How is the GenBank used in typical biological research?

Go to Google Scholar. Enter "Genbank" into the search field and press return. Limit the results to 2013 and later (left side of the results).  Skip the few entries that say only "GenBank." Browse through the pages and pages of search results to get a feel for the many ways that GenBank is used in scientific research. It's used from everything for phylogenetic analysis (relationships among organisms) to determining protein structure and so much more.


Is there any knowledge of physics can be applied in to evolution?

There's some. The basic idea is that entropy, as rigorously defined in statistical physics, can be equated to complexity. This is an idea that has been around since at least the 1957 paper by Jaynes. In a fairly hand-wavey way, one can then say that a system that is being fed a large quantity of free energy (as the earth is by the sun) tends to become more complex over time (i.e. evolve).

Thinking this through a bit, the above argument applies as easily to weather patterns as it does to living creatures. Recently, with the rise of computers and modeling there have been attempts to apply these kinds of general ideas (increasing free energy leading to increasing complexity) to living creatures in a more systematic way. Jeremy England is one researcher working on this problem, and this link goes to a pretty good pop-science-style writeup of his work on the topic.


Does Pasteur's experiment contradict an origin of life?

Consider the context. In Antiquity and the Middle Ages from Aristotle on, people thought that many living things (from microbes to mice) would arise through spontaneous generation. Seemed sensible enough; if you don't pay close attention to animals getting somewhere, and you have no knowledge of anything microscopic, it can easily look like animals just come out of the environment. After the Enlightenment scientists got better understandings of reproduction on the one hand, and made many experiments showing that under certain conditions (like keeping meat sealed so flies couldn't get to it for example), life didn't, in fact, spontaneously generate in the way it was previously thought it did. At this point the idea that all living things come from the reproduction of other living things of the same species became increasingly accepted.

Pasteur's experiment was more or less the death knell of the spontaneous generation hypothesis; some previous experiments had shown microbes growing after a flask was supposedly sterilized, or kept the flask sterile by keeping air out (which opened one to the argument that spontaneous generation required air). His showed microbes not growing in a flask where air could flow but dust did not settle because of its shape, and immediately growing when the flask was tipped and dust fell in.

Pasteur's experiment didn't so much "prove that life only comes from life", as disprove a specific other hypothesis that existed at the time. And in that sense it is still consensus biology: No biologist today thinks that snakes, mice, microbes, or even viruses can arise directly through abiotic processes. If you replace "life" with "modern life", the principle is true as far as we know.

Now biology has advanced a lot, and there is a different context, with people asking different questions and advancing different hypotheses to answer them. The question of the origin of life is one such question, that has nothing to do with what Pasteur was trying to prove. And that's where the "modern life" caveat becomes relevant; while all modern living things are too complex and specific to arise directly via abiotic processes, it doesn't follow that the same is true of the first living things. We know that living things used to be different from how they are now; and in fact when looking into the past via the fossil record and genetic evidence we find clear patterns of gradual development of the modern biosphere's diversity and complexity from simpler and more generic ancestors. While it is harder to find evidence for the evolution of early cells, because the genetic evidence is muddled by the time scales involved and the fossil evidence near-nonexistent for obvious reasons, it is sensible to figure that similar patterns would occur there, and that the earliest cells were as different and simpler than a modern cell as a Precambrian worm is from us.

Here is a video of Nick Lane talking about a promising hypothesis on the origin of life. It sort of illustrates how different, and simpler, those primordial living things could have been compared to current organisms.

https://www.youtube.com/watch?v=gb7pZyks_HE&t=1151s


Acquiring Covid-19 vaccination through kissing with viral vector vaccinated person

No, this is not possible, as the vectors used for the vaccination cannot replicate anymore. Some of the genes necessary for this step have been removed from the viral genome to prevent the uncontrolled spread and replaced by the spike protein which is used as the antigen for the vaccination.
To replicate the virus in the production process, a special cell line with a plasmid carrying the genes necessary for the viral replication has to be used, afterwards the virus is purified and outside of these special cells not able to replicate.
For an overview about the adenovirus type 26 based vaccines, see here:

Vaccines based on replication incompetent Ad26 viral vectors:
Standardized template with key considerations for a risk/benefit
assessment


What is the counter-reponse to a sound stimulus?

All stimuli do not generate reactions. It is the CNS that decides if a reaction has to be generated on receiving the information about a stimulus.

  External stimuli are capable of producing systemic responses throughout the body, as in the fight-or-flight response. In order for a stimulus to be detected with high probability, its level must exceed the absolute threshold; if a signal does reach threshold, the information is transmitted to the central nervous system (CNS), where it is integrated and a decision on how to react is made. Although stimuli commonly cause the body to respond, it is the CNS that finally determines whether a signal causes a reaction or not.

From Wikipedia

The changes that occur inside ear,vibration of tympanum, movement of ear ossicles and all are responses to the stimulus (the mentioned two are mechanical responses) to transmit the information about the stimulus(sound) to the brain.

If the brain finds out that the sound is actually a noise then it would instruct the body (limbs for example) to move away from the source of the sound. This is then called the reaction.

If the sound is not that loud, i.e. not potentially damaging to the ears then the CNS does not instruct to retreat.


Sodium channels are primarily voltage-gated - these are the channels responsible for action potentials.

Many other receptors are ligand-gated, and these are typically the signal that causes the initial voltage change that opens the voltage-gated sodium channels; however, these channels are less selective cation channels and are permeable to ions like potassium as well as sodium. Still, their permeability to sodium is quite important and so they may also be thought of as sodium channels sometimes.

These include neurotransmitter gated channels like nicotinic acetylcholine receptors and AMPA (glutamate) receptors, and transient receptor potential channels like the TRPV1 receptor that is sensitive to painful heat and the chemical capsaicin which makes chili peppers "hot."


What pattern can be learned from the data of RNA seq counts and HiC matrix?

This seems to me to be two independent pieces of data. mRNA seq allows one (in case of linear amplification) to quantify message RNA transcripts of genes of interest. that is, how many copies of mRNA for given gene are in the cell at the moment. It is ultimately, how active this gene is. In neurons different genes will be more active, than in epithelial cells, and vice versa. Genetic expression pattern provides identity of the cell.

Hi-C method, closely related to chromosome conformation capture answers question: what genes are physically interact in the nucleus via stabilizing proteins (e.g. enhcancers). There is more in the video, but general idea is that it allows you to see how genes positioned inside intricate chromatin. Since many genetic elements might physically interact via, for example, enhancers, 3C/Hi-C allows detection of such interactions. Or, at least, quantification of correlation between physical positions of two genes.

Now, the only direct connection between mRNA seq and Hi-C that I can draw is following logic: actively transcribed genes are located in expanded, less tense regions of chromatin. Hence, it will be hard to crosslink genes in such regions and correlation going to be low. Silent genes, if they are located closely in nucleus will be cross-linked with high probability, because chromatin is denser around non-transcribed genes.


Embryos still metabolize the nutrients delivered by the mother. The metabolism takes place in the cells, including in the developing organs. Metabolism produces waste products that must be removed. The allantois is the structure that removes waste from the embryo.

I'm not sure what you mean by the placenta identifying or differentiating waste materials from the embryo. The waste simply diffuses passively into the mother's blood from the embryo. The mother's excretory systems then handle it.


Can swarming locusts act as a vector for any human pathogens?

I have not heard of locusts being a vector for any pathogen. For immunocompromised people, they can on rare occasions be infected by bacteria carried in the guts of insects. For desert locusts, their main gut bacteria is Pantoea agglomerans (Enterococcus agglomerans). This species has been listed as a pathogen of immunocompromised patients.


When does weak selection produce qualitatively different results from strong selection?

It has been shown that predictions based on weak selection can be different from that on strong selection.
In fact, for rare mutations, each strategy has stationary distribution at the mutation selection equilibrium. The rank of the component depicts the relative prevalence of the available strategies. Yet the rank of the components of this distribution can change with the selection intensity. Thus results obtained under weak selection can not generally carry over to strong selection.

For more details, please refer to Fig. 1 in [1] and Fig. 2 in the supplementary information of [2].

1 Julián García and Arne Traulsen, (2012), Journal of Theoretical Biology, Leaving the loners alone: Evolution of cooperation in the presence of antisocial punishment

2 Christoph Hauert, Arne Traulsen, Hannelore Brandt, Martin A. Nowak and Karl Sigmund, (2007), Science, Via freedom to coercion: the emergence of costly punishment


One of the alleles for each gene must come from the parent on the right hand side. That parent only has a and b alleles (is homozygous) - meiotic crossing over will not change this. So the offspring must inherit at least one a and one b. That should point you to the answer.


This translocation is balanced: if it was not there was a specific sign for specific unbalanced event, for example "del" for deletion or "+" and "-" signs etc.


In (human) zygote cell differentiation, do we know how the cells coordinating the process know their current position?

There's a protein called Bicoid in fruit flies (see https://en.wikipedia.org/wiki/Bicoid_%28gene%29) that determines the head/tail axis. I remember from biology class that there's a similar protein that determines the up/down axis as well, although I forget its name.

There's almost certainly something similar in humans.


Why Rh conflict happen but no ABO conflicts?

It happens, but it is very rare.

Anti-A and Anti-B antibodies are IgM type. They do no cross the placenta. Sometimes IgG can be produced and lead to the hemolytic disease of the newborn.

Anti-D antibodies are IgG type and can pass through the placenta.


How did the first self replicating organism come into existence?

Evolution or (as Darwin called it) "descent with modification" is a theory which explains the origin of the species NOT the origin of life.  How the first life arose is completely irrelevant to the theory of evolution.  What evolution does explain is how and why we have such variety of life on earth all descending from the same organism.

What you're asking about is not a theory of "evolution" but rather a theory of "abiogenesis."  Although there are many interesting hypothesis for how abiogenesis happened (e.g. the RNA world, the "metabolism first" theory, etc.), the fact is we simply do not know yet how life first arose.  What we do know is that life first arose between 3.5 and 3.9 billion years ago.  That's a really long time ago compared to lots of other important events in natural history (even the Cambrian explosion where modern animal phyla evolved was only half a billion years ago), and so it shouldn't be surprising that it's a hard problem.


