This is the case when you consume food which is contaminated with some toxins, and those are responsible for development of the poisoning symptoms. The source organisms of these toxins might not be present anymore (killed by heating during cooking, for example). In this case there is no massive invasion of any foreign organisms into the gut.

Alimentary toxico-infection

This happens if you eat the food contaminated with microorganisms, and these start to massively proliferate in your alimentary system causing the symptoms of poisoning. The massive intake of the bacteria (even 2-3 spoons of contaminated food might contain millions of bacteria, like Staphilococcus in contaminated diary products). In this case the balance of gut microflora is dramatically changed due to introduction of a considerable amount of foreign microorganisms.

So, even the poisoning seems to be "minor" (e.g., its symptoms are not so dramatic), there could be different amounts of bacteria invading the guts.

The second important point here is the increased emptying of the gut due to diarrhea that leads to the washing out some of the "good" bacteria from the guts, especially in case of profuse diarrhea. The newly coming bacteria are not necessarily those that are present in normal microflora, and it takes days or even weeks until the microflora reaches homeostasis again.

One last point: even without poisoning, microflora varies, and the amount of different bacterial fractions can fluctuate over time. This is normal and depends upon your eating habits, your environment, immune status, and many other factors.


Why do people dying of immune deficiency diseases appear sick?

Many of the symptoms of disease are indeed related to inflammation, but inflammation depends heavily (though not solely) on the innate immune response.  Patients with AIDS and some of the other immunodeficiencies lose their adaptive immune response, not their innate response.  Therefore they are capable of mounting an inflammatory response that is not effective in clearing pathogens (because it doesn't have help from the adaptive immune system) but can still cause symptoms.

More importantly, many symptoms of disease are not caused by the inflammatory response, but are related to organ and tissue damage caused by the infection.  A patient with pneumonia may have a reduced inflammatory response but will still have difficulty breathing and signs of reduced oxygen supply simply because the lung tissue has been damaged by the pathogen.


A synthetic sieve organ known as kliver?

This term is used in this book (Synthetic Biology, The National Academies Keck Futures Initiative, p.43). This book is a summary of several interdisciplinary team discussions during a  conference held in 2009.

One...

  [...] team considered building artificial organs. Engineered to be hypoallergenic, these could allow for a mass production of personalized organs. Their novel and broad functions could also be useful for medical testing. In a single artificial organ, one might screen potential drugs for both toxicity and permeability.

  For instance, group members proposed the idea of a "kliver", a kidney-liver hybrid. An independent "kliver" could help filter bio-compounds out of drinking water.

There are some more paragraphs revolving around the question how to build a "kliver" and a final paragraph concluding that enough necessary building blocks were available and researchers could start working on it:

  Potential building blocks might be mammalian and microbial cells and their products, such as slime, fibers, small molecules and proteins. The cells might be engineered to hold new electrical, mechanical, and chemical powers.
  [...]
  Cells would be programmed to degrade their organs and DNA if they began to invade other organisms or the environment. A genetic "kill switch" aims to stop contamination or infection.

Summarising this, I wouldn't call it a "popular term".


Safe parameters for external nerve stimulation using electrical impulses

Nice question(s). I will go through them in sequence.

Safe current limits. With regard to electrical stimuli it is current density that determines safety limits. Therefore, in medical devices, it is not a matter of what is a safe maximum current level, but what is the maximum safe current level given the surface of the electrode? And in terms of skin stimulation, it is not the safety limit that is the bottle neck, but the maximum tolerable current density, which is around 0.5 mA/cm2 (Prausnitz, 1996). Higher stimuli result in pain sensations. This is one of the reasons why the BrainPort device is used on the tongue; the moist surface reduces impedance and hence the currrent needed to elicit a tactile response.
Permanent damage. As said, the tolerable sensation limit is more of an issue (a must-read in this regard is Kaczmareck et al., 1991).
Acuity. The best-possible tactile "resolution" is generally expressed in terms of tactile acuity. Tactile acuity varies across body sites, and unfortunately it is about the worst on the thigh (45 mm) and the back (40 mm). A much cited picture on tactile acuities is the following from Weinstein (1968):

These acuities represent the distance in which 2 simultaneously presented, static pressure points need to be spaced to be just noticeable (the so called two-point discrimination threshold). Although your proposed electric stimuli are different from pressure stimuli, these reported values in the figure (40 - 45 mm) give an impression on the inter-electrode distance needed. From my own work I can confirm the ~40 mm using vibratory stimuli. The unfavorable acuity of the back and external bodily skin in general was also one of the rasons to put the electrode grid of the BrainPort on the tongue, which has excellent tactile acuity.

References
 - Kaczmareck et al. IEEE Trans Biomed Eng 1991;38:1-16
 - Prausnitz, Adv Drug Delivery Rev 1996;18:395-425
 - Weinstein S. 1968. In: Kenshalo. The Skin Senses:195-222. Springfield, IL: Thomas


Why does water stress lead to alkalinity of xylem sap in plants?

According to recent studies, drought stress does not consistently lead
to increases in the pH of xylem sap. One article which discusses
interspecies differences is Vit Gloser, et al., "The dynamics of
xylem sap pH under drought: a universal response in herbs?," Plant and
Soil 409, nos. 1-2 (2016): 259-272.

As to what may have prompted the textbook authors to assert this, see an
earlier article by two of the coauthors of the Gloser essay: Sally
Wilkinson and William J. Davies, "Xylem sap pH increase: a drought
signal received at the apoplastic face of the guard cell that involves
the suppression of saturable abscisic acid uptake by the epidermal
symplast," Plant Physiology 113 (1997): 559-573. Wilkinson and Davies
summarize an earlier study: "Hartung and Radin (1989) found that the pH
of xylem sap from water-stressed Phaseolus vulgaris roots increased
from control levels of 6.3 to 7.2." (560)