text:
Origin, or source, of rhesus negative in human blood
This is my first post here, so please be gentle. I recently learned that I have Rh- blood (I'm A-), and was idly looking into blood types on Wikipedia. I was surprised to find that relatively few (~15% of all) humans have it, and most of those seem to be European. Looking just a little further, I found a bunch of crackpot-looking sites that try to explain how people got Rh- blood, and what weird abilities they possess as a result.
I managed to find one site that seemed at least less laughable, which suggested that interbreeding with Homo neanderthalensis (or possibly Homo sapiens neanderthalensis, since the site seemed to indicate that there was some question about how different H. s. sapiens were from H. neanderthalensis) might have accounted for the introduction of the condition.
It seems that from more reputable (medical) sources, the only difference between Rh+ and Rh- is that complications can arise during pregnancy if the mother is Rh- and the fetus is Rh+. Indeed, most sites (e.g., WebMD) seem to explicitly state that there are no other differences of note.
I am not a biologist, or an anthropologist, or a life-science kind of guy at all. However, as a computer scientist, I like to think that I have both an open mind but one which demands scientific and/or logico-mathematical evidence for claims. Lots of the pseudo-scientific, paranormal, etc. theories on the web I basically dismiss out of hand, as explanations which are almost certainly fantasies, but most definitely baseless and untestable.
My question:

What, if any, is the current scientific understanding of the origin, or source, of rhesus negative blood in human beings? Do individuals with Rh- blood have any common (in a statistically significant sense) characteristics or health issues, aside from the issue with pregnancy and tending to be more European than not? Is there anything to continuing to look into this?

For context, I got started down this rabbit hole while looking into different dieting strategies, and found the "blood type diet". Just as an aside, I don't think there's a lot of merit to that diet... sounds like a fad thing. Any sources or information or help on this subject are appreciated.
EDIT:
I have been looking a little more, and I stumbled across a paper entitled, "The influence of RhD phenotype on toxoplasmosis and age-associated changes in personality profile of blood donors" which looks at the effect of the Rh- trait on personality changes caused by toxoplasmosis (if you Google the title, you should be able to download). Using Cloninger's and Cattel's personality factors, they seem to show a variety of things, including (a) personality differences between Rh+ and Rh- individuals not affected by toxoplasmosis, and (b) different reactions to prolonged toxoplasmosis affection in Rh+ and Rh- individuals.
I didn't even know that parasites could affect your behavior; that seems frightening on the one hand, but on the other, it's fascinating if it's for real, especially since the incidence of toxoplasmosis is not insignificant in most people. Anybody who knows anything about this or who reads the paper and can help me understand what it's saying would be doing me a great favor to answer/comment/chat. Thanks!

The blood type diet is a bunch of junk. There is no scientific merit to its claims. Genetic differences could be matched to a diet, but those differences should map to genes relevant to metabolic diseases such as cardiovascular disease, type 2 diabetes and the like. A genetic variant in phenylalanine hydroxylase (PAH) can lead to phenylketonuria (PKU) and specific diets can, usually are, prescribed to alleviate (risk of) symptoms. See http://omim.org/entry/261600.

@Larry_Parnell Yeah, that was my impression as well... blood type should have little to nothing to do with diet, and certainly the guy's reasoning seems to be pure fantasy. It seems like most named diets are fads, and that the best way to live healthy is to eat a varied diet of appropriate quantities of fresh, healthful foods, stay hydrated, and to get some exercise... common sense stuff. Still, I'm interested in the origin of Rh- (interbreeding? mutation?) and what other traits have been observed to be correlated to (not necessarily caused by) it.

For the blood type diet see this question on our sister site Skeptics.SE.

You may wish to also see our question: Is there any advantage to one blood type over another?

Your question has many questions in it.
As for the evolution of Rh factor, Blancher and Apoil (2000) attribute the high level of sequence similarity (92%) of the two RH locus genes, RHD and RHCE to a gene duplication event in the common ancestor of human, chimps, and gorillas. Their analysis of the cDNA from these genes revealed "complex recombination events" after the lineages split.
Basically the most recent common ancestor of apes had the "human" RH genes, which then differentiated after the lineages diverged. Duplicate and differentiate is a common theme in evolution.
As for why it's called rhesus antigen, that's just as experimental artifact:

The term "Rhesus antigen" was introduced by Landsteiner and Wiener,
  who found that rabbits (and later, guinea pigs) immunized with red
  blood cells (RBCs) from a rhesus monkey produced antibodies which
  agglutinated 85% of Caucasian blood samples (Landsteiner and Wiener
  1940, 1941).

They probably weren't even correct about the antibodies being rhesus:

In conclusion, if the term "Rh" was coined by Landsteiner and Wiener
  because of the source of antigens (the rhesus monkey) they used to
  obtain anti-Rh in rabbits, it is highly probable that, in fact, they
  produced anti-LW antibodies.

http://www.ncbi.nlm.nih.gov/pubmed/18766148

RESULTS:
RhD-positive subjects have been confirmed to be less sensitive to the influence of latent toxoplasmosis on reaction times than Rh-negative subjects. While a protective role of RhD positivity has been demonstrated previously in four populations of men, the present study has shown a similar effect in 226 female students. Our results have also shown that the concentration of testosterone in saliva strongly influences (reduces) reaction times (especially in men) and therefore, this factor should be controlled in future reaction times studies.
CONCLUSIONS:
The observed effects of RhD phenotype could provide not only a clue to the long-standing evolutionary enigma of the origin of RhD polymorphism in humans (the effect of balancing selection), differences in the RhD+ allele frequencies in geographically distinct populations (resulting from geographic variation in the prevalence of Toxoplasma gondii), but might also be the missing piece in the puzzle of the physiological function of the RhD molecule.

Welcome to the site. You answers take heavily from quotes, which should be marked as such. Rather than three separate posts, why not try to combine them into a single post with some additional analysis or insights?

http://www.frozenevolution.com/origin-rh-blood-group-polymorphism

The high proportion of Rh-negative persons in the European population
  could be connected with the fact that, until recently, big cats (the
  definitive host of Toxoplasma gondii) were practically not present
  here and thus toxoplasmosis was rare (and Rh-negative persons were at
  an advantage compared to the rest of the population). The low
  percentage of Rh-negative persons in Africa (less than 1%) could be
  related to the high prevalence of toxoplasmosis there, which often
  approaches 100%.

http://www.sott.net/article/228188-Toxoplasma-gondii-Cat-parasite-may-affect-cultural-traits-in-human-populations

Lafferty suggested that because climate affects the persistence of
  infectious states of Toxoplasma in the environment, it helps drive the
  geographic variation in the parasite's prevalence by increasing
  exposure risk. The parasite's eggs can live longer in humid,
  low-altitude regions, especially at mid latitudes that have infrequent
  freezing and thawing. Cultural practices of food preparation such as
  rare or undercooked meats, or poor hygiene, can increase exposure to
  infection, as can having cats as pets. Lafferty added, "Toxoplasmosis
  is one of many factors that may influence personality and culture,
  which may also include the effects of other infectious diseases,
  genetics, environment and history. Efforts to control this infectious
  pathogen could bring about cultural changes."   / this is why I feel
  rh- is a newer blood grouping due to the last ice age conditions.
  these were the conditions in nw Europe back then and the rh- trait has
  persisted in that area. it just all makes sense . you may also search
  out " congenital toxoplasmosis infection " and I believe you will find
  when a pregnant woman gets toxo infection the baby comes out with the
  same symptom ology as erythroblastosis fetalis, rhesus disease.this is
  why all pregnant women are cautioned to avoid cat feces and stay away
  from cat boxes where they defecate.

OPINION ? i'll have you know i'm 61 y old retired medical worker who has studied biology and etc my whole life . this opinion is not just anyone's .  btw i'm o- myself  /

It's my opinion the rh antigen developed from toxoplasmosis infection. I only recently learned that this protozoan can actually insert its genes into a host's genome. Once it's in the genes, it can be passed in the germline. Toxoplasmosis can infect all primates, human and otherwise. Monkeys get it, and so do humans living in toxoplasmosis endemic places. The life cycle of toxoplasmosis is connected with mice and cats as an evolved survival strategy for the toxoplasmosis protozoan. There never were cats in northwest Europe, and that would explain why the people with ancestry from that area were never exposed to toxoplasmosis. I look for the rational biological explaination. One great clue to my thinking is I found a term used in some research writings, the text read "RH strain of toxoplasmosis". Yes they seemed to be doing experiments with the toxoplasmosis found in rhesus monkey.

Can you provide citations to back up your hypothesis? Opinion doesn't go very far.

I am pretty sure there were wildcats in northwest Europe.


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DNA replication Okazaki fragments
I understand multiple origin bubbles; DNA polymerase only synthesizes DNA from 5' to 3' and all that. But what I don't understand is why it has to be in fragments. Yes, DNA is anti parallel, and so the DNA elongates in opposite directions, since DNA polymerase can only go one way. But why not go on just like the leading strand? Why not continue happily along the DNA template continuously but in fragments?

So you mean start at the 5' end of the lagging strand and go the whole way along the chain in one?

If I understand the question, this would require that the entire leading strand was copied first, and then the entire lagging strand would be copied using a primer put in at the terminus of leading strand replication. Apart from any considerations of keeping all of that single-stranded DNA safe from harm, this would mean that replication of an entire dsDNA molecule would take twice as long.

I think you may have been misled by graphic representations of the process: The actual replication fork is very small as, like Rex Kerr mentions, it costs a lot of energy to keep DNA single stranded.
Have a watch of https://www.youtube.com/watch?v=yqESR7E4b_8 at minute 1:45, it contains a relatively realistic representation of the replication fork. Of course you have to imagine all of the space around the molecules in this video to be filled with other DNA, RNA, proteins and small molecules zipping about.
On top of this, we like to think of DNA as a lone double strand where occasionally a protein might attach and do something. Realistically however, most of the DNA is constantly being manipulated by all sorts of proteins (mostly histones for compression, but also transcription factors, methylating and demethylating enzymes, DNA repair enzymes,...). DNA replication has to minimise the interruption it causes to all the mechanisms going on around it, and the most effective way to do this is by replicating the lagging strands in fragments which can be zipped up quickly and left to whatever other proteins might do to it.

