How is the urea cycle regulated with respect to protein deficit?

Preamble

This question is extremely broad because, rather than there being a ‘one-click’ answer, whole areas of amino acid metabolism need to be considered. This is both inappropriate and impossible to do here — even if I understood everthing about it (which I certainly don’t). However I shall provide a specific biochemical answer (or partial answer, as all is not understood) regarding the regulation of the urea cycle, after commenting on some of the assumptions implicit in the question.

Comments on the assumptions of the question

I am not sure that ‘protein deficit’ is a useful metabolic construct. From the point of view of a clinician, yes, one can say that someone is suffering from protein deficiency or malnutrition, but in metabolic terms protein is a not the highest priority and will be broken down to provide glucose for the brain during long-term starvation. And it is well established that protein synthesis is under the control of hormones and growth factors (reviewed here), and this will affect the fate of dietary amino acids or those produced by protein turnover. In addition, the emphasis on hormones in the question seems to ignore the role of the concentration of amino acids and other intermediates in regulating metabolic pathways. Finally, there is control of the expression of the genes encoding enzymes of the urea cycle, which operates over a longer time period.

The Medical Biochemistry site provides a wider perspective on amino acid metabolism and nitrogen metabolism and the urea cycle.

Regulation of the Urea Cycle

The first point that should be emphasized is that the urea cycle does not exist in isolation from other metabolic pathways, but is intimately connected to them. This is shown in the diagram below:

It should be remembered that ammonia for the urea cycle only comes from the deamination of glutamate by glutamate dehydrogenase, and the transamination of other amino acids to produce this depends on a pool of α-ketoglutarate (2-oxo glutarate). A requirement for α-ketoglutarate also exists in relation to the regeneration of aspartate for the cycle itself.

The entry point of ammonia into the urea cycle is the reaction catalysed by carbamoyl phosphate synthetase:

It turns out that this reaction requires N-acetyl glutamate (NAG) for activity, and it is thought that this plays a regulatory role in the urea cycle, as increased intake of protein has been found to increase the hepatic content of NAG. Although aspects of this remain to be clarified or resolved, it is thought that the regulation occurs at the point at which NAG is synthesized from glutamate in a reaction catalysed by the enzyme N-acetyl glutamate synthase:

This enzyme is activated by arginine, giving rise to a model for regulation described more fully in a review by Caldovic and Tuchman, from which I quote the following:

  “… the hypothesis that NAG is a regulator of ureagenesis… If this hypothesis is correct, mitochondrial concentrations of glutamate and/or arginine may reflect the need for nitrogen disposal through their effect on the production of NAG by NAG synthase, glutamate as a substrate and arginine as an effector.”


Evolutionary support for parenting book "The happiest baby on the block"

How many more weeks in utero does Karp think would be ideal? I don't know Karp at all, but a quick search indicates he's known for soothing babies by swaddling. Great. My mother swaddled all her infants many decades ago.
If he is comparing human neonates to  primate neonates, he's correct. Baby primates are born pretty much knowing how to cling onto the mother with four extremities, necessary because primates are quadripedal, and need their arms to walk as well, meaning baby needs to hold on, aided by opposable toes. (Chimps and gorillas do support the baby with one hand longer, though.
But what evolutionary advantage would it serve for our infants to come out grasping? humans are bipedal, meaning we have arms that can be used to carry an infant. If we need our arms, we have the intelligence to fashion slings or carriers.
The same goes for any ability: sight, motor skills, etc. They don't need to be born with these skills, because they are cared for.
Antelopes drop a newborn which is up in minutes and able to see and run. Cats drop a newborn which can wiggle, crawl some, is blind and as helpless as a human.
Babies, through evolution, are able to live outside the womb (assuming no complications) without extraordinary maternal assistance from about 36 weeks on. A look at growth charts show steep rises in both cranial size and weight gain.

But you can see that a baby's head at the 10%ile takes at least six weeks to catch up to a baby the size of one born at 90%ile. Why doesn't that baby just gestate for 6 more weeks?
There is much more than head size going on here. There is the placental size, the amount of amniotic fluid, the possibility of meconium aspiration, etc.
Stillbirths are twice as common at 42 weeks and 4 times as common at 43 weeks.

Approximately 20% of postterm (41 weeks gestation) fetuses have fetal postmaturity syndrome, with chronic intrauterine growth restriction from uteroplacental insufficiency. These pregnancies are at increased risk of umbilical cord compression from oligohydramnios, [low Apgar scores], intrauterine passage of meconium, and short-term neonatal complications (such as hypoglycemia, seizures, and respiratory insufficiency). ...[T]he 4-fold decrease in the incidence of the meconium aspiration syndrome in the United States from 1990-1998 has been attributed primarily to a reduction in the postterm delivery rate [(induced delivery at 41.5 weeks)]. Postterm pregnancy is also an independent risk factor for neonatal encephalopathy and for death in the first year of life.[17, 18]

Maternal complications and death also increase with post-term deliveries.
Are term babies actually evolutionary preemies? I haven't read Dr. Karp's book or heard his reasoning, but it seems superficial to me. Medically, from an infant and maternal standpoint, a 38 week delivery is ideal. Over hundreds of thousands of years, the female uterus and pelvis, and the fetal placenta and amniotic fluid found the most favorable time for delivery into a human environment.
If we gestated for two years, like elephants, yes, our babies would be more capable at birth, but we aren't elephants, and mothers and babies would die.
Postterm Pregnancy (Medscape)
Elephant birthing and calves (Wikipedia)


What causes skewed ladder bands on an agarose gel?

If the ladder is on an edge of the gel, it may be a process of different density as a result of how the gel cooled (or was poured too slowly). I've loaded more DNA loaded in a gel and it doesn't cause this kind of warping for me. It may be the buffer of the ladder is different from that used to make the gel. Your bands don't look particularly sharp, so I would suspect that the running voltage is too high and causing the surface of the gel to heat up and therefore "smearing" the bands. Try running the voltage at 75 V  for a proportionately longer time to see if this solves your problem.


True anatomical/physiological explanation for "metaphysis" etymology

meta-:

  word-forming element of Greek origin meaning 1. "after, behind; among,
  between," 2. "changed, altered," 3. "higher, beyond;" from Greek meta (prep.) "in the midst of; in common with; by means of;
  between; in pursuit or quest of; after, next after, behind," in
  compounds most often meaning "change" of place, condition, etc. This
  is from PIE *me- "in the middle" (source also of German mit, Gothic
  miþ, Old English mið "with, together with, among"). Notion of
  "changing places with" probably led to senses "change of place, order,
  or nature," which was a principal meaning of the Greek word when used
  as a prefix (but also denoting "community, participation; in common
  with; pursuing"). (Etymonline)

physis:

  The growth plate, or physis, is the translucent, cartilaginous disc
  separating the epiphysis from the metaphysis and is responsible for
  longitudinal growth of long bones. (The Royal's Children Hospital Melbourne)

Anatomically and physiologically, meta- in metaphysis means next after physis (growth plate or epiphyseal plate) and refers to the changing (growing) part, which is in between the non-growing parts of a long bone (diaphysis and epiphysis):

  The metaphysis is the wider portion of a long bone adjacent to the
  epiphyseal plate. It is this part of the bone that grows during
  childhood; as it grows, it ossifies near the diaphysis and the
  epiphyses. (Orthopaedicsone)

Picture: Parts of the bone (Radiopedia, Creative Commons license)


Will a bone marrow transplant change one's blood type?

Bone Marrow transplants are extensively matched in order to prevent rejection. Current matching methodology is HLA matching: Stanford Children's Hospital Guidelines

  How are a donor and recipient matched?
  Matching involves typing human leukocyte antigen (HLA) tissue. The antigens on the surface of these special white blood cells determine the genetic make-up of a person's immune system. There are at least 100 HLA antigens; however, it is believed that there are a few major antigens that determine whether a donor and recipient match. The others are considered minor and their effect on a successful transplant is not as well defined.

  Medical research is still investigating the role all antigens play in the process of a bone marrow transplant. The more antigens that match, the better the engraftment of donated marrow. Engraftment of the stem cells occurs when the donated cells make their way to the marrow and begin reproducing new blood cells.

However, because the HLA matching doesn't utilize blood-type and the recipient's marrow is destroyed in the process, then if the donor's marrow produces different red blood cells - then so will the recipient with time:

  Does my blood type change after SCT or [Bone Marrow Transplant]?

  Yes.  The recipients blood type eventually changes to the donor type.  That means if you had a blood type of A+ prior to transplant and your donor had a blood type of O, eventually your blood type would become O.  I may take several weeks, possibly months for your original blood type to disappear, but eventually it will.

What's interesting is that blood-typing is not be expressly necessary with the modern bone marrow transplant process. The danger of mixing two antagonistic blood types in vivo is that the recipient's immune system attacks the foreign red blood cells resulting in body-wide rejection. However, because the immune system's response capabilities are decimated by the destruction of the recipient's bone marrow (usually accomplished via chemotherapy or radiation), it can't mount much of an attack in the first place. That's not to say the body can't mount an attack, or that the donor's tissue can't mount an attack on the recipient (Graft-Versus-Host-Disease [GVHD]) - but the better the HLA match the less likely issues are to arise, which is why we do the more accurate and relevant HLA matching instead of blood-typing.


(How) Does the human digestive system process petroleum jelly, aka petrolatum?

There are controversial case reports about systemic absorption of paraffin used for constipation. These reports mention systemic effects of paraffin absorption and one of them report liquid paraffin accumulations in
abdominal visceral organs. (full text article about paraffin)

  Liquid paraffin is indigestible and is absorbed only to a limited
  extent following ingestion.

+

  As inert substances the ingested mineral oils mostly are excreted
  intact in feces and to some degree in urine. However, some absorption
  form the small intestine has been observed (Stryker 1941). Using
  radiolabeled mineral oil, it was established that the amount absorbed
  in rat was appr. 1.5 % (Ebert  et al. 1966).

  (full text article)


Why did women historically have such a high mortality rate during birth?

That's an interesting question. And it is also a common misunderstanding of evolutionary processes.

Thanks to @Chris comment, we know/can assume that high mortality rate is not a consequence of industrialization but has ever been before the era of modern medicine.