Why don't bacterial cell walls prevent bursting when attacked by the complement?

Although this seems to be a simple question on the exterior, the answer is going to be confusing and unclear because we still don't know the answer exactly.

Short answer - MACs are bactericidal not because of water gushing in. It is due to other mechanisms effected by damage to membrane integrity.

Long answer

First of all, I am assuming you already know the complement cascade, the pathways and the like, and I won't get into it. But to mention in passing, MAC is not the only way the complement can help the immune system. It can also opsonise antigens and release anaphylotoxins to modify the immune response.

Most studies concerning the assembly of the MAC and the resulting membrane lesions have been conducted in model systems, e.g. erythrocytes and artificial lipid bilayers. The advantage of these systems is the ease of characterizing the membrane lesions compared to bacterial membranes. Also, complement fixation tests (which use erythrocytes and complement) have been widely used even diagnostically until not very long ago. The osmotic damage, ion effluxes that you talk of happen here and leads to the lysis of erythrocytes. Even in their case, there are 2 models of how MACs work - one is by making a pore (in the pic) and the other is by forming leaky patches in the membrane. However, the way bactericidal MACs work is thought to be different and a little more complex than this -

This picture may have been used for just didactic purposes but cannot be applied in a bacterial system simply because bacterial cell envelopes are different. The two major groups - Gram positive and Gram negative cell walls are important to differentiate while discussing the mechanism of MAC bactericidality. It is important to note that MAC mediated bactericidal action has been reported predominantly only in Gram negative organisms. This resistance in Gram positives is thought to be not because of the osmotic turgor or turgidity but because of the thick peptidoglycan in Gram positive bacteria, preventing access to the inner cell membrane where the MAC assembles. There are MAC resistant Gram negative bacteria too, but let's not discuss that here. It is not off-track to mention here that species like Neisseria where the capsule is thin and the peptidoglycan is too, are more susceptible to complement damage.

So, assuring that the MAC mediated bacterial lysis is not just water gushing in, how is it thought to happen??

For this, we need to revisit the structure of the Gram negative cell wall. The cell wall structure is quite intriguing since there happen to be two lipid membranes enclosing a periplasmic space which contains little peptidoglycan that Gram positives have much more.

Since there are two lipid membranes, technically, there's a possibility that the MAC can be formed on both these layers (MAC's assemble on hydrophobic membranes). MACs assembling on the OML (outer membrane layer) are not sufficient to cause lysis. It is confirmed that the damage has to occur to the IML (inner membrane layer). Inner membrane damage is thought to be bactericidal since it is more restrictive in its permeability than the OML. Also, the IML is linked to several important cellular, metabolic functions that require proper ionic gradients. One example is the oxidative phosphorylation that takes place around the IML.

This should answer your question in that the mechanisms of cell lysis seem to be slightly different in bacteria than the model systems (erythrocytes), but let us delve a little deeper into this.

One persistent question is "how can something as huge as the MAC, penetrate the OML and the peptidoglycan layer, to reach the IML to cause damage?" The hypotheses that MAC just forms a hole in the OML and other serum factors seep in and cause damage to the IML has been ruled out since complement alone can be bactericidal in nature. To explain this, two models have been proposed -

One, where the complement attaches at special sites in the membrane where both OML and IML approximate (at special sites where large proteins span both membranes) and another where, the complement creates a pore to allow C9 monomers to leak in, in turn polymerizing to damage the IML.

I assume this explains it all. Still, I implore you to refer to the link below and correct me if I've been wrong anywhere.

  Reference : The bactericidal mechanism of the complement membrane attack complex, Lars Ootes, (PDF)


Based on OMIM ID codes
In a broad sense NIH have already divided the IDs. If all you are checking is OMIM code enrichment, this might be an okay resolution since it can tell you the chromosomal locus (autosomal, sex linked, or mitochondrial).

Each OMIM entry is given a unique six-digit number as summarized below:
1----- (100000- ) 2----- (200000- ) Autosomal loci or phenotypes
(entries created before May 15, 1994)
3----- (300000- ) X-linked loci or phenotypes
4----- (400000- ) Y-linked loci or phenotypes
5----- (500000- ) Mitochondrial loci or phenotypes
6----- (600000- ) Autosomal loci or phenotypes (entries created after
May 15, 1994)

Other databases as an alternative method.
If you are interested in specific phenotypes, you may need to get more involved.
OMIM doesn't really attempt to group diseases together beyond their ID nomenclature as far as I'm aware. There have been several projects that set out to do this, like the one the question points out, and the examples below. They mostly use phenotypic data in combination with OMIM information.
Two databases that aim to solve this are:

HPO
LDDB
Enricher web-server see @MaximKuleshovs answer below!

These are tools with controlled vocabulary for phenotypes and associations from OMIM codes. They could help you check for disease/phenotype specific enrichment. This would certainly allow programmatic grouping, although I have not worked with either before and I presume it would be very involved!
It's up to you!
Wikipedia has a list of OMIM codes listed in alphabetical order if you wanted to try to group them manually by whichever criteria you desire.

Without your source code it's hard to tell, but maybe the maximum of one occurrence rate could be a code problem rather than a scientific problem.


Why does the T7 RNA Polymerase require a reducing environment ie. DTT

A quick search on T7 cysteines gave some clues:

  Bacteriophage T7-induced DNA polymerase is composed of a 1: 1
  complex of phage-induced gene 5 protein  and Escherichia coli
  thioredoxin. Preparation of active  subunits in the absence of
  sulfhydryl  reagents  indicates  the reduced form of thioredoxin  is
  sufficient for formation of  the  active holoenzyme. The oxidized
  form of  thioredoxin, thioredoxin modified  at  one  active  site
  sulfhydryl by iodoacetate or methyl iodide, or thioredoxin modified
  at both  active  site  sulfhydryls  by N-ethylmaleimide,  are  all
  inactive,  being  defective  in  complex formation with  gene 5
  protein.

Adler and Modrich, J Biol Chem 258:6956 (1983)

There's a more recent paper (Aguirre et al, Inorganic Chemistry 48:4425 (2009)) that mentions the "the enzyme critical sulfhydryl cysteine groups", but unfortunately I only have access to the abstract.

Update: It seems to be an old finding, rather than a rationale concerning the cytoplasmic redox state. According to Chamberlin and Ring, JBC 248:2235 (1973),

  General Requirements-The general requirements for T7 RNA
  synthesis directed by T7 DNA polymerase are shown in Table
  I. As expected for a template directed polymerase, RNA
  synthesis shows an absolute requirement for DNA, the 4
  ribonucleoside triphosphates and Mg++.

(no surprises there ;)

  The activity of the
  enzyme is reduced significantly if a sulfhydryl reducing
  agent such as b-mercapto-ethanol is omitted from  the
  reaction. The addition of 10^-5 M p-hydroxymercuribenzoate to
  the assay system in the absence of b-mercaptoethanol
  abolished all activity, indicating that the enzyme contains a
  sulfhydryl group necessary for activity.

However, if you see the table I, the remaining activity after removing bme is still 74%

There seems to be 7 exposed cysteines (Mukherjee et al, Cell 110:81 (2002)), but I could not find any paper discussing their roles.


Can DNA test of my grandparent's brother reveal my heritage from that branch of the family?

As Rayoub's answer points, you are likely to share a random part of your genes with your grandparent's brother, and therefore analysing his DNA won't tell you where all your genes come from, since he has some genes you don't have and you have some genes he doesn't have.

However, I understand that you aren't that interested on your particular genes, but on what genetics can tell you on the history of your family - that is, to shed light on who were your ancestors and where they came from. Then, if your grandparent's brother was your grandparent's full brother, his ancestors are your grandparent's ancestors and therefore analysing his DNA can be as useful as analysing your grandparent's DNA.

In addition, since your grandparent and his brother doesn't share all the same DNA (likely just about 50% for full brothers) and each of them just have a 50% of each of their grandparent's DNA, if you could analyse DNA from both a grandparent and one or more siblings, you would be able to gather more information. In fact, you would be getting closer to get the same information you could have got from analysing your grandgrandparents'DNA.


What would happen if you "rewired" your eyes with your nose?

"Rewiring" the brain isn't quite that simple: simply splicing a nerve to another doesn't necessarily mean the axons of that nerve will then grow into area. I am unaware of any studies that cross these specific pathways but as I am writing this answer I see you have already updated your question to ask about other modalities! So, with that in mind...

Crossing Auditory and Visual Pathways

Some related experiments have been done with other modalities: the ones I am aware of involve the auditory and visual systems. Both auditory and visual information traveling to cortex mostly comes through two nuclei in the thalamus: the medial geniculate nucleus, MGN, for auditory information, and the lateral geniculate nucleus, LGN, for visual information.

These thalamic nuclei are adjacent to each other. In Angelucci et al 1998 and Sharma et al 2000, lesions were made to cause retinal projections to innervate the part of thalamus that usually processes auditory information (medial geniculate nucleus, MGN). (note: there are also a bunch of older experiments in rodents and ferrets besides these, I'm not going to do a comprehensive review of the literature here but you can find many relevant citations within those other papers).

Briefly, the technique is to damage both the LGN and the pathways that normally project to MGN. The result is that the retinal axons, which normally synapse in the LGN, will instead path to the MGN. Note that it is important to do this very early in development, such experiments would not work in an adult brain.

The result, in the papers I cited earlier, is that the part of cortex that normally responds to auditory information begins to respond to visual information, and develops a hallmark of visual cortical response properties: selectivity to the orientation of presented stimuli. Therefore, it seems like if you give an auditory cortical area visual information, it doesn't "try to process it as sound" but rather processes it just like the visual cortex would.

