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What is the structure and function of chromosomes during interphase?
Ok, it seems to be easy but I have probably ignored something by accident.
Interphase is the phase where things are growing and the preparation for cell division happens. Its stages G1, S and G2. DNA replication in S stage. So the DNA in some chromosomes must have the pieces of information about how to do the DNA replication. - I am not sure  about thing.
I would say to the part: structure that chromosomes are diploid at the given stage. - It does not feel right anyway.
What would you answer to the main question?

So the DNA in some chromosomes must have the pieces of information about how to do the DNA replication. - I am not sure about thing.

Genomes contain what is called the "origin of replication" - specific sequences in the DNA that tell DNA polymerase where to bind and to initiate replication.
As for your main question, I'm a little confused as to what you're asking. In a general sense, chromosomes function as carriers of genetic information. In eukaryotes, nuclear DNA is organized in the nucleus on linear chromosomes which carry most of the genetic information an organism needs to survive. In bacteria, the chromosome is a circular piece of DNA. In eukaryotes, the chromosome is also bound by histone proteins, which serves to regulate expression of certain genes and to help anchor the chromosomes to the inner nuclear membrane.


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Sitting much, thrombosis and hypoxia
I am thinking the more reasons why sitting much lead to thrombosis i.e. clotting of blood in blood vessels and then hypoxia in the deep tissues eventually.
What are the physiological mechanisms for this to happen?
One student said hormones.
It can be right, but I am thinking how.

Venous return from the limbs is largely facilitated by the action of neighbouring skeletal muscles compressing the veins and forcing the blood proximally past the valves which prevent back flow.  If you are inactive for a long time by sitting, or are sitting in such a way as to impede blood returning from your calves (i.e. with the back of your knees pressing into the edge of the chair) blood movement in this manner is greatly slowed.
Blood that is moving more slowly or turbulently has a greater propensity to coagulate and form a thrombus.  This is similar to the rationale for prescribing anti coagulants to patients with atrial fibrillation - the turbulent and slow movement of blood through their atria leaves them at greater risk of throwing a clot to the brain causing a cerebrovascular accident.
Hypoxia isn't really that relevant in the case you describe as arterial supply is unaffected (much higher pressure) meaning tissues do not become ischaemic. There is also collateral venous drainage from the limb although this can subsequently cause problems in the form of post thrombotic syndrome.  The most significant risk would be that of the thrombus breaking off and lodging in the lungs - a pulmonary embolism.

I think the oxygen supply is deprived in some tissues too. So therefore I think some local hypoxia can occur.

@Masi one hypothesis for the original formation of the VTE is that venous stasis causes the haemoglobin in the static blood to desaturate resulting in hypoxic insult to the vein endothelium that then triggers the coagulation cascade. However, there isn't much of an evidence base behind this and it would be a cause of VTE rather than a consequence.

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Does H. pylori have paracellular activity?
I know that it has transcellular activity i.e. it can pass through neighbouring cells.
However, I am not completely sure if it does not have paracellular activity, see this:

H. pylori did not induce any modification of the paracellular pathway
  (R = 148 ± 10 versus 174 ± 16 Ω · cm2; JNa = 4.16 ± 0.44 versus 3.51 ±
  0.41 μEq/h · cm2; JMan = 0.081 ± 0.01 versus 0.058 ± 0.009 μmol/h · cm2), nor did it modify J3H-HRP (2,201 ± 255 versus 2,110 ± 210 ng/h ·
  cm2 for H. pylori-infected and control cells, respectively). However,
  in the presence of H. pylori, we observed a significant increase in
  JHRPi (520 ± 146 versus 171 ± 88 ng/h · cm2). This effect was not
  dependent of the cag status of the strain and was not reproduced by
  the sonicates or the culture supernatants.

Is there any evidence that Helicobacter pylori has paracellular activity?

I found no evidence for paracellular movement.
Some notes of mine

Mucinase $\to$ lophotrichous flagella $\to$ Transcellular (actin fibrils, tails) movement
ICF Vacuolating cytotoxin (VacA) $\to$ altered T-cell function $\to$
  damages epithelial cells, disrupts tight junctions and causes
  apoptosis.

I think the latter point makes transcellular momevment possible.
I see no way how paracellular movement would be possible.

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How does a fungus protect itself from digestion by other fungi?
If a fungus releases its digestive enzymes outside its body, how does it protect itself from digestion? How do fungi growing nearby protect themselves?
I have tried searching this on google but couldn't get an answer.

Which fungi secret proteases?

usually they do not, but rather ingest via clathrin coated pits I think.  then the proteases are found in a compartment called the proteome.

I think you mean the proteasome.

You would also be interested in fungal autolysis or self digestion. Please refer to the paper "The autolysis of industrial filamentous fungi." PMID: 11958333

In general fungal cell walls are resistant to whatever enzymes or compounds they are excreting to break material down for consumption. Conceptually, it is a little like your stomach lining being resistant to stomach acid. For a more detailed answer you may have to head over to your local university and find a Mycologist.
There is ongoing research on how fungi actually "eat." You can look up fungal endocytosis if you wish to research it more. There may be other mechanisms as Shigeta mentions.


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How effective are restriction enzymes in protecting bacteria?
Bacteria use restriction enzymes to cut DNA of bacteriophages. Virus mutates really fast. Won't a point mutation in restriction site render the restriction enzymes of the bacteria useless ?
So how effective are restriction enzymes in protecting bacteria ?

Note that a given bacterium will probably have more than one restriction enzyme, so the viral genome probably won't ever run out of targets. Even if it did, restriction enzymes could suffer mutations that may change the specificity. When you talk about microorganisms, it's more accurate to think in populations rather than individuals, since the colony would be able to grow again if they have at least one cell. Viruses need a certain density to spread, so even if the bacteria cannot defend against, it may be able to survive simply because the virus run out of hosts before some cells can be infected. This is even easier if the bacteria have some kind of resistance form.
Moreover, restriction-modification systems aren't the only defense line against viruses. Many bacteria have a system called CRISPR-CAS that acts like an immune system, inserting RNA fragments into the bacterial chromosome and using them as "antibodies" by hybridization. In this context, you can assume that restriction-modification systems, alongside other nucleases they usually carry, act as an innate immune system, while the CRISPR-CAS would be an analog to acquired immunity.

Diagram of the CRISPR-CAS system. Source.
Furthermore, not every environment has the same viral density. Some habitats may be protected against viruses by some means, like the gut microbiota (the carbon intake goes through the stomach acid and tons of hydrolases, which is very destructive for viruses); while some others may have an incredible amount due to lack of biodiversity and high cell densities (this is the case of most extreme environments). E. coli, as a gut bacteria, would probably have enough with only restriction-modification enzymes (In fact, while it have a CRISPR system, it seems to be repressed), while many others will need more defenses.

@ Miguel Angel Naranjo Oritz Awesome answer !! CRISPR-CAS system-very interesting !


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Are wasps attracted to UV light emissions?
I remember seeing a documentary where it was shown that bees and wasps are attracted to UV components of a flower colour (please correct me if I am wrong).
Does this mean that they could be attracted by neon lights (that I suspect are emitting also in the UV part of the spectrum)?
I am asking because I have neon lights in my office and if I have the lights on I can't open the window, or a wasp will almost immediately enter the office. I've experimented a bit, and turning off the light makes the wasp go out rather quickly, hence my hypothesis.
I am located in Europe, if that makes a difference for the species involved. Outside the window we have some tall trees, so we keep some lights on even when the sun is out.

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Why Pan_troglodytes-2.1.3 Assembly renamed as a Pre in ENSEMBL?
I began working with panTro3 assembly of the UCSC. This assembly corresponds to CGSC Build 2.1.3. See here: https://genome.ucsc.edu/FAQ/FAQreleases.html
Now, I have to cross annotations with ENSEMBL (Indeed, I need to use Biomart tool: http://www.ensembl.org/biomart/martview/2e4aac505f5cf5e0ac255b4a215a056c). But It seems that between Release 64 and 65 they passed directly from Chimp 2.1 to Chimp 2.1.4. I researched some information and found that Chimp 2.1.3 renamed as a Pre! See here: http://pre.ensembl.org/Pan_troglodytes/Info/Index and here http://www.ensembl.info/blog/2011/06/10/new-pre-site-for-chimpanzee/
Is it a way to solve this problem? How may I use Chimp 2.1.3 assembly in Biomart with GrCh37 as reference genome (I was using an archived versions of the Ensembl: http://grch37.ensembl.org/biomart/martview/cbe191dccbe8e5a314cfebeaa8862ca0), but seems not possible to cross between different releases of the ENSEMBL.

Not that Bioinformatics is off-topic here, but you might get better answers over at Biostars, as they are dedicated to bioinformatics. There are not so many around here.

There may be other ways. Please [edit] your question and explain what you're actually trying to do. What do you mean by "cross annotations"? Do you want to find homologous genes? Syntenic regions? If you tell us what you need, we might be able to help without BioMart.

@Chris, is bioinformatics off-topic? Or do you mean programming/software related problems? I couldn't see anything about this in the help pages.

@ddiez That's what I am saying, bioinfiormatics is not off-topic. But still you might get better answer at biostars. Just for complementation.