Women don't let themselves die in order to improve the species. Those women that carry a gene forcing them to commit suicide in order to improve the species won't pass on their genes, and in consequence no women will ever suicide in order to improve the species. In other words, altruistic behavior cannot appear and spread over time. This is the standard view of selection (and probably the good explanation in our case).

Now, I have to say that I lied in the previous paragraph! There is a field of study called social evolution which aims to study social traits. Social traits are those traits which influence not only the fitness of the individual carrying the trait but also the fitness of other individuals in the population. Theoretically all traits are somehow social traits! Typically altruistic behavior is among those social traits that cause a decrease (a cost) in the carrier fitness for an advantage (a benefit) for one or several other individuals in the population. There are several models (which are still debated in particular concerning the assumptions of these models) to explain the evolution of such traits. The most famous, most commonly used and most theoretically studied one is Kin selection/Hamilton's rule. You'll find some explanations about this rule on this post. The concept of population structure is key in the understanding of Hamilton's rule. Also important are the concept of levels of selection, which gives a possible explanation for the evolution of altruism, the concept of lineage selection, and finally the concept of reciprocity (but that doesn't make much sense in the current context!). Some people would not classify these models as I did, some would add other models, some would melt two models into one…

For one of these models to be correct we would need high lineage split and extinctions in human history which I don't think is really the case. Or we'd need that the death of a woman is particularly benefit to her family. I don't think first human were cannibals. Women were probably very often pregnant and males had to fight to be the father. So dying would probably not free much opportunities for the sisters and brothers…. One would need to write some equations and gather more information than what I have but intuitively I don't think that high mortality rate in women while giving birth is an altruistic behavior.


Which algae grow fastest under optimal conditions?

The answer to your question depends on many variables. To narrow down the list of possible species it might be helpful to list under which conditions you intend to grow this algae and whether you want to give an additional carbon source such as glucose or acetate.

To give you an idea why this is important: the fastest growing alga I have ever worked with is Chlorella sorokiniana with double timings in the range of two hours. However this was in acetate containing medium and it would not have relied a lot on photosynthesis to grow nor would this make a lot of sense in open pond cultivation systems.

In terms of photoautotrophic algae, we have seen the most consistent quick growth (OD) in our system (Algem photobioreactor) for Dunaliella species. But this is based more on experience than rigorously testing a lot of species. In general there also seems to be a correlation between size and growth speed. Some cyanobacteria have a growth rate of around two hours Article


How does the pancreatic beta-cell know how much insulin to secrete in response to glucose?

Yes, pancreatic beta cells can indeed sense the level of blood glucose. They respond to high glucose concentrations by secreting insulin, and stop (or reduce) secreting insulin when glucose concentration falls. This is a classic example of feedback regulation (homeostasis) in physiology.

Exactly how the glucose sensing in beta cells has been the subject of much research for decades; a freely available review is here. You are correct that phosphorylation and further metabolism of glucose by the beta cells is required for sensing. The current theory is that mitochondrial oxidation of glucose leads to increased ATP levels, which is detected by ATP-sensitive potassium channels at the plasma membrane, which in turn leads to secretion of insulin.

When glucose levels fall, beta cells reduce their glucose metabolism because they use the glucokinase enzyme to phosphorylate glucose, and glucokinase is a low-affinity enzyme that becomes inactive at lower glucose levels. Therefore, uptake and oxidation of glucose is reduced, ATP levels fall, and insulin secretion stops.

This is the current consensus I believe. But these metabolic processes are difficult to study, and the precise nature of the connection between glucose metabolism and the ATP-sensitive channels is still somewhat controversial.


Oxidation does not mean inflammation. But oxidation can be a cause of inflammation.

Oxidation processes are part of normal cell metabolism (mostly in mithocondria). They lead to reactive oxygen species ($O_2^-$, $H_2O_2$ and $OH-$) which can trigger inflammation via activation of some transcription factors:

  NF-κB, AP-1, p53, HIF-1α, PPAR-γ, β-catenin/Wnt, and Nrf2 [1]

The metabolic processes also produce some  antioxidants to inactivate those reactive oxygen species. But the excess of oxidants leads to oxidative stress which seem to be linked with inflammation and even to cancer [1].

  rapeseed oil is less saturated and therefore more likely to oxidize

Being "less saturated" I guess it would be better, as studies have found that saturated fatty acid promote inflammation [2], while unsaturated fats decrease the production of inflammatory cytokines and reactive oxygen species [3].

  So my question is this: is it really possible to safely say: "oxidation = inflammation"?

NO. By definition, oxidation is a chemical reaction in which a molecule, atom or ion loses electrons [4]. On the other hand, inflammation is a very complex process, a biological response to harmful stimuli and requires cellular interaction [5].

References:

Reuter S, Gupta SC, Chaturvedi MM, Aggarwal BB. Oxidative stress, inflammation, and cancer: how are they linked? Free Radic. Biol. Med. 2010 Dec 1;49(11):1603-16. doi: 10.1016/j.freeradbiomed.2010.09.006. PubMed PMID: 20840865.
Saturated Fatty Acids and Inflammation: Who Pays the Toll?
Alan Chait and Francis Kim
Arterioscler Thromb Vasc Biol. 2010;30:692-693, doi:10.1161/ATVBAHA.110.203984
Supplement: n–3 Fatty Acids: Recommendations for Therapeutics and Prevention:
Philip C Calder
n−3 Polyunsaturated fatty acids, inflammation, and inflammatory diseases
Am J Clin Nutr June 2006 83: 6 S1505-1519S
Wikipedia contributors, "Redox," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Redox&oldid=621442954 (accessed September 13, 2014).
Wikipedia contributors, "Inflammation," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Inflammation&oldid=625272396 (accessed September 13, 2014).


It's very likely that memory is "lossy" and holographic, such that you can keep adding more information indefinitely, but retain it with less and less accuracy.

Memory isn't a digital storage system with X gigabytes of capacity, and the inputs to memory aren't neat little packets. What we remember are a web of associations and patterns. Vastly oversimplified, we group similar memories together into a baseline, and remember the deviations from that.

If you walk the same route to work every day, you take in a huge amount of information the first few days: stretches of residential buildings, cars parked on the street, portions of curb painted red, trash in the gutters. In successive days different cars will come and go, front yards will get overgrown and trimmed, etc, but these details get mixed in with what you saw the first few days into a blurrier and blurrier sort of average. Trillions of impressions from hundreds of days take up very little more capacity than the first day did, and still tell you what you need to know about the route.

Imagine that there's a particular green car of common make and model, that was parked in front of a certain house about 3/4 of the time for the first hundred days you walked the route. Your memory reduces this to something like "green car usually along here somewhere". If the green car stops parking there, you'll probably notice "green car not there today" because that's a contrast to the common case that you've memorized. But if a week goes by with no sightings of the green car, it's very hard to remember which day you last saw it, because you don't remember individual sightings. (I actually had this happen to me with my own car; I discovered it stolen on a Wednesday and could not for the life of me recall whether I'd seen it on Monday or Tuesday even though I'd walked past the spot it should have been parked both days.)

As you remember more things, you remember them in less and less detail; you can't remember if you've been to New Orleans once or twice; you can't remember which memories were from your first trip to Las Vegas or your second, etc. So the brain never becomes full, it just becomes fuzzy.


Identification of store-bought succulent plant

The only reason I have any clue as to what this could be is because I have one that looks exactly like it and, in a stroke of sheer genius, I wrote the name on the bottom of the pot. I think it is some member of x Pachyveria, which are intergeneric hybrids of Pachyphytum and Echeveria. Because there are so many, determining the exact cultivar may prove difficult. Mine is "Blue Pearl" and it looked very similar until it's untimely demise.

You can check out this website to see some different varieties. Actually, some of the Pachyphytum look pretty close too.

Compare w/ x Pachyveria "Cheyenne" (source):

and x Pachyveria "Little Jewel" (source):


What are "anchor regions" in the human genome?

Good question. Anchor regions are regions that connect to the nuclear matrix. More specifically, in eukaryotic organisms, chromatin is anchored to the nuclear matrix by short DNA sequences of about 100-2,000 bp called matrix attachment regions or MAR. To answer the second part of your question, there are many categories (and opinions about those categories) of anchor regions. The most comprehensive way of categorizing these regions however I believe is by whether they are constitutively (always) or transiently (sometimes) bound to the nuclear structure.


In what animal species is the sex ratio skewed in favour of the fertile female?

It is advantageous to have a skew towards more males. Males can be expendable as they are only required briefly for impregnation and can then focus on providing resources for the mother and young and protection. This breaks down when this is no longer the case, for example in humans we are closer to a 50/50 divide.

This article notes that in aphids, there are twice as many females as males, the same is true for daphnia. I don't think the reason behind this is known. In reptiles, the female to male ratio can depend on temperature of incubation thus this can lead to strong fluctuations.

An interesting principle is Fisher's principle:

  Fisher’s principle explains why for most species, the sex ratio is
  approximately 1:1. Bill Hamilton expounded Fisher’s argument in his
  1967 paper on “Extraordinary sex ratios” as follows, given the
  assumption of equal parental expenditure on offspring of both sexes.
  Suppose male births are less common than female. A newborn male then
  has better mating prospects than a newborn female, and therefore can
  expect to have more offspring. Therefore parents genetically disposed
  to produce males tend to have more than average numbers of
  grandchildren born to them. Therefore the genes for male-producing
  tendencies spread, and male births become more common. As the 1:1 sex
  ratio is approached, the advantage associated with producing males
  dies away. The same reasoning holds if females are substituted for
  males throughout. Therefore 1:1 is the equilibrium ratio.
  Source


How to set the phenotype in GWAS analysis?

Simply, First of all, you can group samples as survived animals and dead samples and you have a binary phenotype.

In a different approach, you can use survival time (time to death) as an ordinal variable phenotype. If you want you can utilize survived sample by assign a large death time value to them.

In the third approach, you can cluster the survival time (time to death) into the desired $n$ groups by the simple procedure like $k$-means. and you have coarse grain ordinal variable you can add survived sample group at the end of The Spectrum.


Why do anaerobic bacteria require a low redox potential for their culture media?