Effects on perception

It is hard to ask the ferrets what their actual perceptions are, but the best guess is that perceptions are built by what we put into the system: there is no way for an area that receives anything but visual input to interpret that information as anything other than visual input. There is no context to interpret it any other way. Cortex develops and responds based on the information it is given. In the animals in these experiments, their auditory systems have been lesioned so there is really no way they could interpret the stimuli they "see" as "sounding like" something.

Similarly, if you send olfactory information to visual cortex, you will process smells in visual cortex. Olfactory processing is a bit different than the other modalities, so depending on where you took this information from things may not develop properly, but that gets into a lot of speculation that is beyond this .SE site.

Crossmodal plasticity in blind individuals

There are some experiments in humans that also look at this type of cortical plasticity. Probably the best ones are those in blind individuals. Again, I won't review the entire literature, but can give some examples: Cohen et al showed tactile representations in the visual cortex of blind individuals, such as when they are reading Braille. Bedny et al, 2015 show that, especially in children who are blind, the visual areas of the brain respond strongly to information from other modalities, especially spoken language. Again, these individuals are not "seeing" these stimuli, beyond the type of "seeing" that you can do when you reconstruct a scene with your eyes closed (if they were at one point sighted). Rather, part of their brain that would normally be used for vision is now being used for other tasks.

Effects on olfaction haven't been studied as often, but in Kupers et al, blind individuals were shown to have olfactory responses in brain areas that don't show olfactory responses in sighted individuals, including areas that usually process vision.

References:

Angelucci, A., Clascá, F., & Sur, M. (1998). Brainstem inputs to the ferret medial geniculate nucleus and the effect of early deafferentation on novel retinal projections to the auditory thalamus. The Journal of comparative neurology, 400(3), 417-439.

Bedny, M., Richardson, H., & Saxe, R. (2015). “Visual” cortex responds to spoken language in blind children. Journal of Neuroscience, 35(33), 11674-11681.

Cohen, L. G., Celnik, P., Pascual-Leone, A., Corwell, B., Faiz, L., Dambrosia, J., ... & Hallett, M. (1997). Functional relevance of cross-modal plasticity in blind humans. Nature, 389(6647), 180-183.

Kupers, R., Beaulieu-Lefebvre, M., Schneider, F. C., Kassuba, T., Paulson, O. B., Siebner, H. R., & Ptito, M. (2011). Neural correlates of olfactory processing in congenital blindness. Neuropsychologia, 49(7), 2037-2044.

Sharma, J., Angelucci, A., & Sur, M. (2000). Induction of visual orientation modules in auditory cortex. Nature, 404(6780), 841-847.


Pretty interesting question: The short answer to it is: Yes, the seasonal O2 levels vary with the season and this can be measured.
The paper in reference 1 says that this is connected to two phenomena: Production of O2 by photosynthesis and also the uptake and release of O2 in the oceans due to higher temperatures (warmer water dissolves less gases).

The paper in reference 2 says that the northern and the southern hemisphere are basically decoupled from each other. The northern hemisphere reaches its peak of maximum O2 concentration in June/July while the southern reaches its peak around January due to the slow mixing in the athmosphere. They also say that due to more ocean area on the southern hemisphere the uptake/release processes in the ocean play a much more important role there.

The graph from paper 3 also shows that the CO2 concentration is inverse compared to O2, since during the photosynthetic period of the year CO2 is consumed.

The following figure is taken from the website of "2° Institute" and is interactive, so can actually check, when the concentration is at which level. The general O2 concentration is getting lower, it is assumed that this happens due to the human CO2 production, the source can be found here.

References (please let me know in the comments, if you can't access the articles):

Seasonal and interannual variations in atmospheric oxygen and
implications for the global carbon cycle
Seasonal variations in the atmospheric O2/N2 ratio in relation to the  kinetics of air-sea gas exchange
Seasonal and short-term variations in atmospheric potential oxygen
at Ny- Ålesund, Svalbard


Would our body adapt to changes that are not in our DNA?

It will be hard to discuss for the specific example you consider, mainly because it is unclear how would you treatment affect the person's height.

That being said, yes, our bodies can change in function of the environment. This is called phenotypic plasticity

  Phenotypic plasticity refers to some of the changes in an organism's behavior, morphology and physiology in response to a unique environment.

Here the term environment does not only refer to outside temperature or other obvious environmental factor. For example, one can ask whether the size of a vein can react plastically to the blood flow. Here, blood flow is the environmental factor toward which, the plastic response is mediated.

Note that some plastic responses are adaptive and some are not. Note also that there are a lot of related terms (developmental flexibility, acclimation, polyphenism, developmental selection, ...) in the field of plasticity and different authors sometimes use these terms with slightly different definitions which can make everything a bit confusing.


What's the difference between life expectancy of cigarette smoker and general population?

The difference in life expectancy between smokers and non-smokers appears to be at least 10 years on average, in a survey of American adults between 1997 and 2004.

The same paper lists causes of death (higher among smokers than non-smokers, as measured by hazard ratio), although this is not exhaustive: lung cancer, other cancers, ischemic heart disease, stroke, other vascular disease, and respiratory disease have an adjusted hazard ratio of 1.7 or more, with 94% of lung cancer deaths attributable to smoking among female smokers, and 93% to smoking among male smokers.

If you have access, you will probably find Table 2 (hazard ratios) of interest.

Figure 2 shows the survival probability:


Coalescence time: Is it different for haploids and diploids in population genetics?

Short answer

The coalescent time is twice as high in a diploid population than in a haploid population

Long answer

Imagine you sample at random one chromosome. Then, you sample a second one and you ask the question, what is the probability that they coalesce in the previous generation. This probability is $\frac{1}{PN}$, where $N$ is the population size and $P$ is the ploidy number (1 for haploids, 2 for diploids). The probability that they do not coalesce is therefore $1-\frac{1}{PN}$. The probability that the two chromosomes coalesce $t$ generations ago is the probability that they don't coalesce for $t-1$ generations and then coalesce. That is the probability that the two chromosomes coalesce $t$ generations ago is

$$P(t) = \left(1-\frac{1}{PN}\right)^{t-1}\frac{1}{PN}$$

You might recognize here a geometric distribution, where the probability of success is $\frac{1}{PN}$. In order to simplify the math, let's assume that the population size is very large. In such case the above formulation is well approximated by

$$P(t) = \frac{1}{PN} e^{-t\frac{1}{PN}} $$

You might now recognize the exponential distribution with rate $\frac{1}{PN}$. We can now compare the mean expected time to coalescent of a diploid population and a haploid population.

The mean of the above exponential distribution is simply $PN$. Therefore, the expected time to coalescent is $2N$ in diploids and only $N$ in haploids.

Details of your post

In your post you talk about structured populations. The calculations are a little more complicated in structured populations and I don't remember on the top of my head how they work.

You talk about divergence $D$. I don't know what you mean by divergence. From coalescent results you can compute the expected heterozygosity, the number of pairwise differences, and even the whole site frequency spectrum. You can as well make those calculations for the structured coalescent model.


How long does it take for a blocked dopamine receptor to be broken down by the body?

Partial Answer and Suggestions
As @De_Novo says, this is a complicated, albeit very interesting, question. There are various reasons for this, such as the fact that the receptors aren't just internalised but also recycled and the fact that there may be antagonist and dose-dependent changes in receptor internalisation. There's the added complexity that receptors can have their expression changed in the short term (by internalisation) but also in the long term (by varying synthesis). You should then note that there's not a set lifespan of the receptors - there's a statistical distribution for how long they'll last at the membrane.
But I'd quite like to stimulate discussion about it so I'm proposing some smaller questions:

Do irreversible dopamine antagonists change the rates of receptor internalisation, degradation or recycling? This is likely to be the case as internalisation of receptors is often activity-dependent. Also, the shape of the irreversible antagonist could change how the receptor fits into a clathrin-coated pit.
Do the irreversible antagonists change the rate of receptor synthesis?
What mathematical models can describe the dynamics of internalisation? This might be a bit tricky since there are feedback mechanisms here (e.g. recycling --> internalisation --> degradation --> less recycling).
How does the proportion of blocked receptors affect these factors?

By answering these questions (or even by finding an experiment that measures the half life of the receptors with blocking), you could come up with an answer for the half-life of the blocked receptors.


Liquid chromatography (LC) allows the peptides from a complex sample to be fed into the mass spectrometer over time. The bottom half of the image shows an MS spectrum from a single precursor scan and the machine is programmed to select the three most intense peaks (parent ions or precursor ions) from this scan for MS/MS (MS2).

This process is repeated throughout the LC-MS/MS run and programs usually include exclusion criteria where a parent ion is ignored for 30 - 90 seconds once it has been scanned 1 - 2 times. Usually the machine will also ignore singly charged parent ions as many of these ions will be inorganic contaminants and you want the machine to be busy with peptides.

Efficient use of machine time is critical to getting good coverage of the proteins in the sample. Proteins that are small create fewer peptides that are amenable to sequencing so these can be missed. Also those proteins that are less abundant may produce peptides that stay below the selection criteria. Good chromatography and efficient use of machine time are critical to getting good results and even in good conditions most peptides will not be subjected to MS2 sequencing. This estimates that of 100 000 peptides with only 16% were 'sequenced'. This explains why proteomics labs are speed freaks, and has driven the development of faster machines. The ~ 1 hour yeast proteome paper demonstrates the 'work' that the newer machines can get through;

  Over a 1.3 h chromatographic method .... collected an average of 13,447 MS1 and 80,460 MS2 scans (per run) to produce 43,400 peptide spectral matches and 34,255 peptides with unique amino acid sequences (1% false discovery rate (FDR)).


What is the relationship between radiation and evolution?

Is background radiation a critical component of evolution? No, it most certainly is not.

The DNA replication and DNA repair mechanisms aren't perfect and errors happen without any external cause or catalyst. You could say mutations happen on their own. There are mutagens that also cause DNA damage or mutations, but they're merely affecting the DNA replication in a negative way, causing it to err more often.