@Chris sorry! I read "note that bioinformatics is off-topic here". My brain decided to complete "Not" to "Note"!


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What are these white areas of coronary thrombosis?
Please, see the picture where the areas (1,2,3) look little yellow:

I think these areas are fat, platelets and/or air.
I think 3 is fat/platelets while 1 is air/platelets.
There also exists white thrombosis, which can explain something here.
However, I do not it is that because those white areas do not contain thrombocytes or leucocytes (not sure, since I have no more closer picture; probably you can see it from this).
I think at the moment that these white areas are endothelium-lined spaces.
However, I am not sure about (3).
What can these three areas be in the coronary thrombosis?

Low density lipoproteins can be taken up by the macrophages under a number of circumstances (typically high circulating levels is the most important). These macrophages are called foam cells. The macrophage can then die and deposit this cholesterol and fatty material onto a vessel wall in the context of atherosclerosis. Additionally tissue damage as a result of release of damaging chemicals from the macrophage can induce an inflammatory response recruiting more macrophages (worsening the problem in a cyclical manner) and result in fibrosis and platelet activation. I think this would cause the white stuff you point to.
In summary I think you're right, it's a combination of fat, cholesterol, fibrotic tissue and platelets. 3 is more likely macrophages and platelets whilst 1 and 2 are more likely a combination of all the above.

Thank you for your answer! I completely missed the term "foam cells".


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Which inflammatory response with Cytomegalovirus infection?
I am thinking about inflammation process with Cytomegalovirus infection.
I first thought it is about chronic inflammation, but then changed my mind because of virus infection.
I think cytokines must be there in activation.
I am thinking which of these is right mechanism for both of these

mononuclear cells and granulocytes (I think this must be chronic inflammation)
granulocytes with scar formation (I think no scar)
cytopathic cytoproliferation inflammation

I think the cytopathic cytoproliferation inflammation is the right one because cytokines are activating the inflammatory response in virus infection.
However, I am not sure if this inflammation is of chronic type.
Which type of inflammation can cytomegalovirus infection lead to?

According to this paper the virus triggers the innate immune system and induces inflammatory cytokines as well as interferon stimulated genes (which is a response to a viral infection).
It seems to be recognized by the cells via the Toll-like receptor 2 and CD14, which subsequently trigger the cytokine production. A schematic view comes from the second paper:

These two articles are interesting in this context, the first addresses CMV in special,
the second is a pretty recent review about how viruses are recognized and how cytokines are involved:

Human cytomegalovirus activates inflammatory cytokine responses via
CD14 and Toll-like receptor 2.
Learning from the messengers: innate sensing of viruses and cytokine
regulation of immunity - clues for treatments and vaccines.


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What are the purposes of granulocytes in acute inflammation?
I heard the phrase

Neutrophilic leucocytes are kings in the acute inflammation.

Neutrophils are granulocytes, while leucocytes are not granulocytes.
I think this statement refers to the fact that leucocytes have neutrophilic properties, instead of being neutrophils itself.
Acute inflammation players are, I think
Granulocytes, monocytes and leucocytes

while in chronic inflammation similar player but the main factor is macrophages so the phrase which I heard

Macrophages are the kings of chronic inflammation.

I think granulocytes are related to the Healing and Proliferation.
Eosinophils for instance in the allergic responses of acute inflammation.
I think granulocytes are phagocytosed by the macrophages and this way spread their functions through macrophages around.
Probably, neutrophiles are attached to the leucocytes such that they spread their function through leucocytes (so called neutrophilic leucocytes).
Let's cover first this, since we can after understanding it go to the chronic one.
What is the purposes of granulocytes in acute inflammation?

Have you read the WP article on neutrophilic granulocytes, the most abundant form? Essentially, they are the first infiltrating cells to arrive at the site of injury at the beginning of acute inflammation (bacterial infection, environmental exposure, etc.).

How are neutrophilic granulocytes related to neutrophilic leucocytes?

As far as I know they are the same thing. Neutrophilic granulocytes is another term (usually) for neutrophils. All granulocytes (white blood cells with granules in the cytoplasm) are leukocytes (or leucocytes), which literally means "white cells." Another term is polymorphonuclear leukocyte, which refers to neutrophils' unusual nucleus, generally having 2-5 lobes or sections.

MattDMo's answer

Essentially, [neutrophilic granulocytes] are the first infiltrating
  cells to arrive at the site of injury at the beginning of acute
  inflammation (bacterial infection, environmental exposure, etc.).

which I agree with.


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Roles of creatine and bilirubin in foetus circulation
I think they are not inputs from maternal placenta.
I think they are the results of foetus metabolism.
However, I do not understand it how and where exactly.
What are the roles of creatine and bilirubin in foetus circulation?

Creatine is an important energy source for body, especially for the muscles, so it is no wonder you can finde it there. I don't think it has a special role besides that. See the Wikipedia article for more information.
For bilirubin this is different, this substance is a breakdown product of the heme metabolism (basically hemoglobine). It is not water soluble and needs to be conjugated to a carrier protein (albumin). In this way it is transported to the liver, where the glucuronyltransferase conjugates it to glucuronic acid. This step makes the bilirubin water soluble and it can be excreted from the body.
Newborns have a higher bilirubin level, since their glucuronyltransferase activity is at about 0.1% of that of adults. This can lead to the typical newborn jaundice. For more details about bilirubin, see here.

Thank you for your clear answer! Creatine for energy, while bilirubin fro hemoglobin, in short.

Yep, thats the short form.


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Can Alzheimer's disease be caused by Slow Prion infection?
I found this claim in my study materials with explanation of amyloi plaques, in comparison to CJD (Creutzfeldt-Jakob Disease).
Its characteristic are

Long doubling time of at least 5.2 days (I think this means the time it takes to double the amount of prions in the target organ)
NO Cypopathic Effect (CPE) in vitro
Long incubation period (about 30 years)
Vacuolation of neurons, amyloid-like plaques
Deficient immunity
Deficient immunoresponse
Deficient Interferen (IFN) production

so this suggests me that the person with infection at a young age can have the disease then at an old age.
Other possible agent could be virus, but it seems that prion is the major one.
Can Alzheimer's disease be caused primarily by Slow Prion infection?

Dr Yong in the paper titled Prion, The unconventional slow Infectious agent states that the formation of amyloid plaque which is a major contributor to Alzheimer's disease is a unconventionally slow infectious disease (Prion). Some papers have also pointed out the similarities between Alzheimers and prion disorders (reference) Cerebral amyloid plaques have also been identified in scrapie which is caused by a Prion. Discovery of a novel prion disorder (reference) with peripheral symptoms have led researchers to believe that protein misfolding, is the basis for most neuro-degenerative diseases, including Alzheimer's disease and Parkinson's disease.
With regard to your question, Alzheimer's has not been completely classified as a prion disorder as of now, but seeing that amyloid plaque formation (reference) and Creutzfeldt-Jakob disease (CJD) (a form of dementia) (reference) have been identified as being part of Prion disorders, it is highly likely that Alzheimer's is too.

I recall that Alzheimer is linked with demyelination or degeneration of motor neurons, particularly. So the target area can be different in Alzheimer than in Parkinson's disease. Intuatively, the main mechanism can be the same in both diseases but the patient's genetic material i.e. processes creating special environments around neurons in different parts of the brain determine where the degeneration is occurring thus determining which disease. It is also possible that there are different types of virion which cause the difference. But I have intuition that both host and virion are players.


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Evolution of Wheat
In the evolution of wheat, there are two instances of chromosomal doubling, when Emmer wheat Triticum turgidum was formed from Einkorn wheat, and when Triticum aestivum was formed from Emmer wheat.
When allopolyploids are artificially made, chromosome doubling is done by chemicals. Here, it occurred by natural endoreplication. But for the entire plant to turn out with allotetraploidy and allohexaploidy respectively, wouldn't it be necessary for endoreplication to occur just after zygote formed--quickly, so all, or most, cells of the plant would have this genotype?
Isn't the probability of that happening twice in the process of evolution, both times in those incidences when the wheat crossed with the goatgrass species, very low? Is it just coincidence that it happened this way, at the right time, to allow for the allohexaploid species to develop naturally?

But for the entire plant to turn out with allotetraploidy and
  allohexaploidy respectively, wouldn't it be necessary for
  endoreplication to occur just after zygote formed--quickly, so all, or
  most, cells of the plant would have this genotype?

Yes, it should have happened right after the embryo was formed in nature.  But in artificial settings, this can be done after growing the seed to a small seedling then dipping its roots in colchicine for 12-24 hours.

Isn't the probability of that happening twice in the process of
  evolution, both times in those incidences when the wheat crossed with
  the goatgrass species, very low?

Yes, it is very low, but consider the fact that nature never sleeps.  Einkorn existed for millions of years before the Emmer wheat came into existence.  And hexaploid wheat only came line 8000-10000 year ago (about half a million years later).  You don't see these events in nature that frequently.  So it is slow.

Is it just coincidence that it happened this way, at the right time,
  to allow for the allohexaploid species to develop naturally?

Yes, it was part coincidence that it occurred naturally.  Right conditions at the right time.  But really important was the role of early hunter gatherers turned farmers who identified the potential of the new allohexaploid and selected it to grow grains.