The higher the redox potential is, the higher the oxygen dissolved in the media will be. Lowering this potential insure that the oxygen concentration is lower and that the anaerobe will be able to grow easily.

Several steps can be done while preparing the media such as boiling to remove oxygen and adding chemical which reduces this redox potential to dissolve oxygen back into the medium.

As for the natural habitat, they naturally have no or really really low amounts of oxygen. If the habitats containing little oxygen have other molecules able to reduce redox potential is a good question.

Lowering the redox potential is mainly important for the medium since there is oxygen involved (hard to remove 100% while preparing media).

I hope my answer helps.


What determines the efficiency of electron production in photosynthetic bacteria?

You may or may not consider this an actual answer to your entire question, but it's interesting nonetheless.

A physicist friend of mine did some work recently modelling the quantum dynamics of photosynthetic complexes, and their coupling constants for passing energy throughout the photosystem. His results showed that, (and I believe this is in agreement with the literature), that photosynthetic systems are actually about as efficient as it is possible to be (not only this, but they are the most efficient energetic systems known to man I believe - over something like ~90% efficient).

If you begin altering positions of chromophores and so on, the photosystems exhibit remarkable robustness and you get a more or less logistic decay in efficiency (i.e. removing one or 2 chromophores results in marginal reductions in efficiency, more still in considerably more severe debilitation, until ultimately it's efficiency is markedly lessened, but further manipulation has a plateau in efficacy reduction).

Much of the work that's been done on the quantum biology of photosystems has concerned the FMO Complex (Fenna-Matthews-Olson) which is a simplified model system from photosynthetic algae - you might find more detailed answers to your queries by reading up in this area.

As for discrepancies seen in photosynthetic effectiveness bought about genetically, there are theories that suggest that the organisms are actually protecting themselves. E.g. to avoid over-production of ROS species. I can't offer you much in the way of a well evidenced case for this though, it's just a conversation I had with a post-doc at work recently, who completed his PhD on photosynthetic cyanobacteria.

EDIT Here's one of the papers about optimality in the FMO:

http://aip.scitation.org/doi/pdf/10.1063/1.4930110


Regarding inherited fertility in animals

No it isn't necessary that the parents should be of the same species. Mules (male donkey X female horse) have been found to be fertile (reference). The wikipedia page on hybrids lists many inter-species hybrids that are fertile including Beefalo (Domestic male cattle X american bison). There are also many canine hybrids which are fertile. Wholphins have been found to be fertile.

  A wholphin or wolphin is an extremely rare hybrid born from a mating
  of a female bottlenose dolphin (Tursiops truncatus) with a male false
  killer whale (Pseudorca crassidens).

So in short, for a hybrid offspring to be fertile, it doesn't necessarily need to be of the same species.


Image analysis of GFP-tagged protein localization bursts

Yep, the Hough Transform is a way to pick out shapes you're interested in, in this case they probably have it set to find circles, and they use that to segment the image.

I think that you have interpreted their methods correctly.  For each cell they make a trace of localization score vs. time, localization score defined in arbitrary units as the difference between the mean of the five brightest pixels and the mean of the remaining pixels in the cell.  I think the lowest 20% refers to the frames in the video that have the lowest 20% of localization scores.  They take the lowest 20% of localization scores, calculate a standard deviation, and then for any frame that has a localization score that is more than 1 standard deviation above the mean of those 20%, you say that frame exhibits a burst of localization.  If I'm understanding this correctly, this process would be repeated on every individual cell.

My interpretation is that the 20% doesn't have anything to do with the signal intensity from the background pixels, and it comes from analyzing the series over time, not a single image.


Both statements are correct, but an understanding of why they are not contradictory requires a bit of explanation.

For "spontaneous" reactions, those which occur naturally, entropy must always increase.  As a general rule, one of the easiest ways to increase entropy is to release energy, so we generally find that spontaneous reactions release energy.*  It's a pretty decent rule of thumb to use.

In the case of an anabolic reaction, we're putting together complex molecules from simple ones, and for these particular reactions we see they don't release energy.  They in fact "consume" energy in their formation.  This is reasonable, so what we find is that such reactions are not "spontaneous."  We don't see them just occurring on their own.

To make an anabolic reaction occur, we need to change the environment such that the reaction becomes spontaneous. We need to change the environment such that the reaction releases energy.  To do that, we start off with inputs which have even more energy than the final product should (such as extra kinetic energy from heat, or a strong oxidizer to reduce one of the reagents, or any one of a number of chemical and mechanical approaches).  Now the formation of the complex molecule can release energy, so it can occur spontaneously.  When we do this, we release some energy, but not all of it.  The rest of the energy is consumed in building the bonds of this molecule that would not otherwise have spontaneously come into being.  The released energy is typically seen as waste, and the energy pent up in the molecule is your desired product.

So in the end, the reason why there's no conflict is the "In general..." bit in the first quote.  You can cause a reaction to occur that consumes energy, but you typically have to do some clever things to put the energy into it.  Reactions which release energy occur spontaneously.  In general, we find "spontaneous" reactions occur far more often, hence the rule of thumb.

* I'm pretty loose with energy and entropy here to try to paint a simple picture without all of the confusion that entropy always brings to a discussion.  As you learn more, do expect to need to be more precise than I am here.


Manual of Clinical Microbiology.

My version is old, but it is an excellent reference considered gold standard in the clinical science industry and by educators.   It has been used by clinical microbiologists for many years and is still coming out with updated revisions. It comes as a two volume set due to comprehensive content. Published by the American Society for Microbiology.

http://www.asmscience.org/content/book/10.1128/9781555817381


What happens when lightning strikes us? How is it fatal?

Minor shocks definitely can paralyze a part!  Get on youtube and watch videos of people who cant let go of electrical wires or who are hit by tasers.

Paralyzing a part does not kill you.  Lightning can kill in two ways.

Arrhythmia.  Having arrhythmia or asystole is what kills most people hit by lighting.  As regards lesser shocks - the handymen who are hanging on to a live wire and can't let go (because their hands clamp down) can stay that way for a while.  Eventually the current produces an arrhythmia in the heart and that is what causes death.  If someone goes down this way from lighting or a lesser shock, you might be able to get them back with CPR.

When you see a whole herd of animals killed by a single strike, that is why. The heart is sensitive.  I do not understand why people's hearts do not similarly stop when they are hit with tasers.  I think sometimes they do.

Resistive heating.  Lightning can burn you.  Mostly the electricity goes over your skin and concentrated at conductors, like your phone.  That hurts but won't kill you.  Lightning going thru you can burn you on the inside which can damage your organs.  That is rare.

https://www.cdc.gov/mmwr/preview/mmwrhtml/00052833.htm
https://en.wikipedia.org/wiki/Lightning_strike


Short answer

Yes, you pretty much nailed it. Inbreeding of (and from) an isolated population.

Long answer

According to wikipedia > polydactyly, there are 39 known polmorphic sites underlying variance in polydactyly. It is therefore not a trait with a simple mode of inheritance.

There are two important (somehow related) concepts to understand to explain the relatively high frequency of polydactyly (and other genetic disease such as maple syrup urine disease) in Amish.

High inbreeding
Important population bottleneck

If you have no absolutely no background in biology, the following might be a little bit complicated. You might want to make sure you know some concepts (such as deleterious, recessive, dominant, homozygous, Hardy-Weinberg equilibrium, locus, allele and of course inbreeding and population bottleneck) by googling them.

Inbreeding

I will, here talk only about one mechanism by which inbreeding causes those diseases.

There is a positive correlation between how deleterious is a mutation and how recessive it is (the more deleterious, the less dominant, the more recessive). The post "Evolution of dominance of alleles" will probably help you to understand why this is true.

Inbreeding increases the frequency of homozygote loci and therefore, increase the probability of a locus which polymorphism explain variance for the disease to be homozygote deleterious. Using Hardy-Weinberg formula with Sewall Wright work, if at a given locus the allele A is deleterious and is present at frequency $p$, then the frequency of the homozygotes AA is $p^2$ without inbreeding (under Hardy-Weinberg assumptions). Taking inbreeding into account, this frequency becomes $p^2 + Fp(1-p)$ (where $F$ is the coefficient of inbreeding). In words, the higher is the inbreeding coefficient, the higher is the frequency of homozygotes (including homozygotes for the deleterious alleles).

In short, inbreeding matters because of dominance. There are other reasons why inbreeding matters though but that would be the subject of another post.

Bottleneck

In population biology, a bottleneck is is a sharp reduction in the size of a population. Imagine you have a population of size $N$ and you selection a fraction $\frac{N}{1000}$ of this population, you are going to lose a lot of alleles due to random sampling. Most of the times you are going to lose deleterious alleles (as they were already present at low frequency in the original population) but sometimes you are going to pick up a deleterious allele. The frequency of this deleterious allele was maybe 0.00001 in the original population and then suddenly its frequency jumps to 0.1. This is a big deal.

The Amish went though an important bottleneck, there was a time when the descendent of the modern-day Amish reproduced with everybody and at some point, they stopped doing so as they decided to create the amish community (I actually know little about the Amish history but I assume something similar happened). This community was formed by about 200 families only (according to this not-necessarily-trustable source, so very little genetic variance) in 1693 in Switzerland (according to wiki). They probably "won" by not having the alleles coding for clubfoot, sickle-cell and cystic fibrosis alleles (just to cite a few example) but they "lost" by drastically increasing the frequency of alleles coding for polydactyly (and some other diseases).


What you might be experiencing is olfactory fatigue, the temporary, normal inability to distinguish a particular odor after a prolonged exposure to it.

It's a form of neural adaptation, a change over time in the responsiveness of the sensory system to a constant stimulus. This adaptative mechanism might prevent the overloading of the nervous system.

However, some people (maybe most of them?) are able to smell their own breath. At least, I know I do. I can't point you to any statistics, but it might be an interesting research project, figuring out how many people can smell their own breath.


This is Hypena obsitalis, aka the Bloxworth snout, a moth of the family Noctuidae.

Personally I hate the word pest, but this little beauty eats Parietaria und Urtica (Nettle) so I can't think of anyone seeing this as a pest species.