So, the effect of background radiation isn't the key here, the key is that the biological processes of DNA replication and repair are not infallible, although radiation does increase the error rate (the rate of mutation) just like many other mutagens do.


Microchaetus rappi
Microchaetus rappi, the African giant earthworm, is a large earthworm in the Microchaetidae family, the largest of the segmented worms (commonly called earthworms). It averages about 1.36 m (4.5 ft) in length, but can reach a length of as much as 6.7 m (22 ft) and can weigh over 1.5 kg (3.3 lb).(https://en.wikipedia.org/wiki/Microchaetus_rappi)

Giant Gippsland earthworm
These giant earthworms average 1 metre (3.3 ft) long and 2 centimetres (0.79 in) in diameter and can reach 3 metres (9.8 ft) in length; however, their body is able to expand and contract making them appear much larger. On average they weigh about 200 grams (0.44 lb). They have a dark purple head and a blue-grey body, and about 300 to 400 body segments.(https://en.wikipedia.org/wiki/Giant_Gippsland_earthworm)


How does heredity work with Endogenous retrovirus?

For a provirus to be heritable, the infection must occur in the germ line. The initial integration would occur at one site in the genome and thus the locus could be described as hemizygous. Inheritance would indeed be probabilistic, depending on whether an offspring inherits the provirus-containing chromosome or its uninfected homolog.

Eventually, the endogenous retrovirus (ERV) can become fixed or lost in a population by genetic drift and natural selection. Additionally, retrotransposition and, more importantly, reinfection can greatly increase copy number and allow ERV persistence despite a lack of fixation at specific loci. It should also be noted that more recently acquired ERVs exist that have not reached fixation in humans.

References and Further Reading:

Boeke JD, Stoye JP. Retrotransposons, Endogenous Retroviruses, and the Evolution of Retroelements. In: Coffin JM, Hughes SH, Varmus HE, editors. Retroviruses. Cold Spring Harbor (NY): Cold Spring Harbor Laboratory Press; 1997.

Belshaw R, Pereira V, Katzourakis A, Talbot G, Pačes J, Burt A, Tristem M. 2004. Long-term reinfection of the human genome by endogenous retroviruses. Proc Nat Acad Sci 101(14):4894–4899.


Is it possible for bacteria to acquire family-wide antibiotic resistance?

The two amoxycillin formulations you mention pair the amoxycillin with a Beta lactamase inhibitor. This is because of the prevalence of resistance to beta lactam drugs including amoxycillin. If we were to invent a brand new never before seen beta lactam drug and started using it irresponsibly, there would probably be resistant bacteria within 5 years. The same beta lactam core structure that makes the drugs work against the peptidoglycan synthesis machinery make it susceptible to attack by beta lactamase. A new beta lactam could avoid the lactamase for a while, but the same evolutionary pressures that selected for resistant mutants against the other beta lactams would select for mutants resistant against the new one.

The same goes for the fluoroquinolines you mention. Their mechanism of action is different, they inhibit DNA synthesis by blocking topoisomerase II activity. But once a bacterial strain is selected for that has resistance against one member of a class of antibiotic it's relatively easy for it to acquire the mutations that confer resistance against other members of the class. Changing the structure of the drug enough so that cannot be defeated by the mechanism of resistance while retaining the drugs mechanism of action is probably impossible, or at least we haven't done it yet. Even vancomycin, one of our most powerful antibiotics, has some bacteria resistant to it.


What were the camels' humps good for back in the polar areas?

In my opinion there might be two reasons why the camel hump (rather than bump) might be one of the adequate adaptations of camels to living in the cold (additional to their flat feet giving hold on both snow and sand and tooth structure, Rybczynski et al., 2012). Both match the humps being fat storages in modern camels.

The first is also provided by Rybczynski et al. (2012):

  Their iconic hump(s), containing fat, also may have been adaptive. As seen in high-latitude ungulates today (Parker et al., 2009), fat deposits could have been
  critically important for allowing populations to survive and reproduce in harsh climates characterized by 6-month long, cold, winters.

Note that this refers to the nutritional value of the fat deposits and does not necessarily relate to maintaining body temperature.

The difference to modern camels would be that the fat storage in modern-day camels serves indirect water deposition (water can be easily gained from the fat stored in the humps and storing the water condensed in fat molecules is way more efficient than storing water directly). This relates to the second reason which, however, is more speculative from my part.

Cold - especially in plants - also implies drought as frozen water is not available. This does not need to apply to mammals as they can thaw ice, e.g. by licking. However, this might be critical as the body might lose some temperature during that process. Accordingly, fat storage might already then have been a means to storing water while keeping body temperature.

Alternatively, and maybe even more likely, the camel hump might have undergone a switch in function from storing a food source in archaic camels to storing water in modern camels as both can be achieved with fat deposits due to the chemical properties of fat.


the meaning of "Non-primary hits" and "tags"

"tag" is a weird term in this context. It used to mean "read", but RSeQC likes using it in an odd way. Suppose you have a read that aligns to a single contiguous (though possibly with InDels) stretch of DNA. This would then count as one tag. Suppose instead that you have a spliced read, that is one where part aligns to one exon and part to another exon. Each aligned part of this read then counts separately as a tag. So this 1 read becomes 2 tags. By extension, if you have a read that is spliced such that is starts in exon 1, jumps to exon 2, and then finally jumps to exon 3, then it'd count as 3 tags. This is only useful if you're interested in splicing, since the higher this value is the better you're able to discern differences there.

For "non-primary hits", suppose you have a read that can align equally well to multiple places in the genome. If there are 5 equally good alignments, then 4 of these will be labeled as "secondary" and one of them will not, which is then the "primary alignment". "non-primary hits" is then an odd way of saying "secondary alignments". The number of primary alignments is equal to the number of reads that aligned.


What is the number density of fungal spores per unit of volume of air?

Bamba et al. (2014) Case study of airborne fungi according to air temperature and relative humidity in houses with semi-basements adjacent to a forested hillside. Biocontrol Sci. 19: 1-9.

This is neither the first nor the last report of this kind. Search PubMed database using this query:

"air"[Title/Abstract] and "fungi"[Title/Abstract] and "spore"[Title/abstract]


What does 'per capita births and deaths' mean?

I will use an ever so slightly more specific scenario than what your book offers.

At the beginning of 2017, there were twenty lotus plants in a pond. By the first day of 2018, eight of those twenty lotus plants reproduced. Using this information, we now want to describe the birth rate of lotus plant population.

To do this, we need the number of plants that produced offspring, and, the population size at the beginning of 2017.

$$\frac{no. \ of \ parent \ lotus \ plants}{initial \ population \ size} = \frac{8}{20} = .4$$

This means that, when considering the twenty lotus plants that first existed at the beginning of 2017, each of those twenty plants contributed an average of 4/10s of a lotus plant offspring for that year.

To generalize this, we say, "a birth rate of .4 offspring per lotus plant per year."

The same method and persective can also be applied to the fruitflies, however, they're considering death rate.


Why doesn't recombination occur in male Drosophila?

This is a venerable fact.  Exceptions in D. melanogaster strain Y-007 have been observed and D. ananassae has consistent male cross-overs, but this work dates back to the 1970s.

This Current Biology 2002 paper is not exactly new, but sheds some light on the issue in question.

  In male Drosophila melanogaster, meiosis occurs in the absence of recombination or a recognizable synaptonemal complex (SC).

The authors used a GFP-lac fusion to observe a series of sections of the male fly in meiosis with integrated lac - specific binding regions.  They see for the most part that the GFP bound segments of the DNA are not associated in cell division.  That is, homologous chromosomes physically associate during meiosis (via the SC) and in male drosophila, they do not.

It seems from more recent work, that the details of how this work is still being worked out but several gene regions and factors have been identified.  Suspected factors that help conspire to align the various homologous chromosomes are being looked into.  Take a look at the P.I.s biblio for more.

This isn't my main field, but as I understand it, many aspects of meiosis are still being mapped out.

As to the question of how this evolved and why; its definitely strange.
 It looks like there is a gender selected trait where the SC doesn't form in males.  Its easy to imagine a mutation that caused males only to lose recombination - the process is so complex its hard to imagine such a trait not showing up.

Still it's surprising to think that the trait has not only survived but become dominant in Drosophila all over the world.  To be a common traits to so many Drosophila species, it must have happened more than 10 million years ago.  Explanations of the advantages of sexual reproduction often include recombination.  Even the human Y chromosome has a self-recombination mechanism that reduces error in the coding regions.  As such, its hard to believe that this is not a huge disadvantage for the flies.  Still, if if it were such a big deal, you'd imagine Y-007 would have dominated and re-introduced the trait.

The only theory I can think of might be called 'lazy males'; that the males got the females to do one more thing for the offspring and it somehow outcompetes the sperm of the recombining males.  Lots of sperm are non-motile; that's a fact for humans, I have no idea what its like for flies that recombine.  Take a look at the variance in morphology as well - sperm are really crazy ugly sometimes and a good deal of the mating process is to help weed out the defective ones.  Without recombination, might it be that males produce viable sperm at a greater rate, helping them in sperm competition, which I'm sure is the case for fly mating - Drosophila are not monogamous too I'd guess?  Anyway that's not a researched idea, just a guess on my part.


What is the difference between non-coding and intergenic regions?