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Why do mitochondria fuse together?
Contrary to all of the textbook images of mitochondria that I have seen over the years, I had just learned that the mitochondria within a cell form a dynamic branching network along microtubule scaffolding by fusing with each other.
Why would they need to fuse together?
When they fuse, would this involve only the outer mitochondrial membrane?
Would it not behoove a mitochondrion to remain distinct from others both physically and genetically?

Mitochondria produce a large quantity of reactive oxygen species (ROS) that damage the mitochondrial genetic material. These cell organelles do have a  DNA repair mechanism similar to that of the nucleus to some extent 3 which is not entirely understood however they have multiple copies and so the fusion and fission of mitochondria work together to maintain as many viable/healthy mitochondria as possible.
When two mitochondria fuse, their genetic material can recombine and thus exchange their damaged DNA. In this way, one of them repairs its DNA at the expense of the other accumulating more damaged DNA. Mitochondria that accumulate too much damaged DNA will 'die' - get eliminated, but they can be replaced by fission of healthy ones. Take a look at this wiki page, it has useful info.
Edit: This article may also be useful. (Mitochondrial fusion and division: regulation and role in cell viability
Giovanni BENARD and Mariusz KARBOWSKI, Semin Cell Dev Biol. 2009 May;20(3):365-74.)

Mitochondria are granular or filamentous organelle, which are present in the cytoplasm of a cell. They are ovoid in shape, with the presence of double membranes.
Mitochondrial fusion is required to distribute mitochondrial DNA to the mitochondrial population and to maintain its respiratory competent and energized organelles. Mitochondrial division is required to efficiently distribute organelles to distal parts of cells.

Can you please add some references to your answer?


text:
What is the point at which abiogenesis is complete and evolution begins?
Is the minimum criterion for life a single cell?  It seems that self-replicating RNA is not enough, but I don't know.
What would be the most basic cell that could fit this criterion and what cells today would be most similar?

Even though it is short, this question is really broad. To answer this you need to get into the definition of life (e.g. the line between "protocells" and cells) and minimum definitions of a biological cell. Also note that you can have evolution in the absence of life, see e.g. Evolutionary computation - all that is needed is variation, selection, heritability and reproduction.

I agree with @fileunderwater. Perhaps the following questions may help you to specify this question into something that can be realistically answered: http://biology.stackexchange.com/questions/22008/simplest-biological-organism/22009#22009 and http://biology.stackexchange.com/questions/1663/are-cells-really-the-basic-unit-of-all-life/1666#1666

@AliceD I agree that it should be refined, and parts of the question is probably a close duplicate to the first Q you linked. For the second question, is also unclear whether the comparison should be against the origin of life (~LUCA) or basic cells that can live under current environmental conditions - the external conditions have changed quite a bit.

Related: Can scientists create totally synthetic life?, How did the first self replicating organism come into existence?, and probably others under the [tag:abiogenesis] tag.

Thanks for the comments everyone!  I didn't realize the line was so fuzzy.  I guess I never would have thought of self-replicating RNA as life but it seems that are people that define it that way.

Why is this too broad? - there is a process called abiogenesis and there is a process called evolution.  I assumed the line is clear, perhaps the answer is that's it fuzzy as the answer below discussed and I commented. It could be that the answer is relative based on the definition of "life", but that itself could be the answer.

Yehosef, one problem is that your question is essentialistic/semantic.  The way you've phrased it suggests that there is an inherent importance to the words "abiogenesis" and "evolution", when in science, the words are just tools used to communicate ideas.  There is no fundamental answer because it all depends on how you choose to define those terms.  In science we use operational definitions for things, and the facts are empirical, stemming from measurements.  This question is like saying "what is life", where the answer is "it's a word with a somewhat arbitrary definition", if you follow.

@TrixieWolf - I understand better what the with issues with the question are and how I might phrase it differently to get the answers I'm looking for.  What now?  I could delete the question, but I think the discussion here is valuable because others may have the same question.  I guess I'll leave it and the powers that be can close it or do whatever they want.

@Yehosef You can just leave the question as it is. Since the question has an upvoted answer it cannot be deleted by you, and, as you say, the discussion can useful for later visitors.

I think it's a mistake to assume that there is such a point. All plausible seeming models of abiogenesis currently under consideration involve evolutionary processes long before they reach the stage we'd consider alive.
Evolution will occur whenever there is (a) replication-with-error and (b) selection (simplifying slightly). This is the case with a self-replicating RNA. It is replicating, but those replicates can be imperfect. Imperfections in replication that improve its ability to replicate will be favoured. That's evolution.

thanks for the clarification.   It seems abiogenesis will go from raw elements until self-replicating molecules and then will combine with evolutionary-type processes until there is "life"(which I'm assuming is at least some self-contained cell) at which point abiogenesis is "done".  Is that the right track?

Yeah, that's it. Although even then I'd be wary of assuming that there is a single clear line dividing life from non-life, so the exact end point of abiogenesis will be ill-defined.


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Haidinger's brush: Is this a by-product of the eye's physics, or are there any evolutionary grounds for it?
The human eye is, very subtly, sensitive to the polarization of light. This is  an effect known as Haidinger's brush (see Wikipedia article of this name).
What, if anything, is known or at least intelligently speculated about the evolutionary "grounding" for this effect?
Another way to put this question: Some cephalopods and the mantis shrimp have sight that is sensitive to polarization of light and this sense is clearly begotten by evolutionary forces as it helps these animals detect prey and predators. So, is our subtle ability to perceive polarized light a leftover from a genetic forebear that benefitted from this ability? Or is it simply an artifact of the physics of the eye? The physics of Haidinger's brush is quite different from the topology of retinal cells that confers this ability in cephalopods and others I have read about.
A second question and related is: what is our nearest common genetic forebear that is known to exploit polarization sensitivity of its sight?

According to the link you provided, the phenomenon Haidinger's Brush seems to be associated with the macula of the retina. The yellow color of the macula may explain the yellowness of Haidinger's Brush. This suggests to me that the brush may be an artifact of the structure of the eye, and others have claimed that Haidinger's brushes probably do not have any ecological significance (Greenwood et al. 2003). If the brushes do not have an ecological significance, then they are very unlikely to have any evolutionary significance.
The brushes may be visible to other primates, such as Macaques (Snodderly et al. 1984), as they have a macula structure very similar to the human macula. This leads me to think the phenomenon would also be potentially visible to other primates such as chimps and gorillas. If so, then our nearest ancestor (forebearer) that could potentially see the brushes would be the common ancestor of humans and chimps.
For a broader review of polarized vision and underlying evolutionary hypotheses, the paper you linked to by Cronin et al. (2003) is a good review. I also came across a book, Polarized Light in Animal Vision. Polarization Patterns in Nature. by Gábor Horváth and Deszö Varjú and published by Springer. The front matter and table of contents are available here.  It appears to be a very thorough review of polarization vision in animals.
Literature Cited
Cronin, T.W. et al. 2003. Polarization vision and its role in biological signaling. Integrative and Comparative Biology 43: 549-558.
Greenwood, V.J., et al. 2003. Behaviorial investigation of polarisation sensitivity in the Japanese quail (Coturnix coturnix japonica) and the European starling (Sturnus vulgaris). Journal of Experimental Biology 206: 3201-3210.
Snodderly, D.M., J.D. Auron and F.C. Delori. 1984. The macular pigmnent. II. Spatial distribution in primate retinas. Investigative Ophthalmology and Visual Science 25: 674-685

Many thanks 3Cat for some fantastic material.


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Why aren't all animals cold blooded?
At least, why don't all animals produce no more heat than the tiny amount that's a byproduct of walking or a bonobo climbing up a vine when the outside temperature is above 0°C? They won't freeze anyway.
After all, the amount of food controls the population size at whatever size makes each individual have just enough food, so shouldn't those with a lower energy demand be more likely to get enough food to rear more children? Shouldn't mutations that make a warm blooded animal able to thrive with a lower core temperature and produce less heat be selected for because there's more likely to get enough food to rear more children?
Also, shouldn't cheetahs evolve to produce extremely little heat in the day during rest even on not very hot days so they will be less hot and can chase their prey for longer? Have they already evolved that way?
If a species did evolve to produce less heat, would that also evolve to walk slower because it takes a lower speed to minimize the energy burnt per distance because they're producing less heat? I know there there will be a nonzero speed that minimizes the absolute minimum possible energy burnt per distance possible to evolve for that speed and a lower speed will actually increase the energy burnt per distance because the animal is walking for a longer time but the rate of energy burnt per time varies less rapidly with speed at such low speeds because of the energy burnt to fight against gravity.

Life on Earth is thriving, it's not just surviving on the edge. This leads to organisms with a high power to weight ratio. Energy efficiency does play a role, the less energy you waste the higher you can make the power to weight ratio for a fixed weight. But there is no need to keep the maximum power at some very low value.

Having a warm temperature allows body chemistry to happen more easily, move muscles faster, etc. That would be the advantage. When it's cold, reptiles can't do much, but mammals can. When it's too hot, reptiles suffer from heat and need shelter just like mammals.