Thank you everyone else i ask just keeps talking about EFFICIENCY! thanks alot that is very helpful indded :)

It's in fragments for efficiency.  Single-stranded DNA is not very stable without proteins to stabilize it.  If you tried to replicate the entire strand in one go, you'd need to keep the entire strand in single-stranded form one way or another (e.g. start at both ends and meet in the middle would still leave each half as an old/new duplex, plus an old single-stranded copy waiting to be filled in from the other direction).
To avoid needing a chromosome or genome's worth of SSDNA binding proteins, it works in fragments.
(That is: if you had organisms that had to produce that much SSDNA binding protein, they'd be out-competed by organisms that didn't have to.)

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How does the human body metabolize gasoline?
A Chinese man has been drinking gasoline to relieve his pain for 25 years. How does the human body metabolize gasoline? Also, what are the side-affects to gasoline?

Hopes the degassing tag is a bad pun

Made my day that one.

Don't discount the likelihood that the original story in your link is either completely fabricated or wildly exaggerated.

Just to add an answer to the 'how does the body process gasoline?' portion of the question, the liver and kidney would be doing most of the work of removing the stuff from the system once it was absorbed in the digestive tract.
The liver does most of the processing of toxins and their removal from the blood and would tend to do the most work in removing hydrocarbons from gasoline.  It has enzymes that oxygenate toxins (adds oxygens) which make them more soluable in the blood, usually less toxic, and also removable from the body by the liver or the kidney. In the case of gasoline the compounds are likely to be just as toxic.
The kidney works by actively filtering out excess water and mostly water soluable wastes like oxygenated hydrocarbons.  Kidney damage occurs when gasoline is ingested in excess.  This may be due to the toxicity of the gasoline, but also due to the compounds the liver is producing.
Gasoline will tend to be fat soluable too, so it will leave the system more slowly, even after being processed by the liver (benzene and toluene in gasoline will tend to become phenols which are quite toxic and fat soluable).
http://www.ncbi.nlm.nih.gov/pubmed/3379185

Gasoline toxicity through ingestions seems to be a topic where there's not a great deal of in-depth information available. I don't know how this works for chronic use, as most literature refers to acute scenarios. Either way, orally ingested, 30-50g is said to be toxic to humans while 350g can be fatal.[3].
So...
Gasoline's Constituents
A lot of components that make up gasoline are toxic to humans. This includes for example, benzene, toluene, xylene and butadiene. It's a mixture of more than 500 hydrocarbons and additives made up of:

60–70% alkanes (paraffins)
25–30% aromatics
6–9% alkenes (olefins).[2].

If you really want to know specifics about metabolism of gasoline, you can probably check out how some of the constituents are metabolised (processed) and their effects. This is because different components have varying metabolic pathways.
If you want to check this out, see Reese, et al at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1520023/pdf/envhper00383-0118.pdf.[3].
Ingestion and Toxicity
Apparently, most reported cases of toxicity from gasoline occur from inhalation or absorption through the skin (intravenous use has also been reported). Even though ingestion is a frequent occurrence, there's not much data on outcomes after oral ingestion.[1],[2]. Gasoline can however be well absorbed through the gastrointestinal tract[2].
The main target organ of gasoline toxicity is the nervous system and at high doses, this effect can cause death within minutes.[3]. However, generally, the primary cause of mortality seems to be related to gasoline's toxicity to the lungs. There are severe effects on the pulmonary system. Other effects of ingestion hasn't been as well documented.[1],[2].
It's suggested that these compounds have a direct effect on lung tissue and  disrupts gas exchange and causes fluid buildup in the lungs (pulmonary edema). This in turn causes the oxygen levels in the body to drop (hypoxemia).[2]. There are many other toxic effects on the lungs as well.
Additionally, liver damage, kidney damage, damage to blood cells, gastric ulcers and toxicity in the heart can occur.[2],[3]. Again, this is discussed in Reese, et al.
Hope that helps!

Rahman I. Gasoline ingestion: a rare cause of pancytopenia. Am J Med Sci. 2009. 338(5):433-4.
Domej W. Successful outcome after intravenous gasoline injection. J Med Toxicol. 2007. 3(4):173-7.
Reese, et al. Acute Toxicity of Gasoline and Some Additives. Environmental Health Perspectives. 1993. 115-131.

The implication seems to be gasoline disrupts membrane integrity and function.

Prolonged exposure to high concentrations of n-hexane (>1,000 ppm) has resulted in decreased sperm count and degenerative changes in the testes of rats but not those of mice.
Acute Data: Gasoline: Dermal LD50>5 ml/kg (Rabbit) LC50> 4500 ppm (Rat) Oral LD50= 18.75 ml/kg. (Rat)
Carcinogenicity: Two year inhalation studies of wholly vaporized unleaded gasoline produced increased incidences of kidney tumors in male rats and liver tumors in female mice. Follow-up studies suggest that occurrence of the kidney tumors may be linked to alpha-2-u-globulin nephropathy, and most likely unique to the male rat. Epidemiology data collected from a study of more than 18,000 petroleum marketing and distribution workers showed no increased risk of leukemia, multiple myeloma, or kidney
cancer from gasoline exposure. Unleaded gasoline has been identified as a possible carcinogen by IARC.
Because solvent extracts of gasoline exhaust particulates caused skin cancer in laboratory animals, IARC has categorized gasoline engine exhaust as a possible human cancer hazard.
Target Organ(s): A two year inhalation study of wholly vaporized unleaded gasoline producednephropathy in male rats, characterized by the accumulation of alpha-2-u- globulin in epithelial cells ofthe proximal tubules, and necrosis and hyperplasia of surrounding cells. Follow-up studies havedemonstrated that these changes are unique to the male rat. Although prolonged exposure to n-hexane, a component of gasoline, has resulted in adverse male reproductive effects in experimental animal studies, no adverse male reproductive effects were found in studies conducted with gasoline.
Developmental: No evidence of developmental toxicity was found in pregnant laboratory animals(rats and mice) exposed to up to 9,000 ppm vapor of unleaded gasoline via inhalation.
All data taken from the Material Safety Data Sheet (MSDS) from Petroleum Products Corp. See this link for more information.

Much of this answer is not relevant to the question about injesting gasoline (not inhaling it, inhaling exhaust, or being exposed to hexane); -1

-1. The question is not about n-hexane toxicity but n-hexane ADME (Absorption, Distribution, Metabolism, Escretion)

Vote up/down as you wish, but information on target organs and developmental effects does indeed give relevant information on how the body processes gasoline.

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What is the pathogenuc mechanism of brown pigment lipofuscin in muscle atrophy?
I think it is autophagy. Lysosomal degradation. Autophagocytosis.
Example of the brown pigment (lipofuscin) here:

I am not sure if autophagy is the right answer to the "pathogenic" mechanism of atrophy.
Is autophagy the pathogenic mechanism of atrophy?
Or what pathogenic mechanism is involved if you see lipofuscin in the histologic slide?

Simple answer: Atrophy through autophagy.

Downvoter! Please, comment or answer better.


text:
Why PPD test in patients without M.tuberculosis often slightly positive?
I got this question which I interpret as

Why PPD test in patients without M. tuberculosis often have slightly positive PPD reaction i.e., a lifelong slightly positive skin test reaction?

because slightly positive -phrase does not make so much sense to me.
I first thought it is about false positiveness, but it does not make sense.
I am reading Murray Microbiology book.
It says there

[An alternative to the PPD skin test,] is in vitro IFN-gamma release
  assays. The tests use immunoassays to measure IFN-gamma produced by
  sensitised T cells stimulated by M.tuberculosis antigens. If an
  individual was previously infected with M.tuberculosis, exposure of
  sensitised T cells present in whole blood to M.tuberculosis-specific
  antigens results in IFN-gamma production.

The question asks PPD test in patients without M.tuberculosis.
It does not say if the patient has previously had infection with M.tuberculosis.
I think this question implies that the patient has never had before infection with M.tuberculosis.
I am not sure how it can be in reality possible for adults, since M.tuberculosis spreads in air.
The reason for false positiveness can be that assays that use PPD use unspecific antigens, in contrast to IFN-gamma and second-generation assays.
The other reason is that once you get infected you always have some degree positive skin test reaction.
So to say patient without M.tuberculosis is faulty in a way because I think most people get exposured to this bacteria at least little in life.


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Contracting muscles in humans
I study biology at school, and unfortunately for me, my program skips the muscles in humans chapter.
I know (and mainly, feel) that the movement in one direction isn't created by the same muscle as the movement in the opposite direction, e.g the Triceps ("front") and Biceps ("back").
I know that the triceps straightens the elbow, while the biceps contracts the elbow.
I also know that, instead of actually moving the arm, I can contract these two muscles (when I show off, for example...) without actually moving the arm. That area becomes hard. Both muscles, as I feel, are contracting. I cannot statically contract only one of them.
My question is whether this action is something "special", or simply both muscles working against each other, resulting in zero movement?

The situation you are describing where muscles are situated on opposites sides of a joint and produce opposing movements is called "antagonism." Most joints are set up where one or more muscles on either sides will produce such movements (e.g., flexors vs. extensors). Here's a question about muscles without antagonists.
When you contract all the muscles crossing a joint (i.e., when you are "showing off"), the muscles balance each other. If not, the bones would move and the joint angles would change. So taking the elbow as an example, in the image below, Arnold is contracting the elbow flexors (biceps brachii, brachialis) as well as the elbow extensors (triceps brachii). In order for the bones to remain static, the forces must be equal and opposite.

Arnold is a good model for studying muscle anatomy in schools.. the exaggerated sizes will help kids find each and every muscle..  :-P


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S. pyogenes' skin infection diagnostics
S. pyogenes is "flesh-eating" bacteria.
It results from life-theatening myonecrosis caused by this organism.
S. pyogenes avoids phagocytosis (mediated primarily by capsule, M and M-like proteins, C5a peptidase), adhere to and invade host cells (M protein, lipoteichoic, F protein), and produce toxins (streptococcal pyrogenic exotoxins, steptolysin S, streptolsin O, streptokinase, DNases).
Suppurative diseases: pharyngitis, soft-tissue infections.
Erysipelas: localised skin infection with pain, inflammation, lymph node enlargement and systemic symptoms.
Cellulitis: infection of the skin that involves the subcutaneous tissues.
Necrotising fasciitis: deep infection of skin that involves destruction of muscle and fat layers.
I think these are most its skin infections. But what about its diagnostics?
I think take biopsy from living tissue, not from necrotic.
If pus, then probably from it.
I think we can do Gram staining, recognise gram-positive cocci like in a string
Then, we can do hydrogen peroxide test - if no bubbles, then suspicion to S. pyogenes, since catalase negative.
The do optochin test which is positive for S. pyogenes.
What is the correct procedure for doing skin infection diagnostics for group A streptococci?