The main reason is that there really isn't any one "cold," but rather the word is used to describe many different infections that simply have the same symptoms. The reason for these same symptoms is that almost all of the symptoms that one experiences in a cold are actually the immune response to said infection. For instance, a fever is used to make the body less hospitable for the infection causing agent and throwing up is used to ensure that harmful substances are removed from the digestive system before they can cause too much harm.

The reason that the body can't simply evolve resistance to all of these possible infections is both because the infections evolve too and because there are simply too many of them that all need a separate method to be defeated. Therefore, curing the common cold is effectivley curing the majority of known ailments.


How much can you learn about species variation from a skeleton?

It seems as if this article is purely speculative. They didn't mention any DNA testing, but instead discussed physical features.

There are two "types" of archaeologists: clumpers and splitters. Clumpers (like the author of this article) believe that there is wide variety among members of the same species, and so it is often wrong to categorize every new hominid fossil as being a different species. Splitters like to "split" their findings into new species, even though there is no evidence that speciation had ever occurred; they just decide that since the remains look different, they must have speciated.

In the future, I hope that archaeologists will have more sophisticated means of sequencing the DNA of ancient remains, allowing them to construct an accurate phylogeny


Is this pCAMBIA co-transformation possible?

Please check and tell me and how do I go about the co-transformation of rice using Agrobacterium starting from E.coli


Microarray images (at least for Illumina arrays) will come in .tiff format and are huge compared to the summarized formats (.sdf/.cel). Most places will not archive the raw images (so you won't find them online) and even when you run the microarray, you will often times need to make a special request to output raw images. iirc .jpg images are useless due to compression artifacts.

You can use the proper bioconductor libraries to extract data from the 'exotic' file formats. There are many bioconductor workshops archived online that will go through the steps of microarray analysis.

http://www.bioconductor.org/packages/release/bioc/html/affy.html

http://www.bioconductor.org/packages/release/bioc/html/beadarray.html

http://master.bioconductor.org/help/course-materials/2007/BioC2007/labs/oligo/BioC2007-oligo.pdf


Why a repeat wasp sting cause an anaphylaxis shock?

The reason is the way anaphylactic shock is caused by massive release of certain cytokins as well as inflammatory mediators such as histamine by two types of white blood cells: mast cells and basophils. This release is triggered by the binding of immunoglobulin E (IgE) to the antigen (the foreign substance provoking the allergic reaction). Antigen-bound IgE then activates so-called FcεRI receptors on the mast cells and basophils. IgE molecules specific to the allergen provoking the allergy are not present in the blood in sufficiently large quantities until after the first (several) exposures to this foreign material. Initial exposure triggers IgE production by specific B-lymphocytes. Only once one or more exposures to the antigen have occurred will there be sufficient quantities of the relevant IgE to trigger this excessive mast cell and basophil reaction.


Do toxin producing strains of E. coli constantly produce toxin or only under certain conditions?

1) That depends on the fact, if the protein in the bacterium is regulated somehow or it is constantly expressed. That could be different for different toxins and even for the same toxins in different strains, so there is no  plain answer for all strains and toxins.

2) That, I guess, also depends on the toxin. There are some that are basically toxins, but do not make people sick. Sometimes, the toxin is produced by the bacterium, but never secreted. Sometimes it is secreted, but has no influence on the host. Sometimes the host does react to a toxin. But the human immune system can also react to the bacteria before they start producing toxin (if it is somehow regulated) or before the toxin concentration secreted by the bacteria starts to be harmful.

In the case of E. coli O157:H7, this paper states it produces two different Shigatoxins (that were supposedly causing its pathogeny), but also some other toxins/toxin-like proteins.

I have studied some E.coli genomes previously, some non-pathogenic had several toxin-related genes, some pathogenic had actually none at all (at least none that could be annotated).


How does low cysteine conditions affect pheomelanin production?

First: Your teacher is right with the statement that a low cysteine concentration affects the synthesis of pheomelanin. To understand this, you need to take a look at the biosynthesis pathway of melanin (from here):

The first steps for both melanin forms are the oxidation of the amino acid Tyrosine to DOPA (L-3,4-Dihydroxyphenylalanine) and the to DOPA quinone by the enzyme Tyrosinase (abbreviated Tyr). In the following step the branches divert, if there is enough cysteine present in the cells, then Cysteinyl-DOPA and subsequently Pheomelanin are synthesized.

If the cysteine concentration in the cell falls below the threshold of 0,13µM (this is taken from this paper), then the switch to eumelanin production occurs.

In the case of you second question, there is a different setting. The overall rate of the melanin production (no matter which flavor) depends on the amount of active Tyrosinase (for the production of the first steps in the synthesis cascade). The production of this enzyme is regulated by receptors in the cellular membrane (and different other factors).

In fair skinned people (classically red-haired and with freckles) these receptors are not fully functional, resulting much less Tyrosinase enzyme in the cells. This results in fewer available precursors for the melanin production and in turn in less need for cysteine. The reason is that the cysteine pool of the cell is not getting exhausted.


Without plant breeding and domestication, would most of the foods consumed by humans evolve to become inedible?

Plant defense against herbivory

Plenty of plant species evolved defense mechanisms. There is a large variety of defense mechanism. Have a look at the wikipedia article Plant defense against herbivory for more information. Such defense mechanism often comes at a cost and therefore the mechanism can be maintained only if herbivory is sufficiently common and costly. Note that herbivory might be beneficial to some animal species typically as it can help to disperse the seeds.

plant-herbivores Co-evolution

Herbivores co-evolve with plants and develop mechanism to deal with plant defense mechanism. Such coevolution often yield herbivores to specialize in feeding in a handful of plant species only.

Human consumption

Most of what human consume is artificially selection. We specifically allow the breeding of individuals that present trait that are pleasant to us. In such condition, a defense mechanism would be a highly deleterious trait.

  Do species evolve to avoid being consumed, especially the animal species which have no need to leave seeds?

I don't understand this sentence. Do you mean "[..] especially plant species being consumed by animal species that don't help spreading the seeds"?

If this is what you meant, then yes. If herbivory comes at non benefit for the plant, the overall cost of herbivory will be more important for the plant. All else being equal, a mutant that present a defense mechanism would have a higher fitness if the herbivores do not offer any benefit to the plant being eaten.


Is there a measure of human genetic variation, where human genetic variation can differ more than 1%?

The question makes it clear that the poster is aware of the different ways of estimating human genetic variation, and he is also no doubt aware of the fact that Wikipedia is written by “people like you” who may not be experts in the field or have updated an old entry based on limited data. Let me address what appears to be the cause of confusion in this question — certainly in other questions on this topic.

For simplicity let us take a suitable round number for the Human/Neanderthal relatedness. Then the poster’s first quotation can be simplified as:

  The proportion of Neanderthal-inherited genetic material in modern Europeans is 2%.

and his second quotation simplified as:

  Neanderthal-inherited genetic material is absent from modern Africans.

A common conclusion drawn from this is:

  The genetic variation between modern Europeans and Africans must therefore
  exceed 2%, rather than being only ca. 0.5%.

Why is this wrong?

This conclusion is wrong because the 2% and 0.5% are measures of different things.

For simplicity, a value of human genetic variation of 0.5% can be regarded as the extent by which the DNA of the coding regions of the genes of two humans differ because of single nucleotide polymorphisms (SNPs) — single base changes in the same gene (that may or may not affect the gene function). This assumes all humans have the same 20,000 or so genes.

Now let us make an overall comparison of the genes of humans and Neanderthals. Since they diverged from a common ancestor their genomes underwent changes due to point mutations, but, as far as I am aware, they maintained the same set of genes. Even if I am wrong on this latter point, the vast majority of genes — and the ones that we are concerned with are common: they both have/had a gene for myosin, for hexokinase 1, for chymotrypsin etc.

Examination of the majority of such homologous genes reveals single base differences, which must have arisen since the divergence. A combination of such Neanderthal variants in one gene — never seen as human SNPs — and the converse situation allow one to designate a chymotrypsin gene, for example, as human or Neanderthal, even though the overall DNA sequence of the chymotrypsin gene may be 95% identical (to conjure a figure out of the air).

Now consider the European/Neanderthal comparison. It turns out that a small number of genes show no (or almost no) variation between the two, but that most of these show the standard ca. 95% difference between Africans and Neanderthals (and hence between Africans and Europeans). These, then, are the 2% of genes that arose from interbreeding of Europeans and Neanderthals, after the exodus from Africa.

But 2% of genes of different origin which still retain 95% sequence identity would only add 0.1% to the modern human variation, cited at ca. 0.5%.

Disclaimer

I do not know the actual extent of variation between most human and Neanderthal genes or the details of the non-African genes of Neanderthal origin. I will be happy to edit this answer if anyone has that detail. I apologize for the geographical generalizations not present in the question, but my concern was to convey the argument without burdening it with continued qualifications.


This may be what you are looking for. The conversion formula is:

$$
\text{Protein concentration (mg/ml)} = \frac{ (\text{Absorbance at 205 nm})} {31}
$$

The first, Scopes, does indicate that nucleic acid contaminants will confounding 205 nm absorbance readings. It seems as though this spetrophotometic calculation is feasible for relatively pure protein species.


Why it can feel chilly close to trees in the evening:

Water coming out of Stomata vaporises, reducing the surrounding temperature.
There is normally no direct sunlight reaching the ground beneath the tree, hence the moisture content of soil is higher, giving it the "chilly feeling"
If there is other vegetation (e.g. grass) growing beneath the tree, then point the first point is repeated for the other vegetation, consequently the combination of point 1 and 2 decreases the temperature noticeably.

An empirical study that estimates the cooling effect of trees from evapotranspiration can be found in Konarska et al (2016). Transpiration of urban trees and its cooling effect in a high latitude city.. In the study, they specifically find a cooling effect at evenings, but less so during nights and at daytime:

With an estimated night-time latent heat flux of 24 W m(-2), tree transpiration significantly increased the cooling rate around and shortly after sunset, but not later in the night. Despite a strong midday latent heat flux of 206 W m(-2), a cooling effect of tree transpiration was not observed during the day.

Why is it more noticeable during the summer?
If the temperature is warm, the atmosphere has a greater capacity to hold water in its vaporous state than if it was cold.
Relative humidity
The ratio between the actual amount of water vapor present to the capacity that the air has at a particular moment. For any given temperature, the air has a particular capacity for water vapor. If that capacity is exceeded, the excess spills out as liquid water.