Cold/warm blooded are misleading categories
The terms cold blooded and warm blooded is very misleading as it gives one the sensation that animals may warm up their internal temperature for the only reason of warming it up.
The terms homeo-, poikilo-, exo- and endo- terms are much more useful in thinking about control of body temperature. Have a look at this post and this post to understand these terms. Make sure to really read these posts to correctly understand these terms and how they interact.
Reformulating your question
What people, in general mean by cold vs warm blooded animals is whether they actively control their body temperature or not. That is cold blooded would mean exotherm while warm blooded would mean endotherm. As such the question becomes "why would any animal care about being endotherm if the body temperature won't go under freezing point anyway?"
Answer
Any metabolic pathway is affected by temperature. A change of temperature of only a few degrees can drastically affect the rate of chemical reactions. Homeotherm individuals (often homeotherm thanks to endothermy) are able to keep a quasi constant level of activity despite external change in temperature. It allow them to forage during hot and cold whether for example. This is a very important advantage but it often comes at the important energy cost. It is a trade-off between the benefit of homeothermy vs the energy cost of endothermy that will define the best interest of an organism.

Absolutely. Also, although it's fairly obvious once you think about it, I would complete the explanation by highlighting that it's easier to achieve and maintain a relatively stable body temperature that is higher than your surroundings than one that is lower than your surroundings...

Maybe for a lot of species, it's because being a poikilotherm would necessarily come with a costly trait because they reproduce sexually. Maybe if they reproduced sexually, they would have evolved to be poikilotherms because that would come with a much smaller costly trait.


text:
are there examples of research harmed by the binary vs. non binary genders discussions?
As a base for my question, here is a link to an article from nature.com: https://www.nature.com/articles/d41586-020-00502-w
In the article, the following paragraph is relevant:

The researchers noticed that male participants’ typical immune
response to infection differed from that of female participants, which
could explain the more severe disease often observed in men. (Nature
recognizes that sex and gender are neither binary nor fixed.)

Obviously the researchers, studying immune response difference between sexes, made two categories: Male and Female.
Then the Nature article, trying to fit with the times wrote that they recognize that sex and genders are not binary, and if they really believed it themselves, they'd probably not publish research as it would be based on a model they say they don't believe in.
My question is: are there known examples where research has been openly discredited (in a publication, or through a public speech on the media) because it is based on the binary definition of sexes and therefore 'not inclusive'?
(for reference I believe Humans are XX or XY and that's it, so this may bias the question / terms I used)

Interesting though your question may be, it is not a question about a biology in the terms of SE Biology, in that it is a question about social influences on scientific practice and publishing, rather than a biological problem. For that reason I have voted to close.

@David, I understand the improper fit. Can you think of another site where the question might be a good fit since I'd like it to be seen by people in the biology field.

Sorry, but I only do hard question and answer sites like Stack Overflow, this and English Language. I happen to subscribe to Nature and noticed the editorial intervention you refer to, but at my age I avoid political discussion with people I do not know. Certainly I prefer to keep this site on topic — I can provoke antagonism easily enough without meaning to just doing that.

I think your logic is a little flawed here. Just because a classification system is not universally binary or fixed (few biological concepts are) doesn't make it useless. If it did, we would have abandon species classifications long ago.
Philosophy or politics would probably be more appropriate stacks for this question.

@Thomas I would possibly recommend dropping the political terminology (i.e. "political correctness") if you want to engage with biologist on this matter, most of whom (like David said) are quite politics adverse.

@4galaxy7, point taken; I'll edit it. Maybe Philosophy is a good place, but I was looking for real examples where this would be an issue in research and I'm afraid Philosophy would be a good place for a debate, but I wouldn't get the answer I'm looking for. With Philosophy, you end up with more questions than when you start usually :D

Your statement that "Humans are XX or XY and that's it" is false. Humans can be XXY, XYY, XXX, XO, and others. Gender and sex are biologically not binary.

I think that you will find that the opposite is the case more often.
First of all, a premise that XX vs. XY has some kind of fundamental truth (which really is a premise of this question) is simply incorrect. There are a wide variety of karyotypes of the sex chromosomes, and these do not line up well with common notions of sex.
Using the XX vs. XY heuristic, and trying to fit e.g. intersex people into it, leads to positively incorrect and unnecessary therapies and surgeries in medical practice. A strong devotion to an XX vs. XY binary simply writes off something like 10% of the population, who are biologically neither male nor female according to that criterion.
Fausto-Sterling's book Sexing the Body was my introduction to this topic, though I am certain that there are more recent works.
So, on the contrary, you are more likely to find instances of people who don't fit the binary being harmed by the binary than people who do fit the binary being harmed by "woke" verbiage.

Very interesting answer. I asked the question as a part of a debate with friends and now I feel like I learned something worth reading a lot more about. Thanks!

@Thomas lovely to hear that. Thanks for taking it seriously- we're all here to learn!


text:
Can anyone (urgently) tell me if this is a bed bug
We just arrived in a place where a lot of people were living before.
This is what we found on the mattress and we are curious to see if this is a bedbug, or some harmless species; To know if we go out right away or not :)
Location: Poland. ;  Size: ~13mm long

Here is a photo with a measuring tape next to it:

Closeup:

Does this answer your question? Insect identification - Is this a bedbug?

Have you tried searching on this site for "bedbug" — there are several very good answers already posted that should put your mind at ease ...

The shape looks different but, not knowing anything about bugs, I have seen a variety of pictures online with different shapes, etc so I would feel at peace confirming what it is :)

By the way, the different shapes you've seen online are just insects being misidentified as bedbugs. In my experience, bedbugs are one of the most often misidentified species on the internet.  Bedbugs have 1 of 2 consistent shapes (hungry vs full), both of which are demonstrated in the post Insect identification - Is this a bedbug?

Since it's clear you still have the specimen, could you try taking a clearer picture under any type of magnification?

@theforestecologist: I added a close up photo; since we're moving right now, I didn't have a way to make a better photo

This is not a bedbug. This is a hemipteran called a leaf-footed bug in the Coreidae family. (Note: bedbugs are also in the order Hemiptera, but in a different family).
Species similar to yours found in Poland include Coreus marginatus (or "dock bug"), which [according to Wikipedia], is found throughout Europe.

 Adult male and nymph shown from dorsal and ventral views. Source: Wikipedia
C. marginatus is typically 13-15 mm long (which matches your updated length) and has a widened abdomen as does your specimen. Additionally, the antenna of C. marginatus is typically red-orange with black ends (as is also seen in your specimen). A more complete description from Wikipedia:

The head, pronotum and abdomen of an adult dock bug are speckled reddish brown. The antennae are composed of four segments, red-orange in colour except for the final fourth segment which is black. Between the antennae are two small projections, known as antenniferous tubercles, which can be used to distinguish this species from other superficially similar species.[6] The pronotum has angular upward facing projections and the scutellum is clearly visible. The rounded edge of the abdomen has lighter coloured markings. Adults are between 13 and 15 mm long and males are typically smaller than females but have longer antennae.

See here for an additional picture showing a specimen with less prominent abdominal markings as in your specimen.
C. marginitus tends to be found in thick vegetation, so unless you've bee around hedgerows, wasteland, or other densely-vegetated areas, it's possible you have some other closely related species.
I haven't been able to find a better matching specimen, though it seems likely I have only gotten you to the right family without being certain of the genus or species. I'll update if I can find more info...
Notes:

Your specimen does not appear to be another common hemipteran found in Poland:  Leptoglossus occidentalis, which is native to the western United States but has invaded Poland for over 10 years [Surce: Lis et al. (2008)1]

You can find a guide to this family of insects (with pictures) for the neotropics (not immediately useful to you, but a good resource) by Fernandes et al. (2015)2

 1 Lis, J.A., Lis, B. and Gubernator, J., 2008. Will the invasive western conifer seed bug Leptoglossus occidentalis Heidemann (Hemiptera: Heteroptera: Coreidae) seize all of Europe?. Zootaxa, 1740(1), pp.66-68.
2. Fernandes J.A.M., Mitchell P.L., Livermore L., Nikunlassi M. (2015) Leaf-Footed Bugs (Coreidae). In: Panizzi A., Grazia J. (eds) True Bugs (Heteroptera) of the Neotropics. Entomology in Focus, vol 2. Springer, Dordrecht


text:
Nose breathing and swimming
If you're standing and holding your nose closed, it becomes quickly uncomfortable; although you can breath fully through your mouth, it still feels like your lacking air since you're naturally trying to breath through your nose and you can feel the restriction.
On the other side, when swimming with a nose plug, you can have your nose totally shut down, breath only through the mouth and somehow you do not have the feeling of nose obstruction blocking your air intake.
Why is this?

Hi Thomas, could you include some kind of citation for the uncomfortable feeling you describe when plugging your nose. Ive never noticed/heard of this phenomenon. Could it have to do with humidity? If you're standing and breathing through your mouth it likely gets dry quickly where if you're breathing through your mouth at a pool, the humidity keeps it from drying out.

I explained the feeling more clearly, where it's a restriction that matters standing on land and one we totally ignore when swimming.

The holding your nose shut is uncomfortable because you are not holding any air in your nose, as for the nose plugs I think you should just blow out your nose while jumping in, it works for me.