S. pyogenes cultured on Blood Agar should show beta-hemolysis. B-hemolytic colonies can be further identified as S. pyogenes by the results of negative catalase (hydrogen peroxide) test, positive L-pyrrolidonyl arylamidase (PYR) reaction (1) and sensitivity to Bacitracin (2). See https://www.inkling.com/read/medical-microbiology-murray-rosenthal-pfaller-7th/chapter-19/streptococcus-pyogenes
PCR may also be used: http://www.sciencedirect.com/science/article/pii/S0923250805000215


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Is this case Histoplasma capsulatum?
A 62 year-old male was admitted to the hospital complaining of shortness of breath. His chest X-ray showed a rightsided cavitary lesions. His medical history indicated he had smoked one pack of cigarettes per day for past 40 years and has had cavitary tuberculosis in about 20 years ago. Recently he is receiving cytostatic therapy for his acute myeloblastic leukaemia. A biopsy specimen of the lung was obtained. Biopsy from lesion shows tubular eukaryotic septated hyphae with diameter of 510 μm that are infiltrating the lung tissue. Culture on Saboraud’ media shows conidia with spores in radiating columns. Which is the most like cause of the findings?
The disease is systemic - affecting lungs.
Organism has septated hyphae with conidia.
Is there any other possibilities for the disease?

Any more information about the pathology?  IPA? Sloughing, consolidation?  IF we had a little more info we might be able to shed more light.

Is the hyphae diameter really 510µm? That seems exceptionally large.  Could this be the length instead?

Is there any other possibilities for the disease?
Yes.  At 37°C, Histoplasma capsulatum usually doesn't form hyphae.

Were the hyphae branching, like this?
If "conidia with spores in radiating columns" means the pictures below,
We have enough to say that this is not a case of Histoplasma capsulatum and there is definitely another possibility for this disease.
Conidia with radiating chains of spores is pathognomonic for aspergillosis.

I do not know if hyphae was branching like that. I have only the text. It is at least septated hyphea like in your picture. No information about temperature where the sample is cultured. Histoplasma capsulatum is a possibility here.

Not the temperature of the culture, the temperature of the biopsy—because the patient is still alive, you have reason to believe that the biopsy was warmer than 30°C. As explained at the previously linked site, H. capsulatum is dimorphic, growing as a mold at room temperature and as a yeast at body temperature.

Tissue morphology
Histoplasmosis: Small narrow base budding yeast cells (1-5um; 5-2um in var. duboisii)


text:
circulating microRNAs are functional?
In plasma and other body fluids, miRNAs can be found. They not only originate from dying cells but also from active secretion and are usually 'packed' into vesicles/lipo-proteic structures (i.e. exosomes) protecting them from the action of ribonucleases. Thus, miRNAs in plasma are very stable, offering diagnostic opportunities.
My question is whether they may also have a functional role. Exosome transfer between cells has been demonstrated, so it is likely that miRNAs can be secreted by one source cell and reach a target cell, similarly to how hormones works. However, this has not been quantitatively assessed. Is the concentration of miRNAs in plasma known? Is it sufficient to hypothesize functional regulation of gene expression in target cells?

See papers by D Bianchi for reports of miR levels in blood of pregnant humans, both of maternal and fetal origin.
A review by Steer and Subramanian offers a number of examples pertaining to your question.
Lastly, Vickers, Palmisano, et al. (2011) show that some miRs are present in the HDL-cholesterol particle and that those levels differ between normal and familial hypercholesterolemia human subjects.


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Are there any forms of heart failure where cell size decreases?
I think hypertrophy happens in most of the cases. However, I am not sure if hypertrophy always happens. I started to think about wet lungs (pulmonary reason for the left-sided heart failure).
Can the decrease of cell size occur in the heart failure?

Literature covers only hypertrophy of the heart.
Atrophy not mentioned.
Theoretically atrophy of the heart would require some factors

mutations (which can destroy the gene to build up the organ),
poor nourishment,
poor circulation,
loss of hormonal support,
loss of nerve supply to the target organ,
excessive amount of apoptosis of cells, and
disuse or lack of exercise or disease intrinsic to the tissue itself.

Atrophy can happen locally in some part of the heart only, like in some parts of myocardial infarction.
However, the surrounding healthy tissue then undergoes hypertrophy so the total heart undergoes hypertrophy.
Some discussion about Cardiac atrophy here.


text:
Some trophoblast excreting digestive enzymes in implantation
I found this paragraph in my study materials about implantation
Original

Simplest trophoblast excretes trypsin related substances and embedding consists of 3 stages:

The blastocyst (composed of cytotrophoblast and embryoblast) stick to the uterine wall
Enzymes digest nische (little hole in the endometrium) to the functional layer and the blastocyst deepens in it. The nische is a closed and destroyed functional layer, in it tissue and blood is used for trophic (called a nischtrophic way of feeding)
Implantation ends in 13½ day when the functional layer covers the blastocyst.
  Implantation normally takes place in anterior and posterior wall of uterus, sometimes in superior or fundus wall.

My suggestion for corrections

Syncitiotrophoblast excretes Digestive Enzymes and embedding consists of 3 stages:

The blastocyst (composed of cytotrophoblast and embryoblast) stick to the uterine wall
Syncytiotrophoblast expresses digestive enzymes which dig a little hole (nische) into endometrium. The hole is usually filled with maternal tissue (so closed) and blood used by the conceptus for histotrophic feeding (nischtrophic way of feeding)
Implantation should end in 13½ day when the endometrium covers the blastocyst.
  Implantation normally takes place in anterior and posterior wall of uterus between glands of the hypertrophic endometrium, sometimes in superior or fundus wall.

I cannot accept the phrase simplest trophoblast and the use of the words trypsin related substances. Really, how can you get trypsin without pancreas? I would not use the word trypsin although the enzymes may have some structural similarities.
How would you reformulate the paragraph?

If you think about what the trophoblast (particularly syncytiotrophoblast) is doing during implantation, then secreting trypsin related substances makes sense.

@kmm Can you call this trophoblast also simplest trophoblast? Where does the name come from?

Maybe it's just referring to the undifferentiated trophobast (before cytotriphoblast and syncytiotrophoblast can be identified as such).

@kmm I made big changes to the paragraph after getting the opinion of another group of students. I tried to fix it so well as I could in the my suggestion.

I have no idea what is meant by 'the simplest trophoblast'. I did, however, find this review, pointing to a role of proteases in the implantation process:

Salamonsen L.A. Salamonsen and Nie, G. (2002) Proteases at the Endometrial–Trophoblast Interface: Their Role in Implantation. Reviews in Endocrine and Metabolic Disorders, 3:133-143

which discusses the roles in implantation of three classes of proteases : matrix metalloproteinases, serine proteinases and cystein proteinases. The reference to 'trypsin-like' presumably relates to the serine proteases. The review reports the results of a number of gene knockout experiments in mice in which genes for individual proteases have been disrupted which indicate that no single enzyme is identified as being essential.
Referring to

Afonso S et al (1997) The expression and function of cystatin C and cathepsin B and cathepsin L during mouse embryo implantation and placentation. Development 124:3415-3425.

the authors of the review state that:

[they] demonstrated that cysteine proteases play a critical role in implantation. Cathepsin B mRNA was expressed by mouse trophoblast throughout the invasive period (days 5.5±10.5) while the proteins for cathepsins B and L were localized to the mature invasive trophoblast giant cells; activity of these enzymes was also demonstrated. Cathepsin L was also present within the stroma particularly in the lateral decidualizing zone. Cystatin C, the major inhibitor of cathepsins, was shown to be a major product of the adjacent decidualizing stroma close to the embryo, suggesting a restraining role. After the completion of placental trophoblast invasion (day 11.5) the trophoblast cells express high levels of cystatin C, probably in association with a switch from an invasive cell type to one providing nutrients to the conceptus [35]. In addition, treatment of pregnant mice with E-64, a synthetic cysteine protease inhibitor, resulted in failure of implantation and normal uterine decidualization.

You are completely right. I think the simplest trophoblast is mistake and the original author meant syncytiotrophoblast. Those enzymes secreted are structurally trypsin related. However, I would never call them such only. The best way to start would be to say digestive enzymes such as trypsinase digging a hole into the endometrium.

Perona and Wassarman (http://www.ncbi.nlm.nih.gov/pubmed/3514318) showed that a 'trypsin-like proteinase' (strypsin) is required to hatch the blastocyst and that it is concentrated on the wall-side cells of the blastocyst.


text:
How does sepsis affect heart function?
I have intuition that sepsis with infection can cause:

spastic functioning of heart during systole
heart working spontaneously in snatches during systole
atrial fibrillation
first contraction of ventricles ends earlier
which follows Action potential from A-V node during relative refractory period
weak second contraction
long compensatory pause

which can be recorded as spikes in the time axis.
With arrhythmic (earlier myocardial infarction) patients, sepsis seems to also cause leaking of valves, weakened compliance of vessels and structure of the heart.
So there are creaking sounds in the spectrum spaces.
How do the symptoms of sepsis affect heart function?
I am thinking if it is possible that this leakiness of valves and weakened compliance last only for short term and occurs periodically, during which also the heart pumps more frequently load during extrasystoles.
Assume that everything listed above is possible.

Can temporary acute/chronic inflammation in the heart cause such symptoms such as sudden weakening of valves and only temporary weakened compliance of coronary vessels?
I think the reason can be thromboembolism which is causing the sudden spastic function and weakened function of vessels and heart structures.