How does most of lymph get back into the blood stream? (I don't mean the lymphatic system)

Technically 'lymph' is used to refer to the fluid found within the lymphatic system. If it's not in the lymphatic system, it is not lymph fluid. Thus, your question is really asking about interstitial fluid or the plasma that was filtered out of blood capillaries.

The answer to your question is based on the Starling equation. Normally fluid leaves a capillary due to a net pressure that favors the interstitium. This net pressure is based on the hydrostatic pressure within the capillary being greater than the interstitial pressure of the surrounding tissues, and the oncotic pressure of the capillary (that draws fluid in) being weaker than the hydrostatic pressure of the capillary (that pushes fluid out). At the venule end of this system, the capillary oncotic pressure is stronger than the capillary hydrostatic pressure, drawing fluid back into the circulatory system.

Remember that albumin is the most important component which establishes the oncotic pressure within a vessel, and that this protein is normally NOT released out of a vessel during filtration. Thus, it passes from the capillary into its corresponding venule directly.

Yes, plasma that enters the interstitium contains many of the same components as when it is in the blood, but the main difference is the protein content, losing the majority of proteins as it enters the interstitium.

Now, if you are asking how the majority of LYMPH fluid re-enters the blood stream, the answer is through the R lymphatic and L lymphatic (aka thoracic) ducts, at the location of the R subclavian or R internal jugular, and L subclavian veins, respectively. Once fluid enters lymphatic capillaries, it goes through a system of lymphatic vessels, trunks, and finally, the above mentioned ducts to rejoin blood.

References:

http://www.biog1445.org/demo/06/lymphaticsys.html
http://intranet.tdmu.edu.ua/data/kafedra/internal/in_mow/classes_stud/uk/med/medprof/ptn/англійська%20мова%20за%20професійним%20спрямуванням/2/№%2003.%20Heart...htm


Are there biological ratchet cycles that are small in number?

First I would in return ask why the actin-myosin coupling should not qualify - the many repetitions of this contractile unit never contract at exactly the same time, and their combined contractile force certainly accumulates in a ratchet-like fashion across the microsecond time scale (with other units contracting before previous units have relaxed). Just because it's a lot of them doesn't make it less ratchet-like :)

With this restriction though, and looking for a "macro-scale" example, I am not aware of anything fitting your description. If I think about it as follows, it also seems intuitive that this wouldn't evolve.

A ratchet as you describe, let's say able to store up x contractions of a muscle for instantaneous release, can also be thought of as a series of x muscle contractions coupled in series across time. It would be equivalent in output to coupling x muscle contractions across space and executing all of them simultaneously. In other words, growing x times the muscles achieves the same benefit.

When it comes to the probability of evolving, what's more likely: an entirely new mechanism to store mechanical energy across time and allow building up, or a simple duplication of the same tissue? The currently existing muscles answer this question: duplication. This can be seen in the different structures that muscles have across living species (muscles in animals, similar contractile mechanisms elsewhere).

The smallest contractile unit in muscles are myosin heads coupled to actin filaments. Duplicate this unit (repeatedly) in two dimensions of space to obtain a myofibril. Multiply the myofibril many times and you reach a single muscle fibre. In fruit fly larvae, this is where it stops - each muscle consists of a single fibre. By the time you're at the adult fly though, the muscles that power the wings consist of a handful of packed parallel fibres. As you go down other routes along the evolutionary tree towards the mammals, you end up at muscles that consist of masses of fibres packed into fascicles, of which many are packed into an individiual muscle. As described above, at each level you have a "many-ratchet", because fibres and fascicles don't contract at exactly the same time everywhere.

So yes, you could evolve a ratchet. Or you could just evolve a bigger muscle. If many animals happen to stop evolving more muscle at around the same absolute potential jump height, that to me suggests that this is a universally beneficial jump height to evolve for terrestrial animals regardless of body size.


Do biologists use the word "solubilize" to mean "dissolve"?

I think I found an answer at Science Direct where multiple definitions are provided, among one from Thomson (2012):

Solubilization is the action of certain chemical reagents on organic materials (such as animal or plant tissue) that effects a structural breakdown (or digestion) into a liquid form that can then be directly dissolved [...]

and from Lau (2011):

Solubilization is the increase in solubility of a poorly water–soluble substance with surface-active agents. The mechanism involves entrapment (adsorbed or dissolved) of molecules in micelles and the tendency of surfactants to form colloidal aggregations at critical micelle concentration levels.

From these definitions I understand that solubilization is a process to make something dissolvable. The process of dissolving thus happens after the solubilization (definition #1) or during the process of solubilization process (definition #2). Thus, solubilization and dissolving are separate processes (definition #1) or dissolving is considered a part of the process of solubilization (definition #2).
So admittedly, at this stage I am unsure to what exactly the two terms mean exactly, but they are certainly not interchangeable terms.
And regarding your comment

...that it's not unusual for experienced biologists themselves to be unsure which is the proper term here. Even native English speakers

I totally second Bryan's response

Language is messy, scientific terminology included...

This is because terminology tends to stick after having been adopted widely, even if it proves to be incorrect. Consider for instance the fact that current always flows from + to - in schematics, but that electrons definiely choose to go the other way around. Scientific terminology is messy indeed.
References
- Lau, Preformulation Studies. In: Handbook of Modern Pharmaceutical Analysis: 173-233
- Thomson, Handbook of Radioactivity Analysis (3rd ed.) 2012: 575-623


When you stop to think about it there is one big reason live birth has an advantage. Lets assume with habe organism A and organism B, A and B both have offspring of exactly the same size and needing the exact same amount of resources (nutrients, etc.) A lays and egg and B gives live birth. A needs to have all of the nutrients its offspring  will need all together at once because once it forms hte egg it cant add anything while organism B does not need it all, they can keep eating and supplying the nutrients over an extended period of time, as they gain it, so they need less "on hand" as it were. A and B may be putting the same amount of resources into their offspring but A does it all at once but B can spread it out over a long period of time meaning it does not need to build up huge reserves before breeding. As an added benefit if times are bad B can dump the offspring and try again later, saving all that would be wasted material for itself, so it can survive famine and drought better.


Question related to L-arginine biosynthesis

The synthesis of N-acetylglutamate is mediated by the enzyme N-acetylglutamate synthase. This enzyme has L-glutamate as its substrate and uses acetyl-coenzyme A as a co-enzyme acetyl donor. Acetylcoenzyme A (Acetyl-CoA) is generally abbreviated in structural formulas, because it is a relatively complex molecule. The only thing of relevance is the acetyl group which is transferred from a thiol group to L-glutamate.

Note that ligands is a term reserved for molecules binding to receptors; substrates is the proper term for intermediates in enzymatic reactions.

N-acetylglutamate synthesis. Source: The Medical Biochemistry page


Confusion about read counts distribution in RNA-seq

Textbook example of multinomial distribution is multiple dice toss. The fair dice has following probabilities:

side 1: 16,66666666%
side 2: 16,66666666%
side 3: 16,66666666%
side 4: 16,66666666%
side 5: 16,66666666%
side 6: 16,66666666%

Lets roll a typical fair dice n = 20 times:

6 5 1 1 3 5 4 3 1 2 4 4 6 6 2 2 5 6 5 2

So this particular outcome of above multinomial variable is:

side 1: 3 rolls
side 2: 4 rolls
side 3: 2 rolls
side 4: 3 rolls
side 5: 4 rolls
side 6: 4 rolls

Multinomial distribution is not restricted to fair dice - the probabilities can be rigged. It also is not restricted to 6 sides - there can be any number of categories. Another textbook example of multinomial distribution is puling colored balls from wery (infinitely) large bag. Probabilities correspond to proportions of colored balls in the bag:

Blue: 53.283%
Green: 19.956%
Orange: 8.336%
Purple: 5.213%
Red: 4.374%
Silver: 3.920%
White: 2.751%
Yellow: 2.167%

Lets simulate n = 200 balls pulled from such a bag in R:

sample(c("B","G","O","P","R","S","W","Y"), replace = T, size = 200, prob = c(0.53283,0.19956,0.08336,0.05213,0.04374,0.03920,0.02751,0.02167))
B S O B B G G P B O B B P G B B G G G G B P G B B P B G B G B S W B B O O G B B O G G B S B O G B B B B B O O O B O B B B B B B O O G B B Y B R G B B B G P W Y G B P W B S R B W G Y B W B G O G B R B B G B B B B B B P R G P B B B G Y G S B B B G P B B B B B G B O G P B G B G P B B G B R B P R B G W B B B B O P G B B B B B B B B G B G G R W B B G G B G O B B B B B G B B B P B B B O R G B B B O B G

So this particular outcome multinomial variable is:

Blue: 102 balls
Green: 42 balls
Orange: 18 balls
Purple: 14 balls
Red: 8 balls
Silver: 5 balls
White: 7 balls
Yellow: 4 balls

In RNA-seq we are "pulling" reads (balls) out of a large set of suitable cDNA molecules fragments in a sample (bag). Each read belongs to a gene (color). We assume fixed fractions of genes in a sample:

gene 1: 0.05217%
gene 2: 0.00319%
gene 3: 0.00073%
...

But what we get from RNA-seq (n = milions of reads) are integer counts of reads:

gene 1: 492 reads
gene 2: 44 reads
gene 3: 5 reads
...

To comment on your idea of using Gausian distribution: Gausian distribution is continuous so using it we would assume we can get fractions of reads per gene which is not the case.


Why is it necessary to have both cone and rod cells in the eye?

First off - both the rod and cone system measure light intensity; both sensory cells increase their responses when excited by more photons (Purves et al., 2001). Hence, your introductory sentence that rod detect luminescence and cones color is incorrect. They are both sensitive to luminescence.

You are correct that rods detect gray scales, while cones perform color coding. Both systems can detect gray shades; while rods are limited to that, cones are not. Rods are very sensitive to light and in a dark-adapted state are capable of detecting a single photon. Hence, they operate under conditions of low-lighting at night and as such they mediate night (scotopic) vision. Cones are photon-hungry and need more light to operate (photopic conditions).