"Intergenic" is, well, an embarrassment, though it can be hard to avoid.  Intergenic means, literally, between genes.  Genes are, as you'd expect, genetically defined as regions of the chromosome with some genetic role.  Between genes, we have, well, junk, spam, without meaning or significance, since otherwise, it would be a gene.  In the 1990s everybody knew most of the genome was "junk DNA" and it was pretty straightforward.  And the central dogma was DNA makes mRNA makes protein and if there was no mRNA making protein, or even no long protein, then they assumed there was no gene.
Well, the problem with using these terms nowadays is, first, it is very hard to show any given piece of DNA never has a role.  After all, you can often remove a whole gene without visible effect on an organism, so how can some noncoding sequence 'between genes' be proved conclusively to be meaningless and of no relevance to either of its neighbors?  And second, DNA definitely does have a role even if all it does is produce non-coding RNA, or act as a regulatory sequence that does.  So for example, on OMIM you can look up many records for "intergenic", with results like H19, for which one term is "LONG INTERGENIC NONCODING RNA H19".  Note also H19 is listed as the HGNC approved gene symbol, so it is an intergenic gene.  Tricky, eh?  (I have great respect for OMIM - this isn't their fault)  Also, enhancers can be quite a long way from a gene, even past the end of another gene or affecting multiple genes, so even though a mutation in the enhancer might genetically act as an allele of a specific gene, it might be described in sequence terms as located in an intergenic region.
Bottom line: the intergenic regions you're reading about are going to be between things that are recognized as genes, and may or may not be known to have some effect on one or the other (or both...).  They won't contain CDS, which is always considered to be a gene, nor 5'UTR or 3'UTR because those are transcribed before or after a CDS.  Past that, how they are being distinguished from "upstream sequence" and "downstream sequence", that could be completely arbitrary.  They might have gone to WormBase and pulled out curated gene records, and added some number of base pairs before the start site as promoter - but I don't know that.  You'll just have to try to find the particular reference for whatever tool you are using.


Why is bacterial meningitis worse than viral meningitis?

One needs to be careful making broad generalizations about meningitis. The term simply refers to inflammation of the meninges (the outer layer surrounding the brain and spinal cord). Meningitis can occur due to a number of causes, most notably viral and bacterial infections, but can also also be due to fungi, parasites, toxins, cancer, etc. There is a vast range in severity of meningitis depending on the aetiology.

For example, rabies infection can progress to a fatal meningitis. Rabies is a virus. You therefore cannot say that bacterial meningitis is worse than viral meningitis.

That being said, what you have likely heard is that viral meningitis tends to be less severe than bacterial meningitis. This is true not necessarily because viruses are worse at causing meningitis than bacteria, but because the common causes of viral meningitis are often more easily cleared by the immune system.

Non-polio enteroviruses and herpesviruses are the most common causes of viral meningitis. These are the same groups of viruses that commonly cause mild cold or flu-like signs. Usually, when we have these signs, we don't go to the doctor to be treated with antivirals, because in healthy individuals our bodies are usually good at clearing the virus. The same is true when the virus is affecting the meninges. However, this does not mean that these viral infections cannot be severe in some cases.

The most common bacterial causes of meningitis in people are Neisseria meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae type b. The pathogenesis of disease is broadly speaking similar to that caused by viruses, but the inflammatory response of the immune system tends to be more severe with these bacterial organisms compared to the common viral causes of meningitis. Bacterial meningitis is also typically accompanied by sepsis affecting other organ systems. While antibiotics exist that are effective at treating these bacteria, many antibiotics do not cross the blood-brain barrier, which makes treatment of bacterial meningitis challenging.

Finally, it is worth mentioning that widespread vaccination may have had an effect on our perception of meningitis severity. For example, at one time polio was a major cause of viral meningitis, but vaccination has vastly reduced rates of this disease in many parts of the world. Similarly, mumps and measles used to be more common causes of viral meningitis, however due to widespread use of the MMR vaccine these are now less common causes of viral meningitis. On the bacterial causes, there are now several common vaccines such as meningitis B/C/Hib/pneumococcal vaccines which are effective at reducing rates of infection with these bacterial organisms.


Can plants be grown using lights in the home?

It depends on what kind of light you are using. I recently did an experiment on this for my school's science fair and I found that you can use LED lights to grow plants. Nowadays you can actually buy LED lights called "Grow Lights" to grow your plant and the only difference is that Now the current LED lights that are used include four LED lights into groups where each light can produce the correct wavelength that will allow for increased production of growth. For beneficial growth of the cannabis plant for example  you want to use your LED lights directed at 439nm, 469nm, 642nm and 667nm. Link http://easy420grow.com/what-is-the-difference-between-hid-grow-lights-and-led-grow-lamps


What signal processors comprise an Event-Related Potential system for EEG?

Event-related potentials are an issue in many aspects of physiology, not just in EEG analysis, so this answer is more general.

The main problem is that electrical or other signals that are associated with some "event" are typically much lower in magnitude than the background noise in the system being examined. Electrocardiograms are the exception in this regard. The trick then is to get the event-related signal out of the noise.

This is done by multiple repetitions of the "event" combined with signal averaging. You mark the electrical record with the time of each event, line up portions of the record by the event markers, and average the lined-up signals around the multiple events. This can be the full waveform for sensory evoked potentials, or if you are examining action potentials in a nerve, the histogram of post-event occurrence times of action potentials.

The particular signal-processing mechanisms used have evolved with technology. I'm old enough to have known people who 60 years ago recorded electric neural activity on magnetic tape and processed the data, after analog-to-digital conversion, on what were then state-of-the art computers with 65,000 words of memory. Even then, there was discussion about the best technologies to use for specific purposes, as this 1959 MIT monograph indicates.

The main problem, the low level of event-related signals to the noise from other electrical activity, still remains 60 years later. The noise is biologic rather than technical, so more recent improvements have more to do with ease and speed of processing rather than the fundamental signal-to-noise problem. For event-related potentials, use whatever technology allows you to collect the electrical data along with linked notations of the event times, then to average the signals synchronized on the events to build up the signal out of the noise. In a standard clinical application of brainstem auditory evoked potentials to evaluate hearing, you may need to average over 500 or more stimulus presentations.

This signal-in-noise problem is also seen in functional magnetic resonance imaging (fMRI) of brain function, which must consider not only the signal over time but also differences among brain regions within individuals and differences among individuals. The Wikipedia page on fMRI goes into some detail on methods for getting specific signals out of the background noise. You should pay particular attention to the issue of "Block versus event-related design" on that page. My understanding is that for "events" of the type that you consider, like "thinking about a turtle," the block design works best in fMRI. The paper by Thierry et al, provided in the helpful answer by @Christiaan, shows how to apply this type of blocking approach to EEG measurements during presentation of visual stimuli.

The methods in that paper by Thierry et al also indicate the type of practical care that is used in professional analyses of this sort. The authors go into detail about the nature and placement of the electrodes, choice of which electrodes to use for analysis, signal-sampling rates, and so on. For example:

  Scalp activity was digitized at a 1-kHz sampling rate from 64 Ag/AgCl electrodes distributed throughout the scalp according to the 10–20 convention using Cz as a reference. Impedances were kept below 7 kOhms. The electroencephalogram was filtered on-line between 0.01 and 200 Hz and off-line low pass at 35 Hz using a zero phase-shift digital filter. Eye blink artifacts were mathematically corrected, and signals exceeding $\pm$ 75 $\mu$V in any given epoch were automatically discarded.

Reading papers like this are probably the best way to learn about what's involved and to find people who can teach you how to do it.


Is the heterotroph hypothesis universally accepted?

I would say the the topic is still very much under debate. This paper by Ferry and House (2006) briefly review the heterotrophic vs chemoautotrophic hypotheses. They include citations from proponents of each hypothesis. Interestingly, Ferry and House propose an "energy conservation" hypothesis that attempts to merge ideas from the other two hypotheses.  Overall, much work remains to be accomplished in this field before we have a clear understanding of the origins of life.

Literature Cited

Ferry, J.G. and C.H. House. 2006. The stepwise evolution of early life driven by energy conservation. Molecular Biology and Evolution 23: 1286-1292.


Why it is important to vaccinate a human newborn within 24 hours since birth?

In the US, infants are vaccinated against Hep B at birth and again a month or two later as well, because of the risk of maternal transmission. If the mother is known to be HepB positive, HBIG will also be administered.

  Perinatal HBV transmission can be prevented by identifying HBV-infected (i.e., hepatitis B surface antigen [HBsAg]-positive) pregnant women and providing hepatitis B immune globulin and hepatitis B vaccine to their infants within 12 hours of birth.

The reason for the HBIG is obvious, but it doesn't last for life. Therefore, the vaccine and its booster.

  Hepatitis B virus (HBV) infection in a pregnant woman poses a serious risk to her infant at birth. Without postexposure immunoprophylaxis, approximately 40% of infants born to HBV-infected mothers in the United States will develop chronic HBV infection, approximately one-fourth of whom will eventually die from chronic liver disease.

In countries where HepB is not prevalent, there is little cause to immunize at birth. However, it is too common in the US.

  Preventing perinatal HBV transmission is an integral part of the national strategy to eliminate hepatitis B in the United States. National guidelines call for the following:
  - Universal screening of pregnant women for HBsAg during each pregnancy
  - Case management of HBsAg-positive mothers and their infants
  - Provision of immunoprophylaxis for infants born to infected mothers,   including hepatitis B vaccine and hepatitis B immune globulin
  -Routine vaccination of all infants with the hepatitis B vaccine series, with the first dose administered at birth

The risk of HepB vaccine is low. The seriousness of the disease is high. It is not only the mother who might be a carrier. There are many unidentified carriers in the US. That makes the risk-to-benefit ratio low. Driving your newborn home in an automobile is probably more of a risk than the vaccine, but most people do so anyway, and do so many, many times over the course of the baby's life.

In the US, we do not routinely vaccinate against TB, so I cannot address that issue with any degree of expertise. The risk-to-benefit ratio is not as low as for HepB. It is given to children who are continuously exposed to someone (say, a parent) with active TB, or in certain communities where TB is very prevalent. Obviously, if the risk of SCID (severe combined immunodefficiency) is high, the risk of the vaccine is much higher, and some infants have died from it.

Discussing the risk to benefit ratio of all infant vaccines is too broad for this venue.

Separating Fact from Fiction in the Newborn Nursery: Hepatitis B Vaccine for Newborns
The benefits and risks of bacille Calmette-Guérin vaccination among infants at high risk for both tuberculosis and severe combined immunodeficiency: assessment by Markov model


What is the difference between these worms: Caenorhabditis elegans and Eisenia fetida?