While the heart is affected during septic shock, it is the result of the chain of events that occur as a result of a systemic release of the pro-inflammatory cytokine Tumor Necrosis Factor alpha (TNF-$\alpha$) that leads to the "collapse of the circulatory and respiratory system." (Janeway's Immunobiology, 8th Edition) See also Tumor necrosis factor signaling.
When leukocytes, mainly macrophages encounter a pathogen or the antigenic product of a pathogen, pathogen-associated molecular patterns (PAMPs) such as endotoxins or exotoxins, their pattern recognition receptors (PRRs), such as the toll-like receptors, are bound and signaling occurs which stimulates the production and release of pro-inflammatory cytokines. In a localized infection, this is a beneficial response, however when the response is systemic, it will lead to a catastrophic cascade that leads to septic shock and often death.
Under "normal" conditions, TNF-$\alpha$ is an inducer of local inflammatory response. When an endotoxin such as lipopolysaccharide (LPS) is detected by TLR-4 on macrophages in the local microenvironment of an infection, the macrophages are stimulated to secrete TNF-$\alpha$. TNF-$\alpha$ produces the following physiological effects:

Activates the vascular endothelium

The endothelial cells will begin expressing a different assortment of receptors that recruit leukocytes out of the blood and into the tissue
This also allows for increased platelet adhesion to the activated endothelial vessels

Increases vascular permeability

Increased entry of Immunoglobulin G into the infected tissue
Increases entry of Complement proteins from the plasma to the tissue
Increased access to leukocytes and activated lymphocytes for extravasation into the infection microenvironment

Increased fluid drainage to lymph nodes

- Janeway's Immunobiology, 8th Edition; p 101
One of the mechanisms that is beneficial to the local inflammatory response, namely platelet adhesion will become problematic in the systemic response and will lead to multi-organ failure. In the local environment, however, it helps to prevent the spread of infection and shunts fluid flow away from the bloodstream and to the lymphatic system where it will be encountered by the components of the adaptive immune system. Locally:

Another important action of TNF-$\alpha$ is to stimulate endothelial cells to express proteins that trigger blood clotting in the local small vessels, occluding them and cutting off blood flow. This can be important in preventing the pathogen from entering the bloodstream and spreading through the blood to organs all over the body. Instead, the fluid that has leaked into the tissue in the early phases of an infection carries the pathogen, usually enclosed in dendritic cells, via the lymph to the regional lymph nodes, where an adaptive immune response can be initiated.
- Janeway's Immunobiology, 8th Edition; pp 107-108

You can begin to see where the inflammatory response triggered by TNF-$\alpha$ may become a catastrophic problem if it is secreted systemically.

Once an infection spreads to the bloodstream, however, the same mechanisms by which TNF-$\alpha$ so effectively contains local infection instead become catastrophic. Although produced as a membrane associated cytokine, TNF-$\alpha$ can be cleaved by a specific protease TACE (TNF-$\alpha$-converting enzyme, formerly called ADAM17) and released from the membrane as a soluble cytokine. The presence of infection in the bloodstream, or sepsis, is accompanied by a massive release of TNF-$\alpha$ by macrophages in the liver, spleen, and other sites throughout the body. The systemic release of TNF-$\alpha$ into the bloodstream causes vasodilation, which leads to a loss of blood pressure and increased vascular permeability, leading to a loss of plasma volume and eventually shock, known in this case as septic shock because the underlying cause is a bacterial infection. The TNF-$\alpha$ release in septic shock also triggers blood clotting in small vessels throughout the body--known as disseminated intravascular coagulation--which leads to the massive consumption of clotting proteins, so that the patient’s blood cannot clot appropriately. Disseminating intravascular coagulation frequently leads to the failure of vital organs such as the kidneys, liver, heart, and lungs, which are quickly compromised by the failure of normal perfusion; consequently, septic shock has a high mortality rate.
- Janeway's Immunobiology, 8th Edition; pp 108-109

So, as you can see, it is the effect of the depletion of clotting factor, the loss of plasma volume and blood pressure, and the alteration of the blood's ability to clot which likely is leading to the arrhythmic effects that you have observed in the heart.
The figure below summarizes both the localized and systemic effects of TNF-$\alpha$ release.
$\alpha$ can have damaging effects when released systemically" />
- Janeway's Immunobiology, 5th Edition; Figure 2.37
Effects of TNF-$\alpha$ on the heart
There is research from the 1990s and early 2000s that deals with the effects of TNF-$\alpha$ both on the heart and expression of the cytokine in failing heart tissue. Below is a brief selection of those articles. The final reference discusses the link between Toll-like receptor 4 activation and the promotion of cardiac arrhythmias:
From Cardiac-specific overexpression of tumor necrosis factor-alpha causes lethal myocarditis in transgenic mice. Kubota, et.al. J Card Fail. 1997 Jun;3(2):117-24.

Tumor necrosis factor (TNF)-alpha, a proinflammatory cytokine with negative inotropic effects, can be detected in myocardium with end-stage heart failure, after endotoxin administration, and during transplant rejection. Various studies suggest that TNF-alpha participates in the pathogenesis of cardiac dysfunction.
Overexpression of TNF-alpha in the heart leads to severe myocarditis and cardiomegaly. These results support the hypothesis that myocardial expression of TNF-alpha can contribute to the pathogenesis of cardiac dysfunction.

From Dilated Cardiomyopathy in Transgenic Mice With Cardiac-Specific Overexpression of Tumor Necrosis Factor-$\alpha$. Kubota, et.al.
Circulation Research.1997; 81: 627-635; doi: 10.1161/01.RES.81.4.627

That end-stage congestive heart failure is associated with a marked increase in circulating TNF-$\alpha$ levels has been reported by numerous investigators. Furthermore, there appears to be a direct relationship between disease severity and circulating levels of TNF-$\alpha$.
In the present study, we demonstrate that chronic overexpression of TNF-$\alpha$ results in the development of a dilated cardiomyopathy that shows (1) ventricular hypertrophy, (2) ventricular dilatation, (3) interstitial infiltrates, (4) interstitial fibrosis, (5) rare myocyte apoptosis, (6) a diminished ejection fraction, (7) attenuation of $\beta$1-adrenergic responsiveness, and (8) expression of atrial natriuretic factor in the ventricle. Additionally, mice overexpressing the TNF-α transgene had a marked increase in mortality. More than half of the mice that died spontaneously presented with exceptional dilatation of the heart, increased lung weight, and pleural effusion, suggesting that they died of congestive heart failure.

From The role of tumor necrosis factor in the pathophysiology of heart failure Feldman, et.al. Journal of the American College of Cardiology
Volume 35, Issue 3, 1 March 2000, Pages 537–544

In summary, both basic and clinical studies strongly support the hypothesis that myocardial expression of TNF alpha is an important step in the pathophysiologic pathway leading to progressive cardiac dilatation and failure.

From Toll-like receptor 4 activation promotes cardiac arrhythmias by decreasing the transient outward potassium current (Ito) through an IRF3-dependent and MyD88-independent pathway. Monnerat-Cahli, et. al. J Mol Cell Cardiol. 2014 Nov;76:116-25. doi: 10.1016/j.yjmcc.2014.08.012. Epub 2014 Aug 25.

Abstract
Cardiac arrhythmias are one of the main causes of death worldwide. Several studies have shown that inflammation plays a key role in different cardiac diseases and Toll-like receptors (TLRs) seem to be involved in cardiac complications. In the present study, we investigated whether the activation of TLR4 induces cardiac electrical remodeling and arrhythmias, and the signaling pathway involved in these effects. Membrane potential was recorded in Wistar rat ventricle. Ca(2+) transients, as well as the L-type Ca(2+) current (ICaL) and the transient outward K(+) current (Ito), were recorded in isolated myocytes after 24 h exposure to the TLR4 agonist, lipopolysaccharide (LPS, 1 μg/ml). TLR4 stimulation in vitro promoted a cardiac electrical remodeling that leads to action potential prolongation associated with arrhythmic events, such as delayed afterdepolarization and triggered activity. After 24 h LPS incubation, Ito amplitude, as well as Kv4.3 and KChIP2 mRNA levels were reduced. The Ito decrease by LPS was prevented by inhibition of interferon regulatory factor 3 (IRF3), but not by inhibition of interleukin-1 receptor-associated kinase 4 (IRAK4) or nuclear factor kappa B (NF-κB). Extrasystolic activity was present in 25% of the cells, but apart from that, Ca(2+) transients and ICaL were not affected by LPS; however, Na(+)/Ca(2+) exchanger (NCX) activity was apparently increased. We conclude that TLR4 activation decreased Ito, which increased AP duration via a MyD88-independent, IRF3-dependent pathway. The longer action potential, associated with enhanced Ca(2+) efflux via NCX, could explain the presence of arrhythmias in the LPS group.

It would be great to understand in which order the dysfunction of valves and coronary vessels commonly occur. I think that the dysfunction of valves can occur earlier in the cascade of TNF-$\alpha$ than the dysfunction of coronary vessels because the hypovolemia leads to the occlusion of the vessels in the late stages. It would be great to understand the pathway differences of Tumor necrosis signalling between the valves and the vessels.

I extended the Synchronicity of TNF signaling in heart's microenvironments to the thread http://biology.stackexchange.com/q/41981/86

@Masi please see edits with additional information on TNF-alpha and TLR-4 in cardiac failure and arrhythmias.

What therapies could be envisioned against septic shock apart from antibiotics when applicable?

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Mechanism of Tear Gas (chloropicrin/Trichloro methane)
Tear gas (CCl3NO2) makes people cry, and crying doesn't seem to be a simple procedure. There has to be a triggering process somewhere. Can someone explain its mechanism / how it works?

The general belief is that these agents are irritants which do not have a very specific effect.  That is to say that there is no specific cell or biological function that they set off, but that they irritate the cells, so the cells respond by putting up general defenses to insulate themselves from the noxious chemicals.
Mucous and tears wash away the compounds.  I'm sure there are all sorts of things going on, but its hard to be more specific.  For instance, onions have many sulfhydryl (-SH) compounds,  many many of them.  In particular propanethial s-oxide causes the tears we get when we cut an onion. This compound is very reactive and reacts with all sorts of proteins and disrupts the membrane, etc.  Its perhaps an example of a specific irritant that is so reactive that it creates tears.
An example of a specific reaction would perhaps be capsaicin.  There is a specific protein that is a heat receptor and the chemical capsaicin activates it, causing the feeling of heat/warmth.
Tear gas and mustard gas appear to fall into the former category, which are chemicals so reactive that they just tear into the cell, damaging all sorts of things in there.


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Manipulating Gut flora in vivo
I am tasked with designing an in vivo experiment in humans that requires manipulating the gut flora in one sample group to gauge its effect. Please suggest ways of doing this besides administering antibiotics.
I am of the view that antibiotics may have unintended consequences and may be unethical; explain any opposing view.

I think it would be helpful if you explained more about what you want to compare, and/or the rationale for experimentation. What do you want to gauge its effect on? Before/after antibiotics is probably the simplest and certainly statistically the most powerful approach.

i'm sure that changes of diet would also substantially change the gut flora mixture.  this has been shown already, but i don't have the reference at hand...