Why have cones? Because color vision helps to detect and differentiate stuff.
Why have rods? Because night vision is helpful.
Why have both? To be successfully equipped to thrive in both light and dark environments.
Do we need them both? No - even nocturnal hunters that don't have rods have been shown to be able to hunt at night. Not only that, these geckos have been shown to be able to detect color in starlight (Röll, 2000). Under these lighting conditions, human retinae rely on the rod system and are unable to detect color.

References
- Purves et al., Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates
- Röll, J Neurocytol (2000), 29(7): 471-84


What kind of ants are these? Are these venomous?

These ants are called weaver ants, they are in the genus Oecophylla.

'Helcium is attached relatively high on abdominal segment III only in Oecophylla'
http://www.antwiki.org/wiki/Formicinae

They use the silk produced by their larvae to bind leaves together to make chambers for their brood. As any ants in the Formicinae subfamily, they do not have a stinger. They can however bite and drop formic acid on your skin, which can cause irritation. They are used in orchard as biological control agents against pests.


How is 16s rRNA used to identify unknown bacteria?

It is not conserved, its sequence is not the same in all bacteria. Indeed, it has a slow rate of evolution (mutation) that make it perfect to build phylogenetic trees.

As correctly suggested by David in his comment, here are some references about the 16s rRNA and on how it is used to identify known and unknown bacteria.

http://www.sciencedirect.com/science/article/pii/S1369527499800526

http://nar.oxfordjournals.org/content/38/22/e203

https://www.ncbi.nlm.nih.gov/pubmed/18828852

https://www.ncbi.nlm.nih.gov/pubmed/27388368

https://www.ncbi.nlm.nih.gov/pubmed/27659439

https://www.ncbi.nlm.nih.gov/pubmed/18353221

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2760787/


You can break down the energy expenditure of the human body in terms of the different organs which use it up: this is done in this biochemistry book for instance, http://www.ncbi.nlm.nih.gov/books/NBK22436/

You can also look at the detailed expenditure of each cell: although the amounts will vary according to cell type (neuron vs. muscle cell, say!), the "budget items" are the same. See this thread: Breakdown of energy expenditure at the level of a single cell


nuhcole is mostly correct.

Airborne particles first pass through the nasal passageways and/or mouth and throat and many are caught, but those that enter the lungs become trapped in mucus.

Your cilia act like a constant escalator, bringing up that mucus from your lungs 24/7.  You reflexively swallow it without even realizing it.  That is why when you are healthy, you might not even notice.

If you are sick (or asthma/allergies), more mucus is produced.  That is when you may notice the increased quantity coming up, and may need to cough to bring more up.

If your cilia are damaged (like in smokers), then mucus does not clear well from the lungs. In this case, people must cough more in order to bring it up.


Can a relationship exist that is mutualistic/parasitic/etc. but not considered symbiotic?

TL;DR: mutualistic/parasitic relationships are members of symbiotic relationships class

So, first of all, there is a way to look it up.

Secondly, the very same article in wiki has subsection on parasitism. Reading it would be useful:

  This is also known as antagonistic or antipathetic symbiosis.

Also, brief search through Google Scholar will show how these words are used in context. papers include such as:

Fungal symbiosis from mutualism to parasitism: who controls the outcome, host or invader?
Mutualism and parasitism: the yin and yang of plant symbioses
Mutualism or parasitism? The variable outcome of cleaning symbioses
Enhanced growth as a manifestation of parasitism and shell deposition in parasitized mollusks. Aspects of the biology of symbiosis.


How do scientists create specific mutations?

Thats basically the oldest method to induce such mutations. For this purpose either radiation (x-rays) or mutagenic chemicals (like Ethylnitrosourea) have been used for this purpose. This method is undirected, so you never know what the outcome will be untill you see the off-springs. Using this method to get specific mutations is relative difficult. Its used for the detection of genes which deliver visible phenotypes (for example it has widely been used for the analysis of pigmentation in mice, since you can easily spot mutations).

Newer methods can target genes directly and either introduce or remove sequence areas. These techniques make use of homologous recombinases. In short you bring in you gene of interest in the modified version on a plasmid into the cell which you want to change. The plasmid also expresses the recombinase (this can be under a cell specific promoter to target specific cells) which then recombines the DNA between the plasmid and the genomic DNA.

An example for that is the FLP-recombinase system (image from the Wikipedia article on it):

Other examples for site specific altertions are the Cre-LoxP-System or the Crispr/CAS-System.


Neisseria meningitidis transformation into a pathogen

It's not like a strain of E. coli that may cause disease in immunosuppressed individuals yet is a part of normal microbiota for other people.

Well, actually, it is kind of like that.
The answer is complicated, but can be boiled down to, virulent serotypes of Neisseria meningitidis infect susceptible populations. For the short answer, just read between the highlighted boxes.

Invasive meningococcal disease results from the interplay of: (1) microbial factors influencing the virulence of the organism, (2) environmental conditions facilitating exposure and acquisition, and (3) host susceptibility factors favoring bacterial acquisition, colonization, invasion, and survival.

Virulent serotypes have capsules that help them evade detection and destruction; they have an outer envelope that helps them invade and infect susceptable individuals.

The virulence (14) of N. meningitidis is influenced by multiple factors: capsule polysaccharide expression, expression of surface adhesive proteins (outer membrane proteins including pili, porins PorA and B, adhesion molecules Opa and Opc), iron sequestration mechanisms, and endotoxin (lipooligosaccharide, LOS). N. meningitidis also has evolved genetic mechanisms resulting in a horizontal genetic exchange, high frequency phase, antigenic variation, and molecular mimicry, allowing the organism to successfully adapt at mucosal surfaces and invade the host.

The most susceptible populations are infants/babies (most frequently), young children and unvaccinated young adults (during outbreaks). These are the populations most likely to have no to low antibodies against the bacteria.

The meningococcus remains a common cause of bacterial meningitis in children and young adults in the USA (132), now mostly affecting children less than 2 years of age (102, 133). Two-thirds of meningococcal disease in the first year of life in the US occurs in infants less than 6 months of age (134). Worldwide, the rates of meningococcal disease are also highest for young children due to waning protective maternal antibody, but in epidemic outbreaks, older children and adolescents can have high rates of disease. Fifty percent of cases in infants in the US are due to serogroup B; serogroup C is mostly seen in adolescents and serogroups B and Y in older adults. Even though peak incidence occurs among infants and adolescents; one-third to one-half of sporadic cases are seen in adults older than 18 years.

Carrier state isn't lifelong or even year long, in fact, it can last as little as a few weeks.

When approximately 10% of individuals from the general population at any time were carrying N. meningitidis in the nasopharynx (Cartwright et al., 1987), the carriage rate was shown to be <3% in children younger than 4 years and increased to 24–37% in the age-group 15–24 years... Then carriage rates decrease to less than 10% in older age-groups.

and

Meningococcal carriage increases rapidly among university students in the first month of the academic year and much of this increase probably occurred during the first week (Neal et al., 2000). The study, performed at the University of Nottingham, UK, showed the carriage rate increased in the first week of term from 6.9 % on day 1, to 11.2 % on day 2, to 19.0 % on day 3 and to 23.1 % on day 4. High social mixing probably caused this increase.

Carrier state is influenced by protective antibodies, local mucosal factors, and lower virulence of the bacteria in carriers. Smokers, for example, are more likely to be carriers than non-smokers. The type of N. meningitidis  also influences carrier vs. infected individuals.

In Norway, approximately 9% of the carriage isolates belonged to two of the known hypervirulent clonal complexes...

That is, of 100 carriers, less than 10% carry a very virulent type. Non-virulence or low-virulence is the norm.
A non-virulent strain can become virulent to others by sharing of DNA.

Because of mixed colonization with other bacteria and because of its duration, the carrier state is an ideal condition for horizontal gene transfer between different strains of meningococci, and between meningococci and other commensal bacterial species. The human nasopharynx may harbour diverse pathogenic bacteria, like N. meningitidis, H. influenzae, S. pneumoniae, as well as non-pathogenic bacteria, such as N. lactamica and the moraxellae.

Again, carriers ave protective antibodies.

Immunity to invasive meningococcal disease is dependent upon the presence of serum immunoglobulin G (IgG) which elicits bactericidal activity toward the infecting organism. Infants may be protected from meningococcal disease by the presence of maternal IgG which is obtained passively during gestation and lactation. Maternal immunity will be replaced by acquired immunity. Exposure to non-pathogenic Neisseria and other cross-reacting species in the nasopharynx increases the level of specific antibodies during childhood (Sanchez et al., 2001, 2002; Troncoso et al., 2000).

And

Carriage of commensal Neisseria, especially N. lactamica, is associated with a high titre of antibodies against N. meningitidis. Highly homologous structures are present in N. lactamica and N. meningitidis (Troncoso et al., 2000, 2001). Sera from mice immunized with N. lactamica and boosted with N. meningitidis have been shown to kill meningococci.
...Mucosal immunity is not able to prevent the colonization of the nasopharynx by meningococci, but it plays an important role in preventing the invasion of epithelial cell (Griffiss, 1995).

If that answers your question, that's what I hoped for, because the rest is a mystery  to me. But remember, you aren't a lifelong carrier. You might be a weekslong carrier, and every exposure to a non-virulent serotype increases your immunity.
Neisseria meningitidis: Biology, Microbiology, and Epidemiology
Neisseria meningitidis: an overview of the carriage state


Are there pre-synaptic alpha 2 receptors in the post-ganglionic synapses of the heart?

The heart of course does have Alpha 2 pre synaptic receptors , the definition states that alpha 2 receptors are present on sympathetic postganglionic endings , so I don't see why heart should be an exception .
I will explain to you how reflex tachycardia occurs .
When you give non selective blockers , presynaptic Alpha 2 are blocked , therefore the pre synaptic neurons cannot sense NE amount in synaptic cleft , so they release large amounts of NE . BUT , post synaptic alpha1 is also blocked , so this large amount of NE cannot act BUT THE HEART DOES NOT HAVE alpha 1 it has BETA 1 receptors which are perfectly capable of being stimulated by this large amount of NE that is released , hence causing tachycardia.