Caenorhabditis elegans is a nematode. Eisenia fetida is an annelid. They both are lophotrochozoans (more specifically, trochozoans).

Time of Divergence

According to Michael Lynch, there are about 41 amino-acid substitutions per site between Annelida and Nematoda. According to Lynch's data, I estimated that this difference is roughly equal 100 million years.

Therefore, assuming the rate of molecular evolution was constant, their common ancestors lived about 100 million years ago.

Difference on Anatomy

Nematodes have pseudocoelom while annelids have eucoelom. Therefore nematodes do not have a vascular blood system. However, annelids do have one. Nematodes also lack a layer of circular muscle, which annelids have. This layer of muscle allows annelids to move by shorten and elongate their bodies.

C. elegans in particular does not have a female gender. There are only male worms and hermaphrodite worms. Only the male can fertilize other worms.

E. fetida is hermaphroditic and two of them can fertilize each other.


What is the prehistory of amino acids in cells?

Edward N. Trifonov is a professor at the Institute of evolution at University of Haifa, Israel. One of the main research topics in his group is the reconstruction of the origins of life. In one of his papers, The triplet Code From First Principles, he proposes the the chronological appearance of the 20 amino acids. There are a lot of hypothesis and testable predictions, among which is the theory of S. Miller that some biological compounds have been abiotically produced in the atmosphere. This prediction has been confirmed by imitation experiments, yielding ten different amino acids, as glycine and alanine being the prevalent ones.

The author tries to predict the chronological order in which the 20 amino acids appeared by taking into account various criteria (studies, hypothesis and viewpoints) that propose some order, as each one of them contributes to the consensus order to a certain extent. This contribution is described in the form of rank. He compiles a list of 60 rankings of 60 different criteria to derive the consensus order. Some of the criteria are:

  N1’. Criteria based on various evaluations of complexity of amino-acids. N1, N34, N35,
  N37 – as in (5), and N44 (6). G, A, S, P, V, C, D, T, N, L, K, I, E, (MQ), H, R, F, Y, W

  N2’. Criteria based on evolution of amino-acyl-tRNA synthetases. N2, N7 (5).
  (AG), (DFHKNPST), (CEILMQRV), (WY)

  N4’. Criteria based on amino-acid compositions of various sets of presumably ancient
  proteins. N4, N26 (5), N41 (7), N45 (8), N47 (9), N48 (10), and N58 (11).

The first ten (earliest) consensus amino acids are the same as in Millers’s experiments. The amino acids appeared last have their respective codons borrowed from already existing ones. The derived consensus order is G, A, D, V, P, S, E, (L, T), R, (I, Q, N), H, K, C, F, Y, M, W.

The author also proposes a reconstruction of the chronological order in which the 64 codons had appeared.


Short Answer

They are marking distance from a reference plane.

Longer Answer

In the images you provided, you are looking at horizontal slices through a brain. The legends are indicating that each plane has that vertical distance from a reference point (if the subject were standing); the positive numbers are dorsal to that reference and the negative numbers are ventral.

A common reference point for MRI images (to define as [0,0,0]) is the midpoint of a line through the pre-auricular point, though ultimately it is an arbitrary distinction.

If the actual reference point is important to you, you will need to verify the reference coordinate system used in the study you are looking at. It's also possible you are looking at coordinates transformed to some reference brain rather than real-life coordinates for that particular subject, but again, whether that matters or not depends on why you care. If you are doing research across subjects, you probably want to know reference coordinates; if you are doing brain surgery on a particular patient you want real-life coordinates.


It looks as though it has a keel along it's back (the area behind the mantle shield.)

If so (and I think it is), it would be a keelback slug, the coloration strongly suggesting a leopard slug (Limax maximus):

Coloration varies but the general pattern is a spotted spotted mantle sheild about a third of its length in size, with a striped tail.

The major doubt I have is the size. It looks smallish in the photo. Leopard slugs are very large. Perhaps it's a juvenile.


Can anyone identify this plant from Bangladesh?

The genus is Lantana, of Verbenaceae. That particular one could perhaps be L. camara. There's a number of papers that exist which study L. camara in Bangladesh, just some examples:

http://link.springer.com/article/10.1007%2Fs11676-007-0060-6

http://www.banglajol.info/index.php/BJB/article/view/1513


If you can digest (break down) the polysaccharides to useable monosaccharides, then they can be incorporated into glycolysis (or some other metabolic pathway!). The metabolic pathways around glycolysis are complex, but here is a representation of some of them:

As you can see in, in the top right corner, sucrose/starch, but also other sugars like nucleosides, can enter the overall simple sugar metabolic pathways. How and what exactly happens to the complex sugars will depend on how they are broken down (if they can be broken down at all) and they will have their own more or less complex metabolic pathways associated with that.


This is a quite complicated question, as melatonin has quite a range of effects on the cells. First, melatonin binds to three different melatonin receptors, which are found in a wide variety of tissues or organs including brain and retina, cardiovascular system, liver and gallbladder, intestine, kidney, immune cells, adipocytes, prostate and breast epithelial cells, ovary/granulosa cells, myometrium, and skin.

Two of the receptors a G-protein coupled receptors (GPCR), the MT1 and MT2 receptors. The third is a quinone reductase called QR2.

For more details, see this papers:

Melatonin receptors in humans: biological role and clinical
relevance.
Melatonin receptors and their regulation: biochemical and structural
mechanisms.

The role of melatonin is pretty broad, see the figure (from this article:"Melatonin: Nature's most versatile biological signal?")

The receptors transport the outside chemical signal (the melatonin) to the inside and activate (or repress) a number of different signal transduction pathways. See the figure below (taken from Qiagen):

This includes MAP-Kinase pathways, proteinkinase C, IP3, adenyl cyclase and so on. This is quite complicated and I recommend reading some of the following articles if you are interested in a deeper insight. Finally these signals are transmitted into the nucleus and result in a changed gene regulation/expression.

Melatonin receptors, heterodimerization, signal transduction and
binding sites: what's new?
Physiological effects of melatonin: role of melatonin receptors and
signal transduction pathways.


There is nothing wrong with the question and it can be explained with not much more than mendelian genetics + linkage.

What do you think are the genotypes of parents?

First hint: If there is more than one phenotype (for the trait) of the offspring at least one of parents must be heterozygote. So the idea of pure lineages goes out of the window here.

Ok, there is at least one heterozygote for each color and smoothness of seeds. What is the genotype of the other parent?

Hint 2: Test cross is a term for cross between recessive homozygote and individual of unknown genome (with dominant phenotype). The test cross reveals genotype of the parent with unknown genome.

Hint 3: 1:1 ratio of phenotypes is typical of cross between a heterozygote and recessive homozygote.

Ok so we have heterozygote and recessive homozygote for both traits. Which traits are dominant and which are recessive?

Hint 4: This question seems to be inspired by original Mendel work. Feel free to read it here to find out which traits are recessive and which are dominant. It is quite a good read, clear in its presentation of evidence and conclusions and I recommend it to everyone.

However, this knowledge is not necessary to answer the question. How are dominant genes organized in parents? Principally we have two options:

(AaBb x aabb) or (Aabb x aaBb)

If we consider organization on chromosomes it expands to basically 3 options:

Option 1:

chr ---A---B---
chr ---a---b---
         X
chr ---a---b---
chr ---a---b---

Option 2:

chr ---A---b---
chr ---a---B---
         X
chr ---a---b---
chr ---a---b---

Option 3:

chr ---A---b---
chr ---a---b---
         X
chr ---a---B---
chr ---a---b---

I leave it to you to figure out which of the tree options leads to result offspring described in the question.


Bee, or other insect stings/bites, will cause a reaction to occur due to chemicals being released from your immune system.  This can result in anywhere from a small bump to anaphylaxis, which can be life-threatening if not treated right away.

From Southern Cross Medical Library:

  An anaphylactic reaction occurs when the body's antibodies respond to the insect venom by releasing chemicals such as histamine and serotonin that trigger the allergic reaction.

Whatever the reaction, it is correct to say that the reaction to an insect sting/bite is a defense mechanism of the body.  An interesting study done by Stanford University School of Medicine was done and discusses these immune mechanisms:

  Innate immune responses occur in subjects exposed to a foreign substance, such as a pathogen or a toxic material like venom, for the first time. [...] Immune cells called mast cells, which reside in most of the body’s tissues, are poised to unleash signals that turn on defense responses when a pathogen or toxin intrudes.  Prior immunization is not required for these types of innate immune responses, nor is the development of specific antibodies. In contrast, during an adaptive immune response, the immune system creates antibodies that can recognize the toxin or pathogen that is invading the animal’s system. Adaptive immunity is typically a faster, more specified and more effective form of defense than innate immunity, the research team explained.

More explanation of the non-specific immune response:

  If a bee stings you, the presence of the bee venom triggers a nonspecific immune response. White blood cells arrive first on the scene to rid the body of bee venom antigens. As war wages between antigens and white blood cells, battle signs may appear on the affected skin. Inflammation (redness, swelling, heat, and pain) results as the body wards off invaders.

  If the body detects an antigen that it previously met, a specific immune response occurs. In this response, the body has been trained to recognize and neutralize a familiar specific antigen; its immune system "remembers" the antigen. Such systemic (not restricted to the initial infection site) immunity enables a faster, longer lasting immune response than does a nonspecific response.

Therefore, these reactions to bee stings and other foreign toxins help us to better develop our immune system to protect against potential future encounters with these insects.


Oscillatory electrical system using a chain of neurons

Short answer
A single pacemaker neuron can generate oscillatory behavior.

Background
Given our exchange in the comments, I will focus on single neurons with intrinsic oscillatory behavior. For example, thalamocortical relay neurons and inferior olive neurons have intrinsic oscillatory properties, mainly through the interaction of a hyperpolarization-activated cation current (Ih) and a low-threshold activated Ca2+ current (IT) (McCormick & Huguenard, 1992, and Fig. 1).