@Thomas, a source for this feeling would still be nice, I have never experienced it, not unless you are talking about the throat drying out.

the best example I can give you is to stand, hold your nose shut. you can breath, but someone it is not very comfortable, you can feel that something is altered. My orl told me a while back that the nose has a sense of air velocity which is used by the brain, but I don't have any data to know if this is the case.

One possible answer for your question could have to do with the level of exercise the subject is doing.
While the nasal passage is the main route for breathing, it provides cleaner air and allows for more even and slow respiration rates, a greater volume of air can pass through the mouth LaComb.
There is no discomfort in mouth breathing during exercise because mouth breathing can deliver greater amounts of oxygen and release greater amounts of CO2; it is the preferred method of breathing for increased activity.
Secondly, discomfort in oral breathing stems from a perception of breathlessness due to stimulation of receptors in the oral mucosa. When patients were required to breath orally with humidified air, no instances of breathlessness were reported (Source).
Based on these two studies, when exercising oral-breathing is required to deliver adequate amounts of O2. Therefore, nasal-breathing is not required and an obstruction of the nasal passage is not percieved. When exercising in a pool, discomfort of oral-breathing is diminished due to the humidity of the surrounding air. When not exercising, and breathing orally in low humidity air, discomfort is felt due to the stimulation of receptors in the oral mucosa.

The study you quote seems to conclude that around 60 L/min of air (for males) people switch from nasal to oral breathing. It is possible that, while exercising, that threshold is reached and nasal breathing doesn't matter anymore. I'll wait for a bit more feedback to see if this is the case.

"Mouth breathing at rest could be uncomfortable because the oxygen delivery is greater than needed and more importantly too much CO2 is expelled." This is just a guess, and an inaccurate one. Breathing is regulated by blood CO2 and O2 concentrations, not the other way around, so mouth breathing will not cause 'too much O2' or too little CO2 unless it is intentionally too deep/frequent (hyperventilation). The reason it's disliked is that we are accustomed (correctly so) to having a moist oral mucosa, and mouth breathing causes mucosal dryness. In the water/shower, this doesn't happen.

Just do it for an hour. No cheating, no drinking, no candy, etc. If you do, and you still need a reference to believe that it causes discomfort, let me know.

I've removed conjecture and provided reference to an additional study which hopefully provides a more comprehensive answer to your question


text:
Can anyone identify this spider

This is in Wroclaw, Poland.
I'll be here a few months and I've noticed that they come in large groups in the evening. They are everywhere outside, but I haven't seen any inside.
They seem to live in colonies because when you see one, there are 50 others next to it, all sizes (age I guess), but always the same type.
The large ones have body about 1-1.2 cm long but the colonies have some significantly smaller with them, like 1/4 of the size.

It's clearly an orbweaver, judging by the typical head-down position in a vertical web.  The scalloped pattern on the abdomen reminds me of one of the Lariniodes species, but I'm not familiar enough with European spiders to be confident of an identification beyond that.  I would assume that there are bright lights, and possibly a pond nearby, given that you mention a lot of them close together.

yes, they gather close to the city's river and are always seen where there are floodlights, at night; can't see any during the day

Most of the night-hunting orbweavers hide near the web during the day (so they don't get eaten), although late in the season, as they get larger, and closer to laying eggs, some may stay in the web during the day.  These are not normally found in clusters, but where there is enough food, they can cram together in surprisingly large numbers.  There is a sewage treatment plant near my home that recently was documented to be something out of a horror movie - masses of webs of orbweavers and thousands of spiders filling the higher levels of a giant open building over the settling tanks..


text:
Speciation and Phylogeny of Lactobacillus
The lactobacillus, also called Döderlein's bacillus is a genus of facultative aerobic bacteria. There are several species such as Lactobacillus acidophillus and Lactobacillus reuteri.
I have several questions, all linked, for the concern of speciation of bacteria species used for lactic fermentation by humans.

Are all species that are used for cheese and yoghurt fermentation part of the genus Lactobacillus?
Do all species used for cheese and yoghurt fermentation form a monophyletic clade?
Did the speciation of this clade occurr before or after the use of these bacteria by humans?
What was the ecological niche of the ancestor(s) before humans used them for cheese and yoghurt?

I deleted your first question since a 3 second search should give you the answer. See NCBI's taxonomy page for Lactobacillus for a list of the various species in the genus.

Isn't that the exact same link I posted in my previous comment?

generally, lactic acid bacteria (LAB) are the ones you should be looking at for milk-based fermentation products. although sometimes species like bifidobacterium are added, which is of a completely different phylum. also, for cheese production, or the Dutch variety I am familiar with anyway, you would need fungi as well.
the lactobacillales order is not monophyletic, as you can see on the wiki page there are at least two different clades.
the wikipedia page 'Yogurt' speculates on the ecological niche of LAB: "Analysis of the L. delbrueckii subsp. bulgaricus genome indicates that the bacterium may have originated on the surface of a plant. Milk may have become spontaneously and unintentionally infected through contact with plants, or bacteria may have been transferred via the udder of domestic milk-producing animals." (source)
EDIT: the LAB are an order, they have been around for quite some time before the humans showed up.


text:
Why there is a very high drop in pressure from arteries to arterioles?
Laplace law explains why the pressure is the same in aorta and arteries (100).
I am thinking why there is so big drop in pressure when going from arteries to arterioles (40-60).
Why there is a great drop in pressure from arteries to arterioles?

While correct, @AndroidPenguin 's answer is only part of the explanation. By far the main reason of the pressure difference is that the peripheral circulatory system has two main compartments:

a resistive compartment, represented by arterioles
a capacitance compartment, represented by capillaries

The reason for the abrupt pressure fall from arterioles onward is precisely that this is the main function of the arterioles: they contract and dilate to adjust capillary pressure. Since a good part of capillary function depends on exchanges along oncotic pressure gradients, hydrostatic pressure cannot be allowed to stay too high in the capillary compartment. So in conclusion, @AndroidPenguin gave you the physical reason, but mine is the physiological reason.

This answer makes sense for me too! Thank you for your answer!

The vessel diameter is the most principal determinant to control resistance. Compared to other smaller vessels in the body, the artery has a much bigger diameter (4 mm), therefore the resistance is low.
In addition, flow rate (Q) is also the product of the cross-sectional area of the vessel and the average velocity (Q=AV). Flow rate is directly proportional to the pressure drop in a tube or in this case a vessels, although there are other factors of blood vessels that contribute towards the difference in pressure drop in bifurcations of blood vessels. These include viscosity, length of the vessel, and radius of the vessel.
Factors that determine the flow's resistance as described by Poiseuille’s relationship: ∆P=8µlQ/πr4:
∆P: Pressure drop/gradient µ: Viscosity l: length of tube. In the case of vessels with infinitely long lengths, l is replaced with diameter of the vessel. Q: flow rate of the blood in the vessel r: radius of the vessel
Assuming steady, laminar flow in the vessel, the blood vessels behavior is similar to that of a pipe. For instance if p1 and p2 are pressures are at the ends of the tube, the pressure drop/gradient is (p1−p2)/l =∆P.
In the arterioles blood pressure is lower than in the major arteries. This is because velocity of flow is increased with decrease in diameter and vice versa.
Source: http://en.m.wikipedia.org/wiki/Blood_pressure_drop_across_major_arteries_to_capillaries
This is important as for efficient exchange at the capillary bed pressure and flow need to be much lower.


text:
Can pulmonary infarction be asymptomatic?
I think it can because there are many parts in lungs.
Like for some COPD patients.
However, I am not sure if COPD patients can have infarction.
Lungs have parallel circulation.
Red infarct is possible there.
Blood can flow there.
One symptom should be at least pain.
So now, I think no asymptomatic possible.
But still, I am not sure.
Can pulmonary infarction be asymptomatic?

No. Based on experience. Lungs are very active organs.


text:
Is nutrient absorption different in Hypersensitive I patients?
I am thinking how the nutrient absorption differs between between patients with allergies (Hypersensitivity I) and those not.
The current guideline about number of eggs in diet is one daily regularly.
My professor says that 1-4 eggs daily can be also ok because cholesterol is inhibited.
However, I am thinking if we have Hypersensitive (allergic) person, what the recommendation should be then.
My hypothesis says that more cholesterol would be absorbed and less inhibited.
However, I cannot find any evidence for this hypothesis.
Hypersensitive response is fast.
I am interested in many responses during long term.
How does nutrient absorption differ in hypersensitive patient and normal patient?

The absorption is itself not different, but the rate of absorbed substances is different because of greater amounts of proteins in the allergic lymphatic circulation.
So less capacity stays for circulation of nutrients and so less absorption in time.

authors: ᴡʜᴀᴄᴋᴀᴍᴀᴅᴏᴏᴅʟᴇ3000


text:
Tc and Th1 interaction and viral immune response
Tc is T cell which can give T killer cells and T helper cells.
T helper cells (Th1) see the pathogen presented by antigen presenting cells (dendritic cells and macrophages).
They then secrete antigens to kill the pathogen.
If there is memory from previous interaction, then it will be easier to protect.
However, since some viruses replicate fast (RNA particularly), this memory benefit is often lost, like in the case of influenza virus A and B types.
However, I am uncertain how to explain this immunology with viruses.
How can you explain this general viral interaction better in the immune response?
I have these pictures in mind:

and

I actually don't understand your text. Can you clarify that?