There are many seabirds smaller than partridges. The smallest seabird (according to the National Trust of Scotland) is the European Storm Petrel, which weighs in at an average of 28g. That's not quite as small as the European Wren (6 - 10 g), but it definitely counts as 'small', nonetheless.

Being seabirds which spend their life at sea except during breeding, storm petrels float well.

Below is a European Storm Petrel weighing in at less than 35 grams in Fig. 1.


The detail about the exact time of heart attack

Acute myocardial infarction (MI) usually happens when a coronary artery is abruptly occluded, typically by a blood clot. The clot can be an embolus that forms elsewhere (such as in the heart itself) and then happens to flow into a coronary artery, or more often it occurs when an atherosclerotic plaque (containing cholesterol) ruptures. Because a ruptured plaque looks a lot like tissues outside the blood vessels, the clotting machinery in the blood responds like it would to stop bleeding from a wound.

MI can also occur in other situations where blood flow is reduced to a level insufficient to supply the cardiac muscle with oxygen, without complete blockage, either from vasospasm or when increased activity (such as exercise) demands more flow than can be delivered through a narrowed atherosclerotic coronary artery.


Can a novel protein domain arise de novo in nature or did all protein domains evolve from a single ancestor?

Yes. Novel protein domains can arise de novo in nature. The evidence is quite solid as those new domains show all the expected mutation patterns and statistical properties (expected for something evolving from DNA that doesn't yet encode for a domain). E.g.: see the following meta-analysis, which also describes how those new domains behave relative to older ones, and how they integrate into proteins: Toll-Riera et Mar Alba 2013, BMC Evolutionary Biology, "Emergence of novel domains in proteins":  https://bmcevolbiol.biomedcentral.com/articles/10.1186/1471-2148-13-47

If you are additionally interested in new genes, the following mini-review: http://www.sciencedirect.com/science/article/pii/S0960982214001547#bib20 .

If you are additionally interested in in-vitro evolution, which is directly observable within the life-span of single humans, the following review: http://www.sciencedirect.com/science/article/pii/S0022175904001309


How to get the average number of pairwise differences among populations?

With relation to the other bioconductor question I would point you towards these packages;

VariantAnnotation: Provides functionality for reading and manipulating vcf files.
GenomicRanges: Provides functionality for creating genome intervals. Also provides overlap functions for calculating overlaps between various ranges.
rtracklayer: Allows you to easily change formats between different biological file formats.
AnnotationHub: Makes many common and uncommon annotation files available in the R terminal in various formats such as TxDb, OrgDb etc. etc.

Here's a tutorial very similar to what you are asking for. It utilises some of the packages mentioned above. Principally, AnnotationHub, GenomicRanges and VariantAnnotation.

If you want the manual of these packages, they are available on the linked pages.


PDB Mining: Why Do I Find Atoms Less than 1 Angstrom Apart?

if you are using NMR structures you might be making the mistake of using several superimposed structures - it would be nice to develop with x-ray structures at less than 2.0 A resolution for starters.

Some of the models at low resolution can be sloppy, but submitted after 1994 or so will not have any center to center distances as that's when the x-ray structures used molecular models rather than just electron density rigorously and wierd steric violations in the structure should be rare.

Still, this might not be wrong - the hydrogen might be pointing right into the aromatic ring's center.  This has been observed quite a bit.  In such a case, the atom to ring plane distance might be very small.

You only need to worry if the center to center distance between atoms is less than the vanderWaals radius.   I would filter for atom center to center distance and see if you see violations.


Look at this scheme -

As I stated before, vitreous is 99% water and is not an organ itself, thus the "replacement of vitreous" is actually = 99% water re-production and the only organ inside the eye which can perform this - ciliary body.

Consequently, if the vitreous was removed and replaced by gas or saline it will be replaced by aqueous which produced by ciliary body - this process takes 8 weeks to completely replace foreign substance as a gas by aqueous.


Micro- and macro- evolution are terms vaguely referencing to arbitrary time scales

The terms microevolution and macroevolution have rather arbitrary and unclear meaning. For this reason, they are rarely used in the scientific literature. When they are being used, it is often in the first part of the introduction where general statements for which inaccuracy matters little are being made.

Typically, the existence of lineages called races (but see below) within a greater lineage called a species are limit cases between what one would want to call macro evolution or micro evolution. But in essence, it really does not matter where such arbitrary boundary is put, it changes nothing to evolutionary processes at play.

The concept of ethnic group

Note also that the concept of race (generally called ethnic group) is a human made concept that sometimes fail to match the reality of population structure in humans. If we were to name lineages based on genetic differentiation rather than socio-cultural cues, we would, if I am not mistaken, end up with a reasonably different result.

Bonus question

For your bonus question, you'll probably want to have a look at the post Does it make sense to classify all humans in a single species? and the post How could humans have interbred with Neanderthals if we're a different species? who discusses the concept of species.

You are right that the increased migration rate brought about by globalization causes increase interbreeding between humans lineages and will therefore rather prevent any further population structure that would have otherwise eventually lead to an event of speciation. There is, for the moment, no sign that any human speciation would evolve any reproductive barrier with any other human lineages. We are for the moment far from any speciation event in humans.


Question about proto-oncogenes and oncogenes?

I am going to add to @MattDMo 's answer a bit.

Proto-oncogenes Function, Developmental Program, and Regulation

Proto-oncogenes are normally functioning genes that are more often than not in the pathways that lead to mitosis and cellular replication. They have important roles in the development, growth, and maintenance of the organism. Proto-oncogene is an accurate description of the genes, but I unfortunately think that sometimes people think that the genes themselves are bad and that isn't the case.

Growth and development in multicellular organisms are highly regulated processes with many checks and balances. Certain cells need to grow in certain places at certain times, and then they need to go into and remain in interphase. If they don't, or they do things at the incorrect times, the multicellular organism will not develop properly or will develop conditions such as cancer.

It is often these points of regulation that become dysregulated when a proto-oncogene becomes oncogenic. If there are regions of allostery that are affected by a mutation in the coding sequence (exon) and a control molecule that represses the activity of the enzyme through conformation change can no longer bind, then that enzyme can remain active, always turned on.

You can also have a situation where you have transcriptional regulators of proto-oncogenes that can be effected making the gene product oncogenic. If there is a mutation in an enhancer (intronic) of the gene that affects the binding kinetics of enhancers leading to a great increase in transcription, this concentrational difference can lead to uncontrolled grown and tumor formation.

You could also have a situation like MattDMo talked about where you generate frameshifts and premature stop codons, though I would think this is more relevant in tumor suppressor gene mutations, as these types of mutations tend to kill the protein rather quickly, but it is possible that it can cause a problem.

RAS

There are however other types of mutations that can effect proto-oncogenes, making them oncogenic. One classic example is RAS. RAS is a G-protein that associates with G-Protein Coupled Receptors at the cell surface and transduce signals into the cell leading to the initiation of the cell cycle. In its inactive form, RAS is bound to GDP. When a signaling molecule binds to the plasma membrane receptor it is associated with the RAS molecule, a Guanosine-Exchange Factor removes the bound GDP, and because of concentration, GTP enters the binding pocket and activates RAS, which activates a phosphorylation cascade, leading to transcription of growth factors.

Normally RAS has GTPase activity and will quickly cleave the gamma phosphate of the GTP in its binding pocket, leading to GDP and inactivating itself. However if the mutation were to knock out this GTPase activity from RAS, then it would have no way to cleave the Gamma phosphate, and therefore it would remain activated and continue the signal transduction, even when it should not.

However, the problem does not need to be with RAS to drive RAS to oncogenesis. If RAS GEF becomes hyperactive and starts to exchange GDP for GTP constitutively, whether or not there is a signal, then RAS will constantly be activated, even if it is still able to cleave the Gamma phosphate and inactivate itself. So there can be Cis-acting drivers of oncogenesis and Trans-acting drivers as well.

I am providing you a link to Scitable's page on Proto-oncogenes to Oncogenes to Cancer. It gives the following summary which is a helpful summary:

  Point mutations, deletions, or insertions that lead to a hyperactive
  gene product
  Point mutations, deletions, or insertions in the promoter region of a proto-oncogene that lead to increased transcription
  Gene amplification events leading to extra chromosomal copies of a proto-oncogene
  Chromosomal translocation events that relocate a proto-oncogene to a new chromosomal site that leads to higher expression
  Chromosomal translocations that lead to a fusion between a proto-oncogene and a second gene, which produces a fusion protein with oncogenic activity


What is the role of the pyrrolidine/piperidine moieties in fagopyrins?

Radical generator

Looking at the molecules they are highly conjugated —must be dark red or similar!
And the disease is photosensitivity. Aromatics + UV? That is a standard UV radical reaction. It may be enough as a catalyst, but you'll get more will a cyclic amine, such as pyrrolidine or piperidine. If you want to go technical confer: Hofmann–Löffler reaction.

The radical will be passed on to other molecules, such as oxygen (generating peroxide), which will damage DNA and will raise an alarm biologically ultimately attracting neutrophils, which are expecting some attack (not poisoning), thus causing local inflammation, which manifests as skin irritation.

Demethylation

With the caveat that secondary metabolism is highly promiscuous and that some modifications are more accidental that anything else, let's look at the methylation and membrane permeability.

Promiscuity and secondary metabolism evolvability

This figure I found has the methylation patterns. A first glance I have assumed it was the usual C-methyltransferase action adding methyl groups, but instead it is a removal twice in the case of fagopyrin B and once in C and D. Specifically, fagopyrin is clearly two condensed anthraquinones molecules (emodin?) —which is a rather interesting non-standard change, I have not looked but so hope that someone has found the enzyme responsible! As you point out an anthraquinone is made by polyketide synthesis: the last acetyl-CoA results in a methyl group on the aromatic structure, which is occassionally oxidised to a carboxyl group (e.g. rhein) and in this case decarboxylated —I do not think a C-methyltransferase can remove groups even with pushed stoichiometries nor do I believe I have heard of one. But anyway. The anthraquinone condensing enzyme may not be able to tell apart the standard and the demethylated metabolites, which is otherwise meant for another pathway, i.e. it could just be promiscuous.

Membrane

Let's calculate the effect on solubility (python3 w/ RDKit).