Fig. 1 Model for an oscillatory inferior olive neuron. Source: Bal & McCormick (1997)

Rhythmic burst firing is created through generation of a low-threshold Ca2+ current (IT), which activates fast action potentials mediated by Na+, K+, and Ca2+ currents (INa, IK, and ICa, respectively). Entry of Ca2+ in the cell during fast action-potential firing and low-threshold Ca2+ spiking result in after-hyperpolarization through activation of a Ca2+-activated K+ current. This afterhyperpolarization activates Ih. Combined activation of Ih and decrease of a Ca2+ activated K+ current (IK,Ca) results in depolarization of neuron, which activates another low-threshold Ca2+ spike. In this manner, Ih modulates frequency of oscillation. In addition, tonic activation of Ih also contributes to average membrane potential, and therefore to presence, strength, and frequency of oscillation
in these neurons.

Regarding the series of sub-questions - these are quite varied. Perhaps it is better to generate another one or two focused, well-formulated questions on this. For now, I will answer them curtly below. Further, the papers I linked contain a wealth of information, and the McCormick & Huguenard (1992) paper is a detailed modeling study. Both papers are awesome and the authors are three of my all-time favorites so far.

I want to know if these kind of oscillations are unique to some special kinds of neuron?
Answer: Yes quite unique, because Ih channels are quite unique (they have been called "funny currents") and they are not present in every cell.

Is the control of oscillation parameter possible in every neurons and isolated neurons?
Answer: No, as the molecular machinery such as Ih channels may be lacking in most other cells.

Can a neuron or any other cell exhibit change in action potential independently?
Answer: That depends whether the cells are coupled through synapses or other means.

Do other cells except neuron and pacemaker cells exhibit oscillation?
Answer: Yes, some cells start to oscillate, for example in the degenerated retina (modeling work only) and there are non-neural cells that when cultured spontaneously start to oscillate.

Can a single neuron exhibit memory?
Answer: Yes, through long-term potentiation or depression.

References
- Bal & McCormick, J Neurophysiol (1997); 77:3145-56
- McCormick & Huguenard, J Neurophysiol (1992), 68(4): 1384-1400


What are the evolutionary reasons behind men being taller than women?

I assume by asking why, you are asking about the distal evolutionary causes, and not the molecular mechanisms that account for these things.

(Important disclaimer: these causes are difficult to be certain about; they require a fair amount of informed speculation.)

With that said: it is widely agreed upon in evolutionary biology that human males, as in other mammals, are thought to be larger mostly due to sexual selection. In other words, size is sexy, and sexy individuals fare better with respect to mate choice, on average. Sexual selection can also work via male-male competition. There may be other causes that are relatively minor contributors compared to this one.

Notice, however, that in humans, females evidently do not remain tiny with respect to males, but they get 'dragged along' in terms of their height, so that males are not drastically different in height (unlike, for instance, in elephant seals). This too may be a result of sexual selection, quirks of physiology across the sexes (e.g. genetics of dimorphism), or even natural selection. Think hip size and the size of human skulls.

Additionally, differences in development time (e.g. length and onset of puberty) can skew body size. Humans certainly exhibit dimorphism with respect to development.


Do dogs have something different about their physiology that allows them to pant without hyperventilating?

This article quotes a professor of respiratory physiology that says "dogs are built to pant just right. The mechanics of their lungs and chest set a precise rate for panting that minimizes the amount of work while maximizing cooling power." They also don't breathe fully when panting, so they can still cool themselves without increasing gas exchange. This is different than humans, who will hyperventilate to get rid of carbon dioxide (or you can intentionally hyperventilate and cause respiratory alkalosis).


Is there a maximum testosterone limit, or is it more accurate to say use?

Whatever is the exact definition of the threshold that the Olympic committee sets, it's going to be relatively arbitrary and unfair to some people.

When it comes down to it, biology is generally messy and blurry, and that includes matters of sex and gender.  Thus, even if most people cluster in a fairly straightforward manner into male and female, there are all sorts of things like androgen insensitivity syndrome that can end up causing a person's normal body state to be judged as too extreme for their gender.

In the end, there is no simple line that can be drawn simply because the biology of gender permits many different ways for naturally occurring variations to form a continuum across any given metric that one might wish to establish.


If oxygen is such a good energy source, why do plants release it?

Short answer
Plants release O2, because it is not an energy source. Instead, it is used to free energy from energy-rich organic compounds.

Background
Plants are solar powered. They release oxygen as a waste product during carbon fixation. Carbon fixation is basically the storage of solar power into carbon-bonds in glucose, a process referred to as photosynthesis or the Calvin Cycle.

To release the solar energy from glucose it has to be burned (oxidized). Oxidation of glucose can be realized via the the citric acid cycle (or Krebs cycle) and electron transport chain to generate ATP. O2 only comes in in the very last step by acting as the final electron acceptor to produce H2O (Fig. 1.)

Fig. 1. Electron transport chain in mitochondria. Electrons are sent through a chain of proteins that drive hydrogen transport out of the mitochondrial space. ATP-synthase uses the proton gradient to generate ATP. Source: Davis University College

Hence, O2 is not the source of energy, it is merely used to free it from energy rich compounds such as glucose. Because it is so abundant in the atmosphere, it doesn't make sense to store it.

Reference
- Berg et al., Biochemistry. 5th edition. New York: W H Freeman (2002)


High blood pressure is caused by an excessive amount of fluid circulating in the blood vessels, or an excessively small mean blood vessel diameter. The later is more associated with stress situations and stressful lives, while the former is more related to the theme of your question: electrolyte balance.

An electrolyte is any molecule that produces an electrically conducting solution when dissolved in water (http://www.medicalnewstoday.com/articles/153188.php). In other words, they are or give rise to ions or charged molecules when dissolved in water. Examples are sodium, potassium, calcium, magnesium, chloride, phosphate, bicarbonate, ...

Water, even though on its own is a neutral molecule, it is still polar. This means that it has parts which are more negatively charged (in concrete, the oxygen atom) and parts that are more positively charged (the hydrogen atoms). These are called poles, and are due to different electronegativities.

The result of this is that water will form electrostatic bonds with charged molecules such as ions, or, in other words, which causes salts to be soluble in water. This also means that water is attracted to places with a lot of charged molecules - places with higher osmolarity. The travelling of water from places with lower to higher osmolarity is called osmosis.

That's what happens when the blood has an excess of ions (and thus higher osmolarity) when compared to the rest of the body and the normal, healthy values. Water starts travelling from the different parts of the body to the blood, being attracted by the extra concentration of salts, and pushing the blood volume over the healthy limits. This also makes it harder for the kidneys to excrete water from the blood, increasing further blood volume and giving rise to hypertension.

As you can see, any charged molecule in excess in the blood can increase blood volume (through higher plasma osmolarity) and create hypertension. In our bodies, the most common and impactful electrolytes are ions, being Sodium the most abundant.

Because sodium is the most abundant in the blood and the most ingested electrolyte, it is usually referred as its excess being the cause of hypertension. The common salt we use to cook comes in the form of NaCl, containing Sodium and Chloride, both electrolytes. They are very useful and fundamental to our organism, but in excess can cause diseases such as this.


Does the size or mass of a body affect the time it takes for rigor mortis to sets in?

One of the main factors that impacts rigor mortis is temperature. Basically, a smaller body would slow down the metabolic processes behind rigor more substantially. Also, one of the first things that happens in rigor is the stiffening of muscles. An increase in muscle mass would increase the time for rigor as well.

Refer to these links: wikipedia and another that talks about rigor mortis within the scope of forensic pathology.

Hope that helps!

n.i.


How animals know which is carnivorous and herbivorous?

They probably don't know and probably don't need to. They tend to run away from potential danger and predators in the same evolution environment because those who don't run away will have fewer offsprings that exhibit similar behaviors.

If an animal suddenly sees a predator that his ancestor has never seen before, then it may not run away from it, to its own detriment. Dodo Bird thought humans were harmless.


There are lots of fish that live in environments without any light (below 1000m in the ocean there is no useful light for vision), however most aquarium fish have not evolved to live in those sorts of conditions. In the future, I think your best bet would be to remove the fish, clean the tank, and then try to manage your nutrient inputs so that the algae doesn't grow out of control.


We get goose bumps because of the flight or fight response or because of cool temperature. The process is that whenever our body experiences such stimuli, the arrector muscles contract and thus the hair follicles straight out. As per the evolutionary point of view, mammals possessed this feature to portray the enemy our response ( in fight). Given photo will tell you the arrector muscle's position so that u can understand how the follicles straight up.
And the thing about cool temperature, the goose bumps appear so that they can form an insulation sort of thing to prevent us from losing our body heat to the surroundings.


Measuring Bioluminescent Algae Intensity

As stated here:

The lunate cysts of Pyrocystis lunula have a bioluminescent emission spectrum with a peak intensity of 477.5 ± 1 nm.

So, almost any spectrophotometer should be able to detect it, it's just bluish visible light.


How is the subunit molecular weight different from the native molecular weight?

Your question is answered in the paper, the protein likely exists as a homodimer in vivo and denaturation (such as performed with SDS PAGE -> Western Blot) separates the dimers into monomers:

"To determine the quaternary structure, size exclusion high-performance liquid chromatography was performed using an Agilent 1100 series high-performance liquid chromatography system with a Bio-Sil SEC-250 column (300 by 7.8 mm) and a mobile phase of 0.1 M Na2PO4, 0.15 M NaCl, and 0.01 M NaN3, pH 6.8. A Bio-Rad standard was used to standardize the column's retention time with respect to molecular mass (supplemental data). All experiments were repeated twice with <0.05 min of deviation in the retention times. The molecular mass of XR was calculated from its retention time to be ∼53 kDa. Monomerization could be induced in the presence of 15% SDS, causing XR to elute as a single peak, with a retention time corresponding to a molecular mass of ∼34 kDa. The data suggest that the native XR is a noncovalently linked dimer. The significant difference between the calculated molecular weight of the dimer and its apparent molecular weight is not uncommon for XRs from other species (7, 21, 33), which also typically exist as dimers. However, to be certain of the protein size, N. crassa XR was subjected to mass analysis by electrospray ionization-quadrupole time of flight mass spectrometry. The highest abundance peak had a value of 38,381 m/z, corresponding exactly with the predicted molecular mass for the His6-tagged XR with the N-terminal fMet removed (supplemental data). Additionally, a 2M+ peak of about 20% abundance at 76,759 m/z corresponds well with the predicted mass of the dimeric form of the enzyme (76,762 Da)."