I think you have most of the key elements.  With a virus, a virally infected cell may present virus antigen on MHC Class I or II and activate T-cells.  The rest looks fine, with "dendritic cells" considered the 'professional' antigen presenting cell that present antigen on their surface, migrate from skin/mucosa to secondary lymphoid organs like lymph nodes/spleen/GALT and drive T and B cell activation and maturation.  Depending on the source, a 2nd exposure may not need to an Innate first step.  Killer T-cells is a catch-all...cytotoxic T-cells may kill cells bearing virus but (cont'd)

its thought that natural killer (NK) cells (lymphoid lineage but lacking T cell receptor) might provide some immunity to nemotodes etc.  So your diagram mileage may vary based on pathogen.  A good immunology textbook should show the differences.

PlaysDice's answer:
Antigen presenting cells migrate from skin/mucosa to secondary lymphoid organs like lymph nodes/spleen/GALT and drive T cell activation and maturation.
T helper cells with CD8 and MHCII complex recognise the virus and kill it.
I think this is what is happening, for instance in HIV infection:

where

dendritic cell (ADCC) presentation of HIV infected CD4+ to MHCII and T helper cell
T helper cell activates cytokine release
Natural killer cells come and lyse the HIV infected CD4+ T lymphocyte


text:
What is the efficacy of Pertussis booster vaccine among different age groups?
The Murray Microbiology book says that it is prefentially 10 years, similarly Estonian and Finnish health associations.
However, my professor says that it can be 5-7 years.
I started to think if the age is affecting here to the result.
When should you take booster vaccination of Pertussis if you are
a) 25 years old,
b) 50 years old,
c) 70 years old, and
d) 90 years old?
My professor says that there is no significant studies about the efficacy of Pertussis booster vaccination among different age groups.
Is this true?

No, it is not true, see references 1 and 2 for this purpose. From these articles which followed up booster vaccinations for pertussis it seems that there is at least some protection 5 and 8 years after the boost.
There is another study, which says that 10 years are relatively safe to assume, as the reduction in antibody levels over time estimated from the 5 year study would still allow protective levels of antibodies. See reference 3 for details.
One of the problems to make statements about the duration of the protection is the lack of data. Additionally there was a change in the vaccine from whole cell (which is pretty immungenic, but has higher number unwanted side effects) against a acellular vaccine. This change happened in the 90s, so there are no longterm data available. See reference four for more details.
The common recommendation at the moment for adults is to repeat the booster vaccination every 10 years (together with tetanus and diphteria) and for people which have close contact to unvaccinated persons every 5 years to prevent infections (see reference 4).
References:

Immunity to pertussis 5 years after booster immunization during
adolescence.
Immune responses to pertussis antigens eight years after booster
immunization with acellular vaccines in adults.
How long can we expect pertussis protection to last after the
adolescent booster dose of tetanus-diphtheria-pertussis (Tdap)
vaccines?
Acellular pertussis vaccine use in risk groups (adolescents,
pregnant women, newborns and health care workers): A review of
evidences and recommendations


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Why is Electrical Cardioversion contraindicated in AF and Digitalis Poisoning?
I am thinking why electrical cardioversion is contraindicated in atrial fibrillation with digitalis toxicity/poisoning.
Cardiac digitalis is also called digoxin and cardiac glycoside.
It is antiarrhythmic agent against supraventricular arrhythmias.
It is contraindicated in Atrial Fibrillation with digitalis toxicity.
The Pubmed's article about the topic is a stub without describing its Pharmacology.
Digitalis toxicity is a complication of digitalis therapy, here used for atrial fibrillation.
This may be due to kidney failure when the medication accumulates in the body.
Its treatment is activated charcoal and gastric lavage.
However, assume that these methods do not help in treatment or that we in acute digitalis toxicity.
I think the reason why we cannot recently do electrical cardioversion in digitalis poisoning is the high probability of repolarizing incidences so the likelihood to stimulate heart at the right moment is very small.
This is because digitalis poisoning is associated with cardiac disturbances: ventricular tachycardia, ventricular fibrillation, SA block and AV block.
Without knowing more precisely about the complication, I think the electrical cardioversion has high risk of failure.
Why is electrical cardioversion contraindicated in Digitalis Poisoning of AF treatment?

The mechanism of action of digitalis-like preparations based on inhibition of myocardial NA+/K+-ATPase as well as of cardiac conducting tissue. The inhibition of latter (conducting) is 2.5 greater than those of former (myocardial). This is why the main feature of digitalis intoxication are arrhythmias due to ectopic electric impulses and spontaneous depolarization (there is overloading of conducting system by Calcium as well as excess amounts of Noradrenaline released from sympathetic endings).
These metabolic changes in a case of digitalis intoxication could lead to irreversible ventricular arrhythmias after cardioversion - there are sporadic reports about this phenomenon. Based on these reports, it was thought that the use of digitalis during electrical cardioversion would provoke ventricular arrhythmias in patient even with clinically desirable concentration of digitalis.
In a study in patients with therapeutic nontoxic digitalis levels determined that these patients may safely undergo electrical cardioversion without reducing or withholding the dose of digitalis. Thus, the cardioversion is not contraindicated in a patient without signs of digitalis toxicity.
Although, the exact mechanism of the ventricular arrhythmias after cardioversion is not well understood, it is clear that mentioned above changes in electrolytes concentrations with electrical stimulation lead to premature beats overtaking restored sinoatrial pace. The rate of ventricular arrhythmias is in direct correlation with the level of the energy used for the cardioversion (this is why there is "pre-cardioversion" with low-energy pulses). Until these metabolic changes are not corrected, the resulting ventricular arrhythmias can be irreversible. This is why, digitalis intoxication is relative contraindication to electric cardioversion of atrial fibrillation/flatter.
Excerpt from the article mentioned:

Excellent sentence The rate of ventricular arrhythmias is in direct correlation with the level of the energy used for the cardioversion (this is why there is "pre-cardioversion" with low-energy pulses). I would like to get more understanding about the nature and characteristics of this energy. What is the energy form? Ellipsoid pulses? Which other energy pulses are provided along the main energy signal? Any more studies about this?

@Masi It is clear that the more energy was used for cardioversion, the more its influence on the conducting system and myocardium. Since, the metabolic changes did not allow "actual" ventricular cardioversion, the higher-enegly impulses would have greater arrhythmic effect.


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What exactly happens if during translation, an amino acid is not present?
Lets say that the cell wants to make a particular protein. Transcription of the appropriate gene is done and the mRNA is made. mRNA attaches to the ribosome and the translation is initiated in a "normal" way.
What exactly would happen if an amino acid required in the protein is absent ? I know that the protein would not be manufactured properly but I want to exactly know what would happen to the ribosome and the mRNA. Are they destroyed? Are they simply separated? Who regulates this?

It is not true that the anticodon of an uncharged tRNA can't bind to the mRNA.
Bacteria have a mechanism called stringent response. This response is complicated, here is a shorter and simplified explanation. Further informations can be found at the wikipedia pages linked in the text.
If during translation a certain amino acid is absent, an uncharged tRNA binds in the ribosome, causing the synthesis of the alarmone (p)ppGpp by activation of the RelA enzyme (in E. coli), associated with the 50S subunity of the ribosome. The translation blocks and (p)ppGpp interacts with β subunit of RNApol causing:

the reduction of its affinity for the σ70 transcription factor and therefore reducing the transcription of rRNA genes;
the increase of its affinity for σS and σN, transcription factors needed, rispectively, for the adaptation at the stationary phase and the lack of N. Also biosynthesis of amino acids is enhanced.

Once the situation is restored, the enzyme SpoT (coli) hydrolizes (p)ppGpp.

Point to know : aminoacyl-tRNA binds to mRNA its not just t-RNA..
So if there is no Amino-acid there is no aminoacyl-tRNA of that aminoacid.. so if there is no aminoacyl-tRNA, the anticodon of tRNA doesn't form a bond with mRNA, so the protein production halts (until the Amino acid produced).
If the protein is not formed within a certain long time, the premature protein folds itself and breaks. Then a molecule (example: ubiquitin for certain type of bacteria) attaches to this premature protein and marks it for degradation.
But there are still chances of protein production with slight mutations.
Mutation: tRNA with the same anticodon and different aminoacid can easily bind to the A site of the ribosome in the absence of the correct aminoacyl-tRNA, so the protein production doesn't stop in this case but the protein has a mutation with different aminoacid.

Could you give a source for your answer?

How can a tRNA with the same anticodon bind to another amino acid ?


text:
Why can't we propose a solid theory regarding origin of life?
What  information is greatly lacking which does not allow us to propose a  solid theory for origin of life ?

The problem is not that scientists are baffled as to how life could have arisen. Rather, the problem is that scientists have many explanations as to how life could have arise, to the point that the appearance of life seems almost trivially obvious; it's just unclear which of the many possible routes was actually followed, and it's difficult to find clues that sort that out. It's as if you found a quarter at the bottom of a hill. The question isn't "Could that quarter have possibly rolled down the hill?" It's "Which path did the quarter follow when it rolled down the hill?"