I can't think of any way to start with an intestinal "blank slate", so to speak, except with antibiotics.
Perhaps it's possible to at least partially homogenize/standardize a sample group's biota with probiotics?
If it's ethics you're worried about, perhaps draw experimental subjects from a pool already being treated with antibiotics (although this, I suppose, introduces it's own biases?).

Thank you Atticus29, this has re-assured me that antibiotics is the way to go..

I'm no expert, but I read this, and I found it very intresting:

In its study, Henry Ford treated patients between May 2010 and June
  2012 with a therapy called intestinal microbiota transplantation
  (IMT), using donated stool from a healthy family member.

Here are the results:

“More than 90 percent of the patients in our study were cured of their
  C.diff infection,” says Dr. Ramesh. “This treatment is a viable option
  for patients who are not responding to conventional treatment and who
  want to avoid surgery."

http://www.henryford.com/body.cfm?id=46335&action=detail&ref=1757

Thanks. I knew that was an option, but not viable for my study. Reason is: I want to gauge low level microbiome against normal. In essence, I need reduced gut flora and not different flora..+1 though. Just realised I cant't upVote..:)


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What causes peanut allergies?
Surveys show that 0.6 percent of the US population has an allergic reaction to peanuts. This prevalent allergy has even prompted some to ban peanuts from schools altogether.
I am completely unfamiliar with the topic, and can't seem to find any specifics in the literature. Thus my question is:
What specifically causes the the allergic reaction associated with peanut consumption, and why is it so prevalent in comparison to other foods?

This article claims that a protein complex Ara H has the allergenic properties.

I just wanted to let you know that I changed the title to reflect that the question is about the causative agent of allergies, rather then the epidemiology of allergies.

Ara H 1, Ara H 2, and Ara H 3 are the three main peanut allergies. AH1 and AH2 are typically higher-acuity anaphylactic type reactions. The molecular cause for this is that some Immunoglobulin E develop a serum sensitivity and bind directly to vicilin and conglutin (the active proteins in AH1 and AH2). There are actually 7 or 8 Ara H complexes, but it is believed the remaining ones have a lesser affinity for IgE, reducing the frequency of allergic reactions and thus their availability for relevant studies.
The prevalence of the allergy is generally attributed to a combination of exposure and genetics. Many people have a genetic predisposition to certain allergies, but to a certain extent the body must be exposed to the allergen before an allergy will develop. The high use of peanuts in the food industry, and even to a lesser degree in skin care products like lotions, can account for early exposure resulting in allergies.
From the other direction, some research suggests that early and frequent exposure from infancy through childhood (albeit the choking risk) can reduce the demographic prevalence of an allergy in a given population.


text:
Why is methylcellulose used in pharmaceuticals?
Why is methyl cellulose used as a pharmaceutical excipient? Is it due to certain chemical properties? What are the reasons for relying on the chemical properties of methyl cellulose?

Methyl cellulose is a dry binder. It is used to make a pill with a small mass of active ingredient and as much binder as required to make the pill a manageable size.
The following properties make methyl cellulose a good dry binder:

inexpensive
non-allergic
vegetarian
soluble in cold water
non-digestable
nontoxic

Most of this information is from the Wikipedia article.

Like cellulose, it is not digestible, not toxic, and not an allergen. Bacteria cannot digest, methyl cellulose, so they cannot grow using MC as carbon source. It is artificially synthesized produced by heating cellulose with NaOH.

It is a filler/binding agent. Thus MC belongs in the context of a drug to the group of so called excipients. The study of the best suitable excipients (as a tradeoff of factors such as cost, and ease of approving the drug) is called
galenics.
Methyl cellulose is also present in your toothpaste and some of the foods your eat and in the construction industry. It can be considered to be metabolically inert for humans, but can serve as a matrix for enhancing bacterial adhesion and biofilm formation.
The gradual smudging and staining of your bathroom washbowl may be largely attributable to MC and bacteria.
MC is a polymer that is sold as dry powder of various mean chain lengths. It is hydrophilic and can retain large volumes of water.

I'd avoid using code formatting for emphasis, it looks a bit out of place and that is not what this option is meant for. There's also bold and italic available, though I wouldn't emphasize that many parts in a post, too much and it gets distracting again.

Unless it is explicitly prohibited, I will prefer that formatting. Thanks for understanding. I consider bold formatting to be more out of place. Different strokes for different folks...

@LoSauer it's considered extremely bad practice across the network, therefore it would be much better not to use the formatting in this way.

@RoryM You point towards an stackoverflow-thread, yet there is a meta-site for this biology community. I put this issue up for discussion on meta. Till then please regard the editing guidelines. thanks.


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How long does it take for E. coli to shift feedstocks?
With our fermentations we're noticing that it takes an appreciable amount of time for E. coli (K12 variant) to change from being metabolically streamlined on amino acids to being metabolically streamlined to glucose.
How long does it take for such microorganisms to adjust to a new feedstock?

This must depend upon the conditions in question, but I think it would not be very long.
The length of a generation for e coli can be 12 minutes or 24 hours, so that gives some idea of a typical time.
I did find this interesting case in the literature. They found that even as you subject e coli to minimal nutrients they are expressing genes that prepare them for a richer nutrient mix.  The bacteria are primed for a flood of carbohydrates succinate or amino acids.
This study incubated the e coli overnight before taking their readings, so this puts an upper bound of about 12 hours.  The implication is that if you are moving the bacteria to rich media it might be just a short time before they are in log phase growth.
In practice moving from LB plates to log phase growth is usually just like 4 hours.  This paper interestingly shows that cold adapted E coli moving to other media react in a few hours, but can show behavioral changes days out.
I would say that 4 hours might be a typical expectation. 12 is typically used in the literature.


text:
What regulates these two methods of splicing?
Alternative splicing can shuffle the exon order and select from the exon sequence of a single gene site to provide a combinatorial selection of possible transcription products from the one gene. Can intergenic trans splicing can do this starting from multiple gene sites?
What regulates these two "non linear" gene combination, transcript-splicing processes?

Are you referring to trans splicing?

As Alan Boyd said, this process is called trans splicing where exons of different RNAs are joined together. Physical proximity is conducive for trans-splicing. This study shows that trans-splicing frequency is higher if the genes are proximal. Proximity not only means closer in the genome but also the 3D proximity governed by chromosomal interactions.
Now, what factors  promote trans splicing is not properly understood.


text:
At what age do babies begin to synthesize their own antibodies?
When babies are first born, they receive their antibodies from their mother (I assume because they do not yet have the capacity to synthesize their own).  So my question is, at what age do babies begin synthesizing their own antibodies?

In the graph above the darker blue line refers to the antibodies the baby receives from the mother in utero, as you mentioned in your question.
As you can see, the red line indicates that babies begin to produce low levels of their own antibodies between 3 and 6 months before birth.  However, these are IgM antibodies, immature 'rough draft' versions.  These have much lower affinity for antigens then their mature IgG counterparts which are the classically thought of antibody.
Levels of an infant's own IgG start to rise after birth, however don't reach a reasonable level until after the child is roughly 1 year old.  Maternal antibodies start to tail off at around 3 months leaving a period highlighted in blue on the graph where infants are particularly prone to getting infections.

I don't think that is correct to say that IgMs have lower affinity. When a cell shifts from making an IgM to an IgG via class switching, the variable domains remain the same, there is no change in affinity - affinity maturation has already occurred during proliferation of the IgM-producing cell line. In fact IgM will bind well to weakly cross-reacting antigens because of its high avidity (due to the pentameric structure of the IgM molecule).

@AlanBoyd this is perhaps a shortcoming in my notes, I was under the impression that affinity maturation has two 'sub-processes', class switch and then somatic hypermutation however I could have easily got the order reversed.

If the fetus gets infected, can it produce antibodies intrauterine to fight the infection ? If yes; is it effective ? Can it be used to test if the infection has traveled from mom to fetus ?


text:
By what mechanism is Streptococcus bovis acting as a risk factor for colorectal cancer?
Streptococcus bovis bacteremia/endocarditis is considered a risk factor for colorectal cancer. What pathophysiological mechanism may link the two together?

As you probably know, there is a lot of literature on the correlation between Streptococcus bovis and colorectal cancer, but very little on possible mechanisms.
In an editorial (Streptococcus bovis: Causal or incidental involvement in cancer of the colon? in the International Journal of Cancer 119(9):xi-xii), Harald zur Hausen referring to this paper:

Biarc J, Nguyen IS, Pini A, Gosse F, Richert S, Thierse D, van Dorsselaer A, Leize-Wagner E, Raul F, Klein JP, Scholler-Guinard M. (2004) Carcinogenic properties of proteins with proinflammatory activity from Streptococcus infantarius (formerly S. bovis). Carcinogenesis 25: 1477–84.

comments:

...used a partially purified S. bovis S300 fraction representing 12 different proteins and triggered the synthesis of proinflammatory proteins (human interleukin-8 and prostaglandin E2, correlated with the in vitro overexpression of cyclooxygenase-2 [Cox-2]) in human colon carcinoma cells (Caco-2) and in rat colonic mucosa. These data could point to a role of oxygen radicals in colon carcinogenesis induced by a chronic infection with S. bovis. The mechanism could be similar to the one suspected for the development of gastric carcinomas after persisting Helicobacter pylori infections. Presently it would still be important to know whether the increased presence of S. bovis in colonic cancers and polyps results from the preferential bacterial colonization of these cancers and their precursors or whether S. bovis represents a carcinogen that is causally involved in colon cancer.

The last sentence summarises the ongoing debate: does the bacterium promote the cancer, or does the cancer promote the bacterial infection?


text:
Are there any bacteria, in our environment, able to break down nitrate under aerobic conditions?
Given a fix volume of water saturated with dissolved oxygen through aeration. Suppose that ammonium, Nitrosomonas, and Nitrobacter are always available in the water. We know that some of the ammonium will eventually be oxidized, by the bacteria, to nitrate. We also know that under anaerobic condition, some of the nitrate, through many steps, will be broken down into Nitrogen by denitrifying bacteria.
Question: Are there any bacteria, in our environment, able to break down nitrate under aerobic conditions? If there aren't, will the nitrate continue to accumulate?