Wikipedia has the SMILES string for the main fagopyrin and it's easy to spot the methyl groups.

from rdkit import Chem
from rdkit.Chem import AllChem
from rdkit.Chem.Draw import SimilarityMaps
# let's make the molecules
normal = Chem.MolFromSmiles('O=C1C2=C(C3=C(O)C(C4CCCCN4)=C2O)C(C5=C6C(C)=CC(O)=C15)=C7C(C3=C(O)C(C8NCCCC8)=C9O)=C9C(C%10=C7C6=C(C)C=C%10O)=O')
demeth = Chem.MolFromSmiles('O=C1C2=C(C3=C(O)C(C4CCCCN4)=C2O)C(C5=C6C=CC(O)=C15)=C7C(C3=C(O)C(C8NCCCC8)=C9O)=C9C(C%10=C7C6=CC=C%10O)=O')
# no need to orient them as the indices are the same. Whoohoo
img=Chem.Draw.MolsToGridImage([normal, demeth],
                              molsPerRow=2,
                              subImgSize=(200,200),
                              legends=['w/ methyls', 'w/o methyls'],
                              useSVG=False).save('/Users/matteoferla/Desktop/mols.png')

Now let's calculate logP (Partition coefficient).
    print('w/ methyls', Descriptors.MolLogP(normal))
    print('w/o methyls', Descriptors.MolLogP(demeth))

w/ methyls 6.71
w/o methyls 6.0

They are really soluble in octanol and insoluble in water. The unmethylated version is less hydrophobic.

Let's look at what is causing the difference by looking at the Crippen contributions to logP. Using the BluePurple colormap (suggestions welcome for best colormap for this descriptor), so that purple is hydrophobic while light blue is hydrophilic. Note that this is not partial charge (Gasteiger).

for mol, name in ((normal, 'meth'),(demeth, 'demeth')):
    AllChem.Compute2DCoords(mol)
    contribs = Chem.rdMolDescriptors._CalcCrippenContribs(mol)
    fig = SimilarityMaps.GetSimilarityMapFromWeights(mol, [x for x,y in contribs], colorMap='BuPu', contourLines=10)
    fig.savefig('/Users/matteoferla/Desktop/'+name+'_crippen.png', bbox_inches='tight')

The difference is a result of the methyl groups, being slightly more electron withdrawing than hydrogens making the carbon between it and the hydroxyl/ketone more hydrophobic. But overall does not change the polar sides, so is in effect unlikely to have an effect on its high membrane permeability.


Are there certain symmetric-pair muscles that are slightly bigger and NOT due to handedness?

There are many variables that could affect the answer to this question. Such as what activities you partake in.

For example, I am a hockey player at the he varsity level in high school. I have noticed that my entire right side is more toned, muscular, and flexible (especially my right latisimus dorsi and deltoid). It just so happens that I rely on my right side for energy and strength more than my left when it comes to shooting pucks and just playing the game.

Typically what we see in humans is the dominant side of their body will tend to show more hypertrophy than the non-dominant side. When you look at a human anatomically, their dominant side shoulder will be bigger and will rest lower when relaxed. Even small things like sleeping habits can effect the visual difference of you symmetry. I will agree though that it is odd that your friend noticeably has more hypertrophy in his neck muscles on one side but is dominant on the other side. This could be due (but not limited) to small habits not taken into account. Like I mentioned before, sleep habits, any motion with the neck in a specific way, chewing could maybe be a factor, or (maybe not likely) a genetic mutation.

This is an interesting topic and I urge you to maybe look at some more people for evidence that dominance has a role in it. 2 people is maybe not enough evidence to really back up a claim you're going to make.

Hope this helped!

-Sartoaster


Humans best at long distance running: purely physiological or is it a function also of ability to pace?

I would argue that the two factors of physiology and pacing are essentially one in the same. A huge component of pacing for distance runners is breath control. This requires indepndent control over breathing while simultaneously maintaing runnning form, which is simply not an option for most quadrapeds.
This stock photo of two gazelle in sprint illustrates why. With each bound, a gazelle's torso compresses (left) and then expands (right) in sync with it's running motion. That compression forces air from the animal's lungs, syncing the rate of breathing with it's rate of running. Because of this, they cannot control their rate of breathing control without also changing their step rate.

The fact that people can learn from coaches and books to get better at pacing suggests there is a cognitave aspect to it, but it's the physiology of bipedal locomotion that allows for more efficient pacing in the first place. It's not easy to separate the two factors in a scientific (non-speculative) way, since we can't train an animal to do something that it's not physiologically capable of doing.
There are some interesting discussions here about the Iditorod, which I imagine involes some amount of the human driver pacing the sled-dog team.


Why do people have antibodies against other blood types?

According to the Wikipedia entry for the ABO blood group system:

  Anti-A antibodies are hypothesized to originate from immune response towards influenza virus, whose epitopes are similar enough to the α-D-N-galactosamine on the A glycoprotein to be able to elicit a cross-reaction. Anti-B antibodies are hypothesized to originate from antibodies produced against Gram-negative bacteria, such as E. coli, cross-reacting with the α-D-galactose on the B glycoprotein.

The cited reference is Van Oss, CJ (2004) Letter to the Editor: "Natural versus Regular Antibodies The Protein Journal 23:357, available here. This source contains this statement:

  ..."we have known for more than four decades that these bloodgroup (antibodies) arise out of minor infections occurring very early in life..."

The cited references are:
Pettenkofer et al. Z. ImmunForsch. 119: 415-429
Springer, GF (1960) Klin. Wschr. 38: 513-514

Unfortunately I have access to neither of these articles, and besides they are presumably written in German.


Is it possible to have undamaged healthy cell, that is dead?

There is a great bit on the podcast "The Infinite Monkey Cage" wherein Brian Cox recurrently asks "When is a strawberry dead?"

If you think about it, it is a difficult question: when a berry is growing on a plant, it is easy to say it is living because the cells are actively dividing and functioning. But when the berry reaches maturity, the autosomal cells no longer divide. This is called Programmed Cell Death or apoptosis. This is a physiological process. However, one could still argue the strawberry is alive in the sense that the seeds are still viable and can actively produce new strawberry plants. These cells are quiescent. What though, if a strawberry is crushed to smithereens or a disease infects all of the cells? In this case the "death" of the cell has ceased function as in apoptosis, but this is externally mediated. This type of non-programmed cell dysfunction is called necrosis.

So, in direct answer to your question, you must taken into account the mechanism (internal or external) for cessation of function and the permanency. Internal and permanent = apoptosis. Internal and temporary = quiescent. External and permanent = necrosis. External and temporary = ...maybe injury?

To be clear, I've used a multicellular plant as an example (because it is easier to relate to than yeast), but the principles are the same for unicellular organisms.

@Flo made the good suggestion to add references for those interested:

Buttner et al. (2006) Why yeast cells can undergo apoptosis: death in times of peace, love, and war. Journal of Cell Biology

Gordeeva et al. (2004) Apoptpsis in unicellular organisms: mechanisms and evolution. Biochemistry


Melting point of animal fat and plant fat

Plants contains monounsaturated fats while animals contains saturated fats. The high proportions of fatty acids in animal fat means it takes longer to heat it up. I don’t know the melting points of different things off the top of my head, but you can find a meat that is as unsaturated as possible and compare it to the most saturated plant fat to test your last question.


Is 1 g/l living biomass for a Biogas fermenter plausible?

I've done experiments with yeast, and they can easily ferment glucose at the rate of 4g/L/d.  Probably faster, if one were to optimize it.  So your numbers don't seem crazy.


"So my question is, in general, how many different flavors of carcinogens are there?"
As mentioned in the comments, almost all carcinogens act by damaging DNA.  In general there are three ways to do this:

Alkylation, a good example is pyridine.  These compounds covalently modify the DNA and either cause a mutation by misincorporation during DNA replication (where the wrong base is incorporated across from the alkylated base), or by generation of double strand breaks during DNA replication that result in a mutations during the repair process (the details of which are not in-scope here).

Intercalation, my favourite example being ethidium bromide.  These compounds literally insert themselves between the bases of the double helix, where they cause "fork collapse" during DNA replication, and the ensuing repair process mutates the DNA.

Ionization through radicals.  Yes, carcinogens can generate radicals that will generate DNA damage.  A good example is doxorubicin, which is a highly effective chemotherapeutic, but also a carcinogen in its own right.  Some heavy metals can also generate radicals under the right circumstances.  These compounds typically oxidize the bases of DNA, and result in broad misincorporation during DNA replication.  Radicals can also result in breakage of the phosphodiester backbone, which cause mutations during repair. This mechanism is taken advantage of in some methods for studying the primary and secondary structure of RNA molecules, and in "foot printing" methods.  Incidentally, it is this mechanism of carcinogenesis that causes antioxidants to be associated with the prevention of cancer.  Compounds like vitamin C soak up the radicals generated by the carcinogen (or radiation), thereby preventing the damage from occurring.

An interesting point: pyrimidine dimers, which are generated whenever you get a sunburn, are a carcinogenic form of DNA damage somewhere between the ionization and alkylation mechanisms.  UV light induces a redox reaction that results in covalent linkage of two neighboring pyrimidines.  A dedicated repair process can cause a mutation at the site of the dimer.

However, the take home point is that the DNA damage itself is not usually the mechanism of mutation!  Mutation occurs when the damage is repaired, either as part of a dedicated repair process, or by (non)homologous recombination after a stall in DNA replication.

I hope this answers your question.  It is a complicated subject, and I doubt I covered everything here.


How do pet gecko lizards pose a health risk?

If you're referring to keeping geckos as pets, like all reptiles, amphibians and birds, they come with a small but finite risk of contracting salmonellosis. Having said this, the infection is easy to avoid if you maintain basic hygiene.

On a personal note, I know dozens (perhaps hundreds) of people who keep or have kept reptiles as pets and have yet to meet anyone who contracted salmonellosis. Basically, if you wash your hands after touching the gecko, keep it away from food preparation areas and don't put the lizard in your mouth, you should be fine.

If you're talking about geckos living free in your home, as is common in many tropical places, I have never heard of any health risks associated with them. If anything, I would think that the geckos would reduce health risks by eating insects such as cockroaches and mosquitoes that are prominent disease carriers.