I think this greatly overstates our understanding of the origin of life. I'm certainly not an expert on this, but as far as I know there are large gaps in all current hypothesis.

The first animal must have produced only 1 simple protein/product in large numbers... like mucus for example... in a long chain with no end, and then the second animal must have been when the long chain of mucus incorporated a copy of the first animal in it. they would have had no cells, no nucleus, just a complex molecule that made a huge amount of mucus, or another simple product which served as protection and food simultaneously. that's a fairly good theory for the first animal. the first animal was perhaps just a 50 atom molecule that made mountains of mucus out of heat and co2 and water.

Because the planet was sterile, the first animal didn't have to defend itself against anything, it just required the right PH of pure water, and an energy source, like sulphur, or volcanic vent compounds, it didn't need an outer shell that much, because everywhere was pure minerals and water.

What do you mean by "solid theory" because supported theories do exist.

First of all, we do have some solid theories to explain the origin of life. That said, the main thing missing in order to be able to accept one of these theories with a decent amount of certainty is the ability to run a planetary scale experiment for a few billion years.
The theories are fine, the problem is that we cannot really test them. In order to test a theory that describes the origin of life, we will have to recreate the original conditions (think of a test tube the size of the Earth) and then pump energy into the system and watch what happens over the next few billions of years. This is not really feasible, for obvious reasons. I really doubt you will be able to get funding for an experiment that will run that long.

The mice are working on it as we speak...

@Amory I just hope they finish before the Vogons get here.

The reason for no single, solid origin of life (OOL) theory is that there are
many and none of them explain or resolve the overall or the detailed issues of OOL, encompassing wide differential and even conflicting approaches, e.g., reproduction vs metabolism, and RNA vs DNA. Further, all are using naturalistic processes, requiring validation by the laws of physics and experimentation. While there are numerous theories, they are either geochemically irrelevant or outside the laws of physics. Whether RNA world, panspermia, hydrothermal vents, small warm ponds, all embrace various levels of chemical evolution for the initial, intermediate and ultimate biochemical assembly of increasingly more complicated levels of organic elements considered vital to OOL. No viable processes have been found to naturalistically create life.
Increasingly, wild speculation of geochemical conditions and trivialization of biochemical assembly, metabolism and reproduction are being proposed. The intractable problems that apply to naturalistic theories begins with the fact that chemical evolution of non-living compounds produces no viable pathway to increased complexity, that is, there are no cosmic evolutionary processes capable of the complex structure, design, order and operation of biochemical systems required for even the simplest organism.
The universal challenges that must be fully resolved in all theories include:
1. The homochirality essential in nucleotide amino acids,
2. The homopolymerization of the DNA side chains,
3. The nucleotide coding using information design,
4. The cell membrane formation essential encapsulation.
5. The chicken and egg issue of proteins and complex structures.
These are affected by requirements for colocation. coincidence, contamination mitigation and concentrations that are absolutely precise.
Finally, lab experiments must accurately reflect geochemically relevant conditions and not overly manipulated by experimenters, which would simulate intelligent design but produce questionable results.
The number of sources that could be listed is extensive. A simple search internet of the main descriptive words would provide detailed definition and additional detail. Regarding the 5 universal challenges: 1. homochirality relates to the right/left handedness of the amino acids since they are not symmetric. DNA amino acids must be 100% left handed or DNA will not work. One of the challenges to get comprehensive sourcing is due to the reluctance of present biological entities to fully acknowledge the delineated intractable issues.

Welcome to Bio. Can you add sources to your answer?

The high number of sources that could be listed are very extensive. A simple search internet of the main descriptive words would provide detailed definition and additional detail. Regarding the 5 universal challenges:

If there are so many sources to find it shouldn't be too difficult to put a few in your answer. Your answer is downvoted because it lacks references. Sources allow other users to background-read on your post.

"DNA amino acids" do you mean nucleotides? With errors like this sourcing becomes even more important.


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How bad is ethidium bromide in your plasmid for downstream applications?
I want to transfect Adipose Derived stem cells using a clone of my own. My problem is that I get a lot of contamination (not only genomic, but due to the nature of the technique, I get undesired products I haven't been able to get rid of).
So I was thinking about running a gel with my plasmid DNA samples and gel purify my desired bands. I don't know, however, if Ethidium Bromide contamination in my sample would be a problem or if a regular gel extraction kit gets rid of it.

No, there is absolutely no problem with that. And you get rid of the EtBr in the purification anyway.

Ethidium toxicity is probably not as bad as they make you think, they use it at like 1 mg/kg in cattle to prevent parasite infections.

And I should point out that it's not efficient to use plasmid purified from gel directly in a mammalian cell transfection. You should consider a larger scale prep. If its a problem of incorrect plasmids, transform your plasmid mix in bacteria, pick several SINGLE colonies and miniprep them, sequence and try again.

Possible duplicate of http://biology.stackexchange.com/questions/14047/ethidium-bromide-and-mutagenesis-on-cloning

Thanks for your insightful answers!
To answer user137:
I cannot expand my plasmid in bacteria to use a larger prep since the OriR sequence is excised and degraded from the construct after induction with arabinose. This is what I'm trying to get: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4144359/
Again, thanks

@Varekai I've used minicircles before, it's a pain, but you'll probably have to go back to the bacteria step and grow up your minicircle parental plasmid in large volume and go through the recombination step to remove the bacterial elements, then gigaprep the plasmid. If you don't get 100% conversion of parental plasmid to minicircle, consult your manual's troubleshooting section and do it again.

Purification and isolation of DNA bands by cutting them from agarose gel is commonplace (Lee et al., 2012). The purification step after excision of the band gets rid of most of the EtBr and other impurities. E.g., see the websites from Isogen and Sigma-Aldrich.
Reference
- Lee et al. J Vis Exp (2012); 62: e3923


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HIV and open reading frames
In Wilk et al. 2001 I saw that HIV has 3 open reading frames. In the Watts et al. 2009, I noticed they mentioned HIV has 9 open reading frames. I don't understand this very well.
e.g.

[ATG] GAT GTA AGT
A[TG G]AT GTA AGT
AT[G GA]T GTA AGT

Could anyone explain this to me?

Can you please link to the two articles you mention?

An open reading frame in this sense can, and in this case indeed it does, refer to transcribed regions.

Three: http://jvi.asm.org/content/75/2/759.full

Nine: http://www.nature.com/nature/journal/v460/n7256/full/nature08237.html


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How does evolution produce complex organs
I've been wondering lately how evolution manages to produce complex organs. It is pretty obvious to me how evolution would select some minor traits like size, resistnce to illness or climate. There is a mutation where some organisms are slightly different and better traits are selected. However I cannot imagine how an organism will mutate to have lets say lungs at once and unless organism has a functional organ there is no reason for the trait to be selected. So how does evolution produce complx organs?

The answer is 'gradually'. All other answers will be longer ways of saying the same thing.

This is, fortunately, not true. See Evo Devo below.

It is true, there is no sudden transition from no organ to a complex organ. It happens gradually.

You might find some relevant material if you search for "What use is half an eye", the classical question about how complex systems can evolve. Typically the answer is along the lines of "from smaller systems which in themselves are useful or at least not impeding".

@Armatus if this was an answer I would mark it as accepted. Found really simple explaination here - http://www.dbskeptic.com/2008/07/06/what-good-is-half-an-eye/

@Stilgar: Nice article, though I think it's worth mentioning that the human eye has not evolved from this line ;) The mammalian eye develops as an outgrowth of the brain whereas the given examples all develop first and then attach to the brain (according to biology year 12 which may have been wrong of course)

Still it make sense to me (as total Biology noob). First some tissue forms that works in some very basic way and then it evolves to form an organ.

Watch The Christmas Lectures by Richard Dawkins, here https://www.youtube.com/playlist?list=PL24C9639BE2DD4223 In one of them he shows how an eye can evolve incrementally. You don't need much biological training or knowledge to appreciate them.

you may be interested in cloacal breathing in turtles and things called swim bladders. both are ways incomplete lungs can be useful.  There is no such thing as an irreducibly complex organ.

The best introduction to evolution of complex phenotypes via master control genes is Endless Forms Most Beautiful: The New Science of Evo Devo and the Making of the Animal Kingdom by Sean B. Carroll. You might also want to have a look at a more recent Evolutional developmental biology (Evo Devo) book like those you get when searching for "Evo Devo" in Google Books.
In summary, it is possible for a mutation to change a shape by changing the spatial distribution of a transcription factor during embryo development. What's more, by changing the distribution of two mutually dependent factors, formation of any shape is possible if the distributions overlap. Such transcription factors are highly conserved in evolution and the most important cause of the endless forms we see.

Excuse my ignorance but I have only studied high school biology 15 years ago and in another language. If I understand your answer correctly it is possible for a mutation to create a functional organ at once?

No. You said above there are always small steps, and I said this is not true. The shape of an organ, when it is already evolved, can change drastically because it is determined by processes that are very sensible to the environment and to some mutations.

PS. There are indeed mutations that can 'create' a functional organ at once, because there are mutations that can make organs disappear. Just do the reverse change. I know the reverse would be near impossible in evolution.