My initial reaction upon reading this question was to think that the answer was: no, denitrification is a process in which nitrate is used in the absence of oxygen as an alternative electron acceptor. However I decided to check the literature, and I have discovered that there is, in fact, a lot of new evidence that many bacterial species may be able to use both of these electron acceptors simultaneously. This article is a good place to start if you want to find out more:

Chen & Strous (2013) Denitrification and aerobic respiration, hybrid electron transport chains and co-evolution. BBA Bioenergetics 1827: 136-144

This is a review which summarises the area from the point of view of bioenergetics, but most importantly for this question, includes a Table summarising the experimental evidence for the phenomenon.  Referring to this Table, they state:

It appears that in most cases, the evidence presented is not sufficient to support the conclusion that denitrification really proceeded in the presence of excess oxygen. It should be noted that the aerobic denitrification rates were much lower than the anaerobic denitrification rates measured for the same strain while aerobic respiration rates remain high. This implies that the major electron flow in the respiratory chain is towards complex IV rather than the NOx reductases, and that aerobic respiration is still the preferred pathway for growth. Apparently aerobic denitrification can be an auxiliary pathway next to aerobic respiration.

The last sentence answers the OP question.


text:
How is consciousness linked to the brain?
Could the brain be working without consciousness? Does the brain interact with consciousness? Alternately, is it that consciousness can't really control the brain, and you only have the impression that you make the decisions, but your brain does.
If the answer to the last question is yes, it is impossible to know if someone else has a consciousness? Even if he doesn't, he'll say he does, because the brain thinks he does.
We can't be made only from matter. If we would, we'd be a mix of chemicals interacting with each other. What makes us be aware of our feelings, what we think, and our 5 senses?
When and how is consciousnesses created?

Unfortunately, although this is a very well researched area in neuroscience, I think we do not know the answer yet. Anyway good question! I would slightly edit it, however, to make it a bit more "biological" and a bit less phylosophical

Note that consciousness and mechanicism are not mutually exclusives. We, at the same time, can be both conscious and mere chemicals. Because this question lie at the limit between philosopy and biology I suggest you to search at http://philosophy.stackexchange.com/, for example here and here. Good question, though.

"A mix of chemicals interacting with each other" is a great way to describe organisms.

@Someone Great question. One point I'd make though is that 'We can't be made only from matter' is a statement that makes assumptions about the nature of matter. Matter is not like Lego. From what I remember from my uni physics courses, matter is actually pretty weird... i.e. non-intuitive. At least on the smallest scales.

A non-subjective definition of consciousness is needed first . I would go with "a created system that decides pro-activity and is given freedom to think for itself "


text:
Can Naegleria fowleri enter through wounds into the bloodstream?
All the sources I've read said that Naegleria fowleri enters the brain through the nose. But lets say that someone had cuts on their arm or leg and they are swimming in water that is conducive to Naegleria fowleri growth. Could it enter the cut into the bloodstream and then into the brain or cause some other type of damage if it enters the bloodstream?

No, Naegleria fowleri is a free-living excavate form of protist that lives in warm fresh water. Fowleri finds its way into the brain by eating through the olfactory neurons in the nose where it multiplies itself greatly by feeding on nerve tissue.
Once it penetrates the nervous tissue, fowleri's feeding  results in significant necrosis of and hemorrhaging in the olfactory bulbs. The protist then climbs along nerve fibers through the floor of the cranium via the cribriform plate and into the brain.
Since the protist travels by feeding on nervous tissue, fowleri could not enter the brain via bloodstream.
Just some more facts about Naegleria:

Death usually occurs within 14 days of exposure due to destruction the autonomic nerve cells of the medulla oblongata.
Luckily for everyone this disease is rare. There were only 300 cases as of 2008

Maybe the blood-brain barrier would also deter the fowleri from entering the brain. Could the fowleri thrive in the bloodstream?

I know antibiotics would not help. But that is never a concern since it is rarely (if not ever) identified in time to save a life.


text:
Systematic difference of diversity between sister taxa?
When looking broadly at the tree of life, my feeling is that, after a divergence there is almost systematically one taxon that speciates way more than the other.
(There will have some approximations below it is not really the point of my question to discuss whether the urochordata is a sister group to the vertebrates or not.) Let's look at the kingdom Animalia for example:

Chaonflagellata vs "the others"
Sponges vs "the others"
Cnidaire and cténaire vs "the others"
Protostomia vs Deuterostomia (both are fairly equally diverse diverse! Some might not be happy with this claim!)...let's continue with the Deuterostomata
echinodermata vs chordata
cephalocordata vs vertebrata

etc ...
My questions:

Is there really a systematic difference in diversity between the branches?
Is this difference can be explained by chance?
Is it only a bias due to out ability to recognize more species in animals that look more like us (or a bias due to something else)?
Does it make sense to say: the more diverse is a taxon, the more likely it is that it gets even more diverse (because each species might have an equal chance to speciate or something like this)?

Neat question. I'm tempted to assume that this must be related to where we recognize splits as being? I.e. its an artefact of our typology, rather than a property of the external world. It bears thinking about, though! You might use "key trait" or "key innovation" as a search term (I think I remember Galis gives a good introduction)

Bond and Oppell address your question points one, two and three empirically by looking for what they call "unbalanced bifurcations" as a sign of adaptive radiations in a well-resolved phylogenetic tree (spiders), and find that the number of unbalanced bifurcations does indeed exceed what they would expect to occur by chance.
As you mention and as I suggested in the comment, there are some serious problems that arise in trying to answer your question. Many of these are well presented in Cracraft, including assuming that higher taxa are comparable with one another, making arbitrary choices about what rank of taxa to compare, ignoring counterexamples, and qualifying rather than quantifying diversity. I think that Bond and Oppell effectively address most of these problems through rigorous, apriori definitions.
There's a diversity of opinions and evidence from biological systems on your fourth question point. Bond and Oppell connect these significantly unbalanced bifurcations to key traits (like orb-weaving) that open up new adaptive zones. I suppose therefore they might say that there's a fundamental factor (a key trait, and therefore open adaptive zones) driving diversification, and therefore might not agree with you that diversification would necessarily beget more diversification (at least, not in the absence of open adaptive zones). For instance, in Hawaiian tetragnathid spiders, ecomorph niches on an island are filled either through immigration from another island or through adaptive diversification (Gillespie). No ecomorph is represented by two sympatric species, so a niche filled by immigration will presumably not spur adaptive radiation. However, species radiations in Andean lupines (Hughes and Eastwood) and plethodontid salamanders (Kozak et al) seem not to have been accompanied by any key traits or particular ecological opportunity, and could theoretically be driven by the self-reinforcing mechanism you propose. As a related point, I suppose more diverse lineages could be less likely to go extinct; which could support diverse lineages becoming more diverse.

 Bond JE, Opell BD. 1998. Testing adaptive radiation and key innovation hypotheses in spiders. Evolution 52: 403–415. (Behind paywall, free pdf here).
 Gillespie R. 2004. Community assembly through adaptive radiation in Hawaiian spiders. Science 303: 356–359. (Behind paywall, free pdf here)
Cracraft J. 1990. Origin of evolutionary novelties: pattern and process at different hierarchical levels. p. 21-44 in Evolutionary Innovations, ed. M. Nitecki, U Chicago Press.
Hughes C, Eastwood R. 2006. Island radiation on a continental scale: exceptional rates of plant diversification after uplift of the Andes.
 Kozak KH, Weisrock DW, Larson A. 2006. Rapid lineage accumulation in a non-adaptive radiation: phylogenetic analysis of diversification rates in eastern North American woodland salamanders (Plethodontidae: Plethodon). Proceedings of the Royal Society B: Biological Sciences 273: 539–546.

Thks a lot for this excellent answer!


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Blood pressure during exercise
What happens to blood pressure when we exercise? Does it increase, decrease, or remain the same? If it does increase, why are patients with high blood pressure recommended to exercise?

As pointed out in the answers above, your blood pressure increases transiently as you exercise because more oxygen and nutrients are consumed by your muscles. However, regular exercise increases your "cardiovascular reserve"-this means your body will be able to function well at lower blood pressures. However, caution must be taken in hypertensive patients whose blood pressures are already up the roof. In these patients, gentle exercise and life style modifications (diet, stopping smoking, weight loss etc) may reduce their blood pressures over time. This will also reduce their risk of cardiovascular catastrophes in the future.
So whilst exercise will reduce blood pressure, it is not recommended as a first line of life style modification in hypertensive patients because exercise itself is stressful initially and stress is also bad for a hypertensive patient. Hence, exercise is good but gentle exercise is recommended for hypertensive patients. But again I doubt gentle exercise will do maximum good to your cardiovascular system because the type of exercise that helps lower your blood pressure is one that makes you sweat (e.g tread mill, etc). But once the blood pressure of a hypertensive patient is under control, then they can safely exercise and this should help lower their blood pressure long term. I hope this makes sense.

Blood pressure increases during exercise as shown in this paper, but the reason that experts recommend exercise for hypertensive patients is that increases in fitness decrease blood pressure (demonstrated nicely in this study of >2000 children, measuring fitness and blood pressure changes over 12 months).
In a way, the doctors aren't saying that exercise itself will decrease blood pressure, more: "increasing fitness will decrease blood pressure, fitness will increase with regular exercise, therefore you should exercise more."
Caution should be used though for taking up new exercise regimes and doctors should be consulted.
There are of course other well documented benefits to regular exercise and personally I find it is great stress relief which could indirectly aid lowering of blood pressure (stress increases blood pressure, mine is 80/50 - very low - and I would describe myself as quite easy going :D).

Increases during exercise, but as we get fitter it decreases. Vessels become more optimal, they grow to supply muscles better, the heart beats less as it becomes more efficient. However this goes beyond that, hypertensive patients are at risk of stroke and heart attacks. Exercise reduces many risk factors: stress, obesity and coronary artery disease and many others. Thus exercise is really helpful.


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Which texts are good for beginners to understand evolution on the genetic scope?
Are there good texts to study the evolution, how it works, and how mutations and changes lead to evolution of the organism ?
And how does the information increase through the long time using mutations and other mechanisms?
Can you recommend specific texts?

what level are you looking for; popular science for the general public, high school level, undergraduate, graduate in graphic design, graduate in evolutionary genetics? you say beginner but beginner at what level?

having looked at your profile I see you are a high school student, I'd suggest heading towards Dawkins' popular science texts first, then Ridley's evolution for some finer detail.