Genetic information storage and the extent to which it controls appearance/structure

The common phrase I've heard is "DNA isn't a blueprint, it's a recipe". More specifically, the nucleotides in DNA correspond to which proteins get made (coding DNA) and when and where (regulatory DNA). Just like a recipe doesn't specify the exact color of a cake or the position of each raisin, but does say "cook the cake for this long" (which will, in interaction with the heat of the oven, determine its color) or "put in this many raisins, at this general point in this general area", DNA doesn't contain the exact information of how you end up looking (hence why identical twins aren't really identical), but it does say how to make you how you are.

It also illustrates how much has to be "programmed" initially; how we are really needs to be understood as an interaction between DNA and the environment through the process of development, just as you can't completely understand a cake just from the recipe, you also need to know how chemistry and physics cause the things in the recipe to have the effects that they do. A lot of what goes on in development is cells growing, changing or dying depending on the chemical environment they're in, which includes what their neighboring cells are. The information in DNA basically consists of affecting that via what proteins get made when and where during development.

As for whether complete information about the entire organism's structure is stored all over the body, yes and no (but mostly yes). Yes, by default every cell in your body inherited its whole genome from the original zygote that started things, and you can indeed in theory clone a whole person from many random cells in the body. However in practice it depends on the cell: some cells lose their nucleus entirely, like red blood cells, so of course they don't contain the body's whole genome. Other cells could theoretically multiply or eliminate certain genes in a similar way as they specialize for the specific task they need to do, meaning they won't end up with the same genes as all the other cells in the body, but this isn't thought to be a common phenomenon especially in humans (cells will vary more in the expression pattern of their genes without necessarily changing the DNA sequence itself). This is also ignoring the ordinary mutation rates in DNA as the cell divides, which will yield differences between different cells of a given body even without that being a deliberate process. Hence cancer !

Some references on the possible variations of DNA in somatic cells (i.e. not ova or sperm)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3497787/

  It is commonly assumed that all healthy cells that arise from the same zygote possess the same genomic content, with a few known exceptions in the immune system and germ line. However, a growing body of evidence shows that genomic variation exists between differentiated tissues.

Elimination of actual DNA in nematodes and lampreys :

https://www.ncbi.nlm.nih.gov/pubmed/23123092

https://academic.oup.com/mbe/article-abstract/33/9/2337/2579241/Characterization-of-Somatically-Eliminated-Genes?redirectedFrom=fulltext

Quote from the first abstract:

  Chromatin diminution is the programmed elimination of specific DNA sequences during development. It occurs in diverse species, but the function(s) of diminution and the specificity of sequence loss remain largely unknown.

I have found no mention of it happening in humans however.


Doesn't meiosis form two pairs of similar cells and two pairs of opposite cells?

Great question - I think there are two misconceptions in your question that are interfering with your understanding.

First, crossing-over occurring at just the "tips" is just for clarity in textbooks so you can easily follow the different pieces of chromosome.

Although crossover events tend to occur at particular sequences, these don't have to be at the tips. There can also be multiple crossovers on the same chromosome, or none at all. See this link for some estimates of recombination rates for different species.

Second, gamete diversity doesn't depend only on crossing-over during meiosis, it also depends on the incorporation of just a single chromosome from each pair. Humans, for example, have 23 pairs of chromosomes. There are therefore 2^23 = 8388608 different combinations of chromosomes - with NO crossing over! Therefore, even without recombination, the odds of two genetically identical sperm fertilizing two genetically identical eggs are incredibly small.


How to interpret this cuffcompare result? Sensitivity over 100?

I don't know if this is still needed but I went through the source code of cuffcompare to see if this phenomenon is indicative of the false positive rate or an issue with the tool (and to provide a more thorough answer). It seems like it may be a bug in the code for cuffcompare (which is a massive amount of code). If you look at line ~1518 in the source code at this URL:

https://github.com/cole-trapnell-lab/cufflinks/blob/master/src/cuffcompare.cpp

There are several statements that suggest Sn values > 100% would be possible and should be reassigned to 100%. These results may occur from keeping "redundant" transcripts if they start with the same 5' intron. How do your "fuzzy" Sn and Sp compare to this result? are they are similar?

The developers are no longer maintaining this software in favor their new faster version, Hisat/Stringtie. However I find the output to be more complete from Tophat and Cufflinks. To get a better understanding of the output, you could compare the number of potentially novel features in your cuffcmp.combined.gtf to the total number of features in your new cuffcmp.combined.gtf using overlapping and contained features as a proxy for false positive rate. Comparing these values with the total number of lines in your reference annotation may provide you with another Sn estimate without performing qPCR.

# to count the number of potentially novel
grep -c "\"j\"" cuffcmp.combined.gtf

# to count the overlapping and contained features
grep -c "\"[c,o]\"" cuffcmp.combined.gtf

# to count the number of exact matches
grep -c "\"=\"" cuffcmp.combined.gtf

# To count how many features are identified for each gene
cut -f4  -d ";" cuffcmp.combined.gtf |   uniq -c

# To count how many known genes gene were identified
cut -f4  -d ";" cuffcmp.combined.gtf |   uniq -c | wc -l

# To count number of features in the reference gtf
wc -l reference_annotation.gtf

or if you prefer to use Bioconductor packages like rtracklayer in an R environment, you could read the cuffcmp.combined.gtf file and analyze the data further

library(rtracklayer) # if you have the package installed
rtracklayer::readGFF("~/full/path/to/cuffcmp.combined.gtf")


Why is there now only one Salmonella species?

Simply put, old habits die hard; physicians and other medical personnel have grown up with the old species designations so will continue to use them.  This is somewhat the reverse of the case with E. coli, where 80-90% of the genome is variable across strains.

Lin-Hui gives a brief history, where strains identified early were given specific names within Salmonella like typhi, typhimurium, panama, etc.  In 1966 it was proposed to lump serovars together among three species S.
choleraesuis, S. typhosa, and S. kauffmannii.  Shortly thereafter in 1972 with the advent of DNA techniques, it was shown they really should be all piled together.  There is one exception, Salmonella choleraesuis subsp. bongori, separated in 1989.


How far does your center of mass move from stance to stance?

You can find the relevant math here:

http://hypertextbook.com/facts/2006/centerofmass.shtml

The key factors are the body mass distribution, height, standing center of mass, heartbeat, clothing, etc. You can approximate the center of mass for a given stance as:

  In order to determine the center of mass of a person, we used the formula for torque:

$\Sigma\tau = r \times F$

  The torques due to the weight on each end of the person were set equal to each other. The displayed weight on the scale was the force, and there are two different radii. The first radius is the distance to the center of mass from the person's feet, and the second radius is the length of the board minus the distance to the center of mass from the person's feet. The net torque of the system is zero and therefore the torques on the opposite sides of the boards must be equal:

$w_1\times x = w_2\times (l~-~x)$

  where w1 is equal to the weight at the person's feet, x is equal to the distance from the person's feet to his/her center of mass, w2is equal to the weight at the head, and l is equal to the length of the beams. The resulting formula, when solved for the distance to the center of mass from the person's feet (radius one) is:

$x = \underline {~~~w_2\times l~~~}$

$\hspace {11mm}w_1~+~w_2$

  After determining the location of each person's center of mass, the ratio of the center of mass to the height of each person was calculated using the formula:

$x/h$

  where x is the location of the person's center of mass and h is the person's height.


Are there enzymes for every given reaction?

This will probably be a difficult question to answer definitively without some hand-waving or redefining the question; I can't imagine proving the negative result that no enzyme is possible for a given reaction, except for some cases where the reaction is just thermodynamically impossible outside of incredible conditions (for an extreme example, what about hydrogen fusion: the reaction exists, but the conditions necessary are outside the tolerance of protein-based catalysts).

As @tomd pointed out in a comment, enzymes do not change equilibrium, so enzymes are only possible for reactions that are thermodynamically favorable. However, some enzymes couple reactions that are thermodynamically unfavorable with highly favorable reactions to produce a net thermodynamically favorable reaction, which greatly increases the number of reactions that can theoretically be catalyzed.

As for whether any shape can be created out of polypeptides: given the diversity of amino acids and the structural effects of the tertiary structure of proteins, there is a near limitless array of combinations which exceeds human comprehension, but not a truly mathematically infinite number. There are interesting projects such as this one that seek to harnessed underutilized computing power to iterate all of these possibilities to search for useful drugs and explain the causes of disease.


Possible to get Furniture carpet beetle specimen for collection?

You might try calling up a local exterminator (ideally not a franchise) and asking them to save you a specimen the next time they are called out to deal with such insects. Donate some beer/weed/customer referrals by way of thanks and they'll help you out with future specimen hunts.


NADH vs. NADPH: Where is each one used and why that instead of the other?

The phosphate group in NADPH doesn't affect the redox abilities of the molecule, it is too far away from the part of the molecule involved in the electron transfer. What the phosphate group does is to allow enzymes to discriminate between NADH and NADPH, which allows the cell to regulate both independently.

The ratio of NAD+ to NADH inside the cell is high, while the ratio of NADP+ to NADPH is kept low. The role of NADPH is mostly anabolic reactions, where NADPH is needed as a reducing agent, the role of NADH is mostly in catabolic reactions, where NAD+ is needed as a oxidizing agent.

You'll find some more information about this in chapter 2 of "Molecular Biology of the Cell by Alberts et al.