Adding to previous answers. For basic textbooks I've been happy with (earlier editions of):

Evolution, Futuyma
Genetics: From Genes to Genomes, Hartwell et al.

EDIT:
I should also mention the free pdf book Theoretical Evolutionary Genetics by Joe Felsenstein, with latest update from 2013. He uses it for a course in population gentics. So far, I have only browsed it myself. It is fairly math-heavy, but I thought that it could be of general interest.

Books on my shelf right now (I'm an evolutionary genetics grad student)...
Entry level:
Evolution - Mark Ridley (not Matt Ridley)
A primer of ecological genetics - Connor & Hartl
Intermediate:
Elements of evolutionary genetics -  Charlesworth & Charlesworth
Advanced:
Principles of Population genetics - Hartl & Clark
Introduction to quantitative genetics - Falconer & Mackay
Further basic/popular-science books include R Dawkins' Selfish Gene/The Extended Phenotype/The Greatest Show on Earth and of course The Origin of Species by Darwin


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Inverse of dopamine reuptake inhibitor?
The wikipedia article on the dopamine transporter gives examples of some drugs whose effects are mediated by the inhibition of the dopamine transporter, such as cocaine and amphetamines.  Are there any drugs or substances whose mechanism of action involves increasing the activity of the dopamine transporter, i.e., a "DAT releaser?"

It's important to note the difference in mechanism between cocaine and meth. While cocaine blocks reuptake, meth makes VMAT - vesicular monoamine transport - leaky and actually reverses the transportation of dopamine, so that instead of transporting dopamine into the axon terminal, it actually transports dopamine out as it leaks from the vesicle that carry it. This is what is meant when referring to 'reverse transport' of dopamine through DAT. Feel free to read this abstract and the sources it cites (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2631950/).
Regarding the possibility of a DAT agonist of sorts, looks like current research has identified some potential targets. One of which seems to be luteolin and its derivatives (http://www.ncbi.nlm.nih.gov/pubmed/20971650). Current studies find new derivatives and test the EC50 to assess pharmacological efficacy.

Amphetamine isn't a DAT inhibitor. It actually causes exocytosis of dopamine vesicles. That is why cocaine is activity dependent as it's mechanism depends on presynaptic activity whereas amphetamine is activity independent.


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Natural selection and the Galapagos Islands
Woodpeckers found on the South American mainland are able to peck insects from the bark of trees. Would the woodpecker finch have been able to survive if woodpeckers had found their way to the Galapagos Islands where this finch is found?

Dunno, depends on who eats more. Perhaps both would have diversified into different species or one of the two would have gone extinct, or both or whatever. We have no way of knowing what would have happened.

While this is an interesting question, I think it's too hypothetical for the SO format of questions and answers.  Invasive species can and do happen, even without human intervention, but it would be entirely speculative to try and model how a habitat invasion would play out here.


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Why does a blood test show ethanol when no alcohol was consumed?
Why would ethanol show up in a blood test if a person had not been drinking alcohol in many years. What are other reasons for showing ethanol?

There are some situations when ethanol-like compounds can be present in the blood stream:

[...] exposure to hand sanitizers, after shave lotions, perfumes, medications, hygiene products, cosmetics, foods [...]  Uncontrolled diabetes mellitus can cause false positive alcohol tests.

Source: Dr. Kokil Mathur. Answer on: False-Positives for blood alcohol content. Available from MedHelp forums.
Other causes as pointed on eHow.com:

low calorie diets
gasoline, paints, lacquers
lower hematocrit values
diabetes mellitus

Thank you Dr. Kohl for your answer, but none of the above seems to apply. I was in the Hospital Emergency with H.Pylori, Gastritis, Duodenal inflammation. It showed WBC of 15.4 and Ketones 15. I'm not a diabetic

Convincing answer was given
In Syrups or injections Drugs to dissolve the active ingredients use different types of alcohol use or alcohol is also used in some Toothpaste that maybe cause +alcohol test


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What is the reason for fear induced defecation?
I started to handle mice for my job and noticed that they tend to defecate and/or urinate when they are scared. The fear is induced by me, because I need a long time (due to inexperience) to grab the mice and then move them from one cage to a new one. My question is why?
I tried to look up literature for this behavior and there are different fear behaviors for different animals some shake in fear, some play dead but I could not find something for fear induced defecation. Therefore my question: What is the reason behind the "Fear induced defecation"?
I am especially interested into the neuroscience pathway behind it.

Just a guess - but this could be a mechanism to try to deter their attacker, the smell of urine and faeces may ruin the meal

Just to share, if I'm nervous or am afraid, I feel like saying Hello to the bathroom.

Even if you're a pro, handling certain strains of mice for any length of time will cause them to void. It's not just you :)

If your mice are stressed or scared during those manipulations, as we can expect them to be, defecation can be a consequence of the "Fight-or-Flight response": in this situation, the organism try to focus its energy to act quickly, and a wave of specific neurotransmitters (noradrenaline in particular) is released. In consequence, mice's bladders relaxe, which cause them to urinate, the digestion stops, but the transit of the faeces in the colon is accelerated: they defecate.
This is all controlled by the activity of the sympathetic nervous system, which secrets acethylcholine and noradrenaline.


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How does horse extract the energy to needs from a relatively small digestive system?
Recently I saw Inside nature's gaints episode on horse, and was fascinated about its internal organisation. And my question is that they have a very large lungs to accommodate, but a relatively smaller stomach. But other herbivores like the hippopotamus have a very large digestive system even though they need less energy than horse. How does horse manage this problem? How do they get that much of energy even though it had small digestive system and more over it is an herbivore?

Horses (and rhinoceri) are hindgut fermenters unlike cows which are foregut (stomach) fermenters. I don't know about hippos, but the hindgut fermentation in horses allows it to eat more frequently.

So, the horses eat a lot frequently.

The digestive system of a horse is by no means small:

They have 15 to 21 m (50 to 70 ft) of small intestine, with a capacity of 38 to 45 L.
They have a 1.2 m (4 ft) long caecum that holds 26 to 30 L.
They have 3.0 to 3.7 m (10 to 12 ft) of colon, capacity up to 76 L.
(Figures sourced from Equine Anatomy (Wikipedia))

Certainly horse stomachs are comparatively small as they are hindgut fermenters, but that is not where most energy and nutrients are absorbed. Some food passes from the stomach to the small intestines before it is fully digested, which enables more continuous eating to keep up with their energy and nutrition requirements. Most proteins, carbohydrates, and fats are absorbed in the horse's small intestine. Some nutrients are absorbed in the large intestine as well, see Is there nutrient absorption in the large intestine of hindgut fermenters?.
The hippopotamus is a pseudoruminant, having a 3 chambered stomach (unlike the 4 chambers of a cow). Hippos are therefore considered to be foregut fermenters, and are not comparable to horses. In terms its digestive tract, the hippo is much more similar to a cow than a horse.


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Effect of interruption of photoperiod in a short day plant
When a short day plant is exposed to its critical period of darkness it flowers. But when it is exposed to a small period of red light which exceeds the critical period it doesn't flower.
But when it is exposed to small and equal amounts of red light and far red light it flowers even though it exceeds the critical period of light.
How is this possible?

can you add the source of this info? more importantly, is it homework?

I read it in a magazine

which plant species?

It is not mentioned in it...


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What are the odds of being an albino human and have Down syndrome?
I know the odds of a human to be an albino. In Europe and the US it is 1 in 20,000 people (source) and for Down syndrome it is 1 in 1,250 (source). So that means the chance of giving birth to a child that has both albino and Down syndrome is:
$20,000 \times 1,250 = 25,000,000$
i.e., 1 in 25,000,000 correct?

Probability of independent events
Assuming the albinism and Down syndrome are independent traits, then the probability of having both traits is the product of the probability of having each trait.
For more information see wiki > probability (especially the section on independent events).
Albinism and Down Syndrome
If (and only if) albinism and Down syndrome are independent events (see below), then the probability fo having Down Syndrome is $\frac{1}{20,000}$ and the probability of having albinism is $\frac{1}{1,250}$, therefore the probability of having both is $\frac{1}{20,000} \frac{1}{1,250} = \frac{1}{20,000 \cdot 1,250} = \frac{1}{2.5\cdot 10^{7}} = 2.5\cdot 10^{-7}$.
So, yes you were correct! Good job!
Validity of the assumption of independence
I want to highlight again the importance of the assumption that albinism and Down syndrome are independent traits. If a person with Down Syndrome has a different probability of being albino then a person that does not have Down Syndrome, then the probability of having both traits will NOT be the product of the probability of having each trait. The only way to know whether these traits are independent is to look at empirical data. I failed to find any evidence of such correlation (but I might have missed it). If this is a homework question, you should be fine just stating Assuming the two traits are independent,... at the beginning of your answer.

Thank you very much for your great answer. Do you know if there was ever a human that was born this way?

It is correct if (and only if) albinism and Down syndrome are independent events, that is, if albino people is not more nor less likely to have Down syndrome than non albino people (and vice-versa).
However, doing a quick Google search I can't find any source relating albinism and Down syndrome, and therefore independence seems a reasonable assumption unless more information arises and your numbers are right - at least, as right as the sources you are based in.
But beware that your sources are not very representative of what you want to get, or at least not very consistent:

Your source for albinism (and its reference) gives prevalence, that is, number of albino people in the whole population of living people in Europe and USA. Please notice that proportion in living population may differ from proportion of births since albino people may have a different life expectancy.
Your source for Down syndrome gives a "baseline probability" for a given mother age (young) in some unspecified country. For older ages, probability becames larger.

Then, "the chance of giving birth to a child that has both albino and down syndrome" may differ from that you calculated, specially if you want to use it in circumstances that differ from those your data came from.
Anyway, if you just want a rough estimate, you can use your numbers.

This answer is fascianting. Thank you very much. Do you know any case where a human was born this way?

I'm sorry but I'm not expert in albinism nor Down syndrome - my answer is mostly from statistics. Anyway, according to your numbers we could expect just a few hundred people in the Earth with both, so it's not very likely such cases having been reported.

do you think there are around 100 people or 0 on earth?

Using your rough approximation, 1 out of 25,000,000 means 280 out of 7,000,000,000. Therefore, if albinism and Down syndrome are actually independent and your sources are representative enough, we could expect a few hundred people on Earth with both. 100 seems more likely than 0.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Hybrid vs introgression zone in natural populations
In the book An Introduction to Molecular Ecology, the authors say that

Introgression is the diffusion of alleles from one population or
  species into another as a result of interbreeding or hybridization
  between them.

And that hybridization is (roughly) the breeding of two distinct species.
I thought that when we were talking about introgression zone and hybrid zone, it was the same thing.

But here is my interpretation:
See the image below. Across an area, you would have 2 populations of 2 species (A-E). They could interbreed in the middle, this would be called the hybrid zone (in C). But the change of allele (or the transfer of allele) between two populations is not only done by hybridization (B vs C). It can be done by a new hybrid breeding with a non hybrid (backcross, in B). Then, B to D would be the introgression zone.
I don't really know what would happen in that case when 2 hybrids breed together for the colours!
So my question is: What is the difference between introgression zone and hybrid zone (is my interpretation correct?)?

I think you're correct. See Harrison, R.G. and E.L. Larson. 2014. Hybridization, introgression, and the nature of species. J. Hered. 105: 795–809. Also see https://www.differencebetween.com/difference-between-hybridization-and-vs-introgression/
Interesting that you're received no responses to this. It's an interesting (and I think important) question.


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What does the "*" in haplogroup I2A1* mean?
I have been told that the "asterisk" in the Haplogroup 12A1* means it doesn't move down stream? What exactly does that mean in layman's terms?

From the 23andMe website:

Sometimes there are a few lineages that don't fit into any subgroup of a haplogroup. Since there isn't a mutation that links these lineages, they don't get their own subgroup. Instead, these lineages are given the main haplogroup label plus a star (*) to indicate that they are part of the main haplogroup but don't fit into any of the known subgroups

So there are defined subgroups for I2A1 (I2A1A and I2A1B) for which more information is available, but you dont fit into any of them.
What "doesn't move down stream" means, I have no idea.


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Dinuclei cellular mechanism
I am no biologist, but I have this question buzzing in my mind. It's a matter of curiosity
What happens when two nuclei occupy the same cell? Would we expect the embryo (if it lives) to have complex cells (assuming the nuclei are from different species, i.e., genetically incompatible with each other)?

It depends on the kind of organism.
When the cell with two nuclei will try to go through mitosis, the nuclear membranes will fragment, releasing all genetic material to the cytoplasm, where it will behave normally, as if it came from only one nucleus. The DNA will divide and move into two daughter cells, each of which will assemble its one nucleus from the membrane fragmnets. However, each daughter nucleus will have double the normal number of chromosomes - one whole set from each of the old nuclei.
(In fact, this is what happens in humans after fertilization - the male and female pronuclei never merge, they just copy their DNA and divide it simultaneously into two daughter cells. The pronuclei are haploid, so the resulting daughter cells are diploid.)
What happens later, to the tetraploidic cells from your question, when they try to develop into a full organism, may end better or worse.
For exapmple many plants will just grow normally, only form bigger plants (modern wheat is such an example - it may be tetra- or even hexaploidic, meaning it has up to 6 sets of chromosomes).
For animals this is usually fatal, but some, like the xenopus, seem to be unaffected.

the second sentence is very obscure. Due to this, it is absolutely not clear, how you relate binuclearity to polyploidy.

I hope it's better now.


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Beginning of the urogenital system
Are any invertebrate nephridia (proto/meta) homologous with vertebrate kidneys in the sense that embryologically they also begin together with the genital system?  When did the embryologic association between reproduction and osmoregulartion/metabolite elimination begin in terms of evolution?

I dont think invertebrates have urogenital system.

So which one, excretory or reproductive, is homologous to the vertebrate urogenital system... I understand that invertebrate is a polyphyletic category of exclusion, but I'm talking about the closest related animal phyla to vertebrate... I guess I should'look deeper into lancets and hagfish...

The urogenital system as a cohesive functional unit probably evolved very early in vertebrate history. Hagfishes and lampreys have separate systems for reproduction and excretion. More derived groups of fishes use kidney tubules and ducts for sperm delivery outside the body (Helfman et al. 2009).
The vertebrate nephron may be homologous to the invertebrate nephridia (Ruppert 1994). The genetics underlying the development of vertebrate female reproductive organs shows many homologies with invertebrate reproductive organs (Kobayashi and Behringer 2003)
I would hypothesize that the both the reproductive and extrectory systems of vertebrates show corresponding homologies to invertebrate organ systems (at least genetic and developmental homologies) but evolution of the urogenital organ system did not evolve until the early vertebrates.
Literature Cited
Helfman, G.S. et al. 2009. The Diversity of Fishes. Biology, Evolution and Ecology. Wiley-Blackwell, Oxford, UK.
Kobayashi, A. ad R.R. Behringer. 2003. Developmental genetics of the female reproductive tract in mammals. Nature Reviews Genetics 4: 969-980.
Ruppert, E.E. 1994. Evolutionary origin of the vertebrate nephron. American Zoologist 34: 542-553.

authors: Костя Дряхлов


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How many consecutive cell divisions are required to form the adult human body from the single cell zygote?
The preferred question would have been what is the total number of cells in a full term human foetus and how many cell divisions are required to reach that number. However estimates of total cell numbers in foetus could not be found. From the abstract of the July 5, 2013 article published in Annals of Human Biology, the adult human body consists of approximately $3.72 \times 10^{13}$ cells (37.2 Trillion). The question is: what would be the approximate number of cell divisions required to reach that number (Ignoring the fact that different tissues may reach full differentiation at different times)?

Sounds like just a math problem if you allow that cells dying and different rates of division are not to be accounted for:
$2^N = 40 \times 10^{12}$
$log_2(40 \times 10^{12}) = N$
$N = 45.185$
so 45 or so divisions.
is that what you are looking for?

I think you want 40T, not 4T.

@ shigeta - Isn't 45 pretty close to the 'Hayflick limit'?

@RamManoharM Supposedly it's between 40-60, so yeah.  But if that means anything...

@ Amory - By the time you are 20 (young adult) your have near exhausted the capabilty for cell division (broadly speaking). Just wondering if the loss of Telomere has more important role during development other than merely ushering in senescence.

The Hayflick limit is entirely unrelated to this issue as the foetus develops firstly from embryonic totipotent stem cells, then pluripotent stem cells, and even in the adult body there are still multipotent stem cells, some of which are capable of indefinite replication.

that still leads me to the question of how does a whale get so big?  are the cells larger or how does a very large organism obey the hayflick limit? is it multipotent cells reasserting themselves to regenerate the tissue?

@shigeta I'm not sure what the answer is for whales specifically, but different species can have different telomere lengths. In fact, different people can be born with different telomere lengths. The Hayflick limit of 40-60 divisions is a statement about homo sapien cells.


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Is there a realtime molecular clock within the genome to co-ordinate the developmental sequences in an embryo?
It is difficult to assume that the massive number of co-ordinated developmental sequences in a developing embryo is controlled by molecular signalling alone. Is anyone aware of a molecular or developmental clock within the genome which control the on off states of the genes concerned with developmental sequences? If it has not been reported is it likely to exist? (This is not about the molecular clock in evolution.)
Assuming there is a molecular clock, is it possible that the clock is switched on at the time of fertilization, and the zygote transfers the elapsed time to the progressive generations of the cells?

You think it is difficult to believe that development is only timed by molecular events, but you are asking whether there is a molecular clock? Seems a bit contradicting... Anyway it has been shown that disruption of clock genes leads to developmental defects: for instance (these are just two random papers I found, but there is surely more) http://www.ncbi.nlm.nih.gov/pubmed/22884368 http://www.ncbi.nlm.nih.gov/pubmed/17963275

Thanks for the comments Nico, I did not say events, i said molecular signalling and molecular clock. by molecular clock I meant something like a run time clock or a timer for that matter for referance.The circardian rhythm is too slow for temporal refernce control of the fast paced developmental process in an embryo.

Ok, now I understand what you mean. In general when speaking about "molecular clock" one refers to a set of genes and their derived proteins that govern circadian rhythms and that indeed act as a "24h timer". See also my explanation here: http://biology.stackexchange.com/questions/2299/how-is-human-biological-clock-modelled-in-modern-science/2856#2856 . Now, although these genes are involved in circadian (~24h) rhythms, they possibly also have a role in shorter (<24h, ultradian) and longer (>24h infradian) rhythms, although this is still very much an unresolved question.

I think that the "molecular clock" that you refer to and the "molecular signaling" that you are skeptical of are one and the same thing.
In the 1960s, nuclear transplant experiments established that molecular signals in the cytoplasm can dedifferentiate terminally differentiated nuclei, "resetting" your molecular clock, or in the more common terminology "rerunning" the "developmental program" to yield viable animals.
This "developmental program" metaphor has been frequently used to describe this process, seeing development as a series of gene regulatory cascades; they called it a program because they were thinking of procedural computer programs. It isn't really a clock so much as a complex process by which different sets of genes are turned on and off in a concerted fashion, where one step depends on what happens in the previous step. An undergrad course discussing some of the mechanisms of this is posted here.
We've known for many decades that interrupting cellular processes such as transcription, translation, and DNA replication tend to arrest development at different points (for one early example see here).
A good example of a step/series of steps in the developmental program is the maternal-to-zygotic transition in metazoans, where embryos transition from using maternally deposited mRNAs as molecular raw material to de novo transcription of their own mRNAs.
From the linked review:

As development proceeds, two processes are triggered that together form the maternal-to-zygotic transition (MZT): first, a subset of the maternal mRNAs is eliminated; second, the transcription of the zygotic genome begins. Initially, the destruction of maternal mRNAs is accomplished by maternally encoded products. However, zygotic transcription leads to the production of proteins and microRNAs (miRNAs) that provide feedback to enhance the efficiency of maternal mRNA degradation. In addition, among the earliest mRNAs synthesized de novo in the embryo are transcriptional activators that enhance the efficiency of zygotic transcription. The net result is that the control of development is transferred from the maternal to the zygotic genome.

Figure 1. A comparative overview of the maternal-to-zygotic transition (MZT) in several model organisms. Key embryonic stages for each model organism are depicted schematically above the corresponding cleavage cycle and time after fertilization. The red curves represent the degradation profiles of destabilized maternal transcripts in each species. The light and dark blue curves illustrate the minor and major waves, respectively, of zygotic genome activation. The last embryonic stage presented for each organism is the developmental point at which there is a major requirement for zygotic transcripts.

This transition requires that the developmental steps based on maternally-deposited mRNAs have completed successfully before de novo transcription of embryonic RNAs can begin.