This is a bit too simplistic. For sure we did not get from unicellular organisms to organisms with a stomach, hearth and lunghs just with a couple of mutations. Several small adaptive steps exist in the middle.

This is a strawman argument because I never stated that, either.

Just because the inverse of something is true, does not make that thing true. Organs disappearing with a single mutation is not evidence that they could ever have evolved with one.

And complex phenotypes are not equivalent to organs - do you have an example of an organ which evolved as a result of a master switch?

@rwst: -1, if your intention was not to state that then you have not really answered the question... You may want to quote relevant extracts from the books you refer to, in order to improve your answer.

Part of organ complexity is shape, and that can well be changed with a single mutation or even small change in environment. The question isn't about lungs popping into existence. It's about lungs with all their complexity, and part of that can change drastically. As you're not inclined to accept anything from me, I will close this now

@rwst: I am very sorry that you are taking this so personally. The only thing I am interesting into is to have a good answer, I don't care who writes the answer. The OP states: I cannot imagine how an organism will mutate to have lets [sic] say lungs at once so it is clear that he is asking for how lungs popped into existence, not how they were modified from a previous existing respiratory apparatus.

Yeah I am interested in how organs pop into existence. I am fully aware that they have been changed and improved slowly over time but unless they somewhat worked from the start evolution would not select for this trait

@rwst it's not a personal attack, it's just that the interesting point you've made (that complex phenotypes can appear rapidly in evolution due to master switches) does not demonstrate that organs arise suddenly, but that they can change form quite suddenly. It doesn't answer the question. It remains that gradual accumulation of small changes still accounts for evolution of the molecular networks which might be rearranged by a master switch mutation. For what it's worth, I do think your answer was interesting :). Please don't stop contributing just because of this.

-1 While certainly relevant, I don't think this answer is actually answering the question. Will undo if improved of course :)


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How good is information transfer between the hemispheres of the brain?
I sometimes listen to lectures on my phone using ear buds, but occasionally with only one ear bud in. Is the other half of my brain losing out on any aspect of the lecture? Just how good is the corpus callosum at sharing information between the hemispheres?

Have you read experiments in which patients with corpus callosum  severed were asked to do various things ? You will then appreciate the functioning of it .

Auditory information is routed to cerebral hemispheres via the brainstem and midbrain.  Structures in the midbrain receive information from both ears and combine it (including differencing it for spatial location) before sending the combined information on to both cerebral hemispheres.  Usually only the left hemisphere interprets the sound for language content, but it is doing so based on the sounds perceived from both ears.  The corpus callosum would not be involved in the hearing pathways.  So sound coming from the left ear should work as well as sound from the other if the perception level is adequate and not interfered with by sounds from the other ear.  It is likely the sound perception is somewhat better if both ears are receiving input from the source.


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Do Viruses produce a biomagnetic field?
From wikipedia:
Biomagnetism is the phenomenon of magnetic fields produced by living organisms.
The present scientific definition took form in the 1970s, when an increasing number of researchers began to measure the magnetic fields produced by the human body. The first valid measurement was actually made in 1963,[1] but the field began to expand only after a low-noise technique was developed in 1970.[2] Today the community of biomagnetic researchers does not have a formal organization, but international conferences are held every two years, with about 600 attendees. Most conference activity centers around the MEG (magnetoencephalogram), the measurement of the magnetic field of the brain.
Do viruses produce such a field?

viruses are not bio, but they can be magnetic. Just ask any virologist... ;)

possible duplicate of Do viruses have a magnetic field?

Hi user1432.  You've got the right idea in trying to improve your questions to get answers, however please use the edit link to do so rather than creating a new question.

Noted. Thanks. I'll try to delete the closed one when I have more time.

Viruses are bio.  Something does not need to be alive to be biological.  For chemistry all that is required is that it contains carbon.  Would you consider a random strand of DNA not biological?

Interesting related article suggesting perhaps biologists are over-estimating biomagnetism.

Please excuse the phrasing, which is not scientifically rigorous. The post only serves as a starting point.
Any electric current (the net movement of electrons) induces an magnetic field, and any magnetic field in turn induces an electric field. Indeed, each other is just one side of the same coin. The first to join these two into what is known as electromagnetism was JC Maxwell in his four fundamental equations.
Biomagnetism results from the flow of electricity within special functional tissues, located in organisms. (Some organisms have pure electrical junctions rather than 'interconnects' which rely on chemical messengers as vertebrae do. See this classical paper, and Evolution of nervous systems )
Certain heavy atoms have asymptotic magnetic field effects (a thankful property for many  NMR structural biologists).
As such, even if a metalloprotein with such heavy metal-atoms were to move inside the virus, driven for instance by a chemical oscillator (which would eventually come to a standstill), the effect would really have to be theoretically predicted first, and then empirically measured, rather than coincidentally just discovered (like say Penicillin). That is because it is very expensive to do science at such small scales, and the required hardware and human resources are in competition with projects that promise greater outlooks.
Further Questions:
My answer would be another question:
What sense would it make for a terrestrial virus to potentially benefit from producing an electric current inside, to motivate theoretical scientists to look into such a matter?
Or, what virus features would account for the sufficient flow of electricity to be considered a mechanism ( - as the magnetism at these scales is just the 'side effect') ?
Considerations:
( During the life-cycle of a typical virus, the virus does produce a magnetic effect, as the information-carrier molecule is charged, and the production of a new virus requires the net transport of charged molecules. Note, that by convention viruses are not living entities. )
Afaik, the field of biomagnetism only really took off due to the invention and commercialization of the SQUID.
This is just a starting point, motivated by the challenged notion of viruses. Virologists have a much better and up-to date grasp on the matter.
Killing a virus:
On a less serious side-note, one way to kill any virus is to put it on a Magnetar.
I hope this helps as a starting point...

What sense would it make for a terrestrial virus to potentially benefit from producing an electric current inside, to motivate theoretical scientists to look into such a matter?

First - let's leave off the motivations of theoretical scientists to theoretical scientists.
My core notion is to find evidence that running your biomagnetic fields at certain frequencies and amplitudes through emotional regulation naturally functions as shield.
In furtherance of "Darwinism", if viri tune themselves to the biomag attractor for suitable hosts - we can up the sales of mind-heart meditations.

Many living things have significant magnetic fields.  they are mostly the result of bacteria who assemble a tiny cluster of magentite within their cell bodies.  These tiny iron magnets are sensitive enough to respond to earth's magnetic field, which seems to be the best known function of the magnetic particle.
Symbiotic magentobacteria are one of the mechanisms of migratory bird's uncanny ability to find their way along their magnetic route.
I don't believe a virus has ever been a magnetic particle discovered in a virus, though you never say never in biology, esp with microlife.
There are other means by which electrical and magnetic fields may be sensed by living things, but the individual magnetic fields of typical atoms in biological samples are too weak to sense without a big-ass magnet.  I don't know of any verified theory that gives any validity to this being important except maybe metal atoms inside proteins whos electromagnetic fields help guide ions and electrons along specific paths in the cell.  These are very local phenomena - spanning only 100 nm or so.

My markedly unverified theory is that we should be able to alter our own magnetic fields to improve resistance to viruses, similar to the manner in which the earth's EM field shields us from solar excretions.

From what I can see, this is hard theory to support.  Its hard to verify a theory when the magnetic fields cannot be measured.  the magnitudes of field you seem to be pointing at wouldn't stop something as large as a viral particle.  The fields are weak partly because non metals can't make magnets in the sense that we typically see them.  Look up ferromagnetism for more details on this.

Apart from that, what kind of magnetic field would you need to influence a virus? Not influencing your own cells at the same time?

it would be hard to influence a virus with a magnetic field - if this were obvious how to do this it would certainly be tried.  you might want to study MRI and how it differentiates between different kinds of tissues.  this might be a good direction, but it is still a bit of a long road to making something work.

@shigeta RNA and DNA can be partially aligned in a magnetic field in an NMR spectrometer due to their elongated shape. You could likely do the same with viruses, as long as they aren't globular. But that still wouldn't do more than slightly change their preferred orientation in solution.

@MadScientist Good point.  It seems like MRI/NMR might be able to pick up DNA, though the signal is really weak compared to that of water. Like you say, it seems unlikely you could use this as a handle to differentiate viruses from other cells in a mixture like a living thing.

@shigeta Viruses consist mainly of nucleic acids and proteins, just like cells. Without isotope labelling or very high levels of overexpression you have no chance of distinguishing specific components of such a mixture.

To be fair MRI can differentiate between some bizzare things. for instance tumor cells vs non tumor cells and metabolic processes, without using isotopic labeling.   Though I think we both agree; the density has to be within the resolving capabilities of NMR and its doubtful that most viral loads are enough to be seen much less manipulated.

Every atom produces a magnetic field, so the formally correct answer would be "yes" (assuming that viruses belong to the tree of life, which is disputed -- otherwise, one would not use the prefix 'bio').
However, biomagnetism as a science (and not pseudoscience) is concerned with more measurable effects. The biomagnetism of a virus will be negligible compared to all the surrounding cells, and hardly measurable.

Given that viruses are using the same building blocks as the rest of the known organisms (RNA/DNA), claiming that they do not belong to the tree of life sounds odd.  Of course they do (as in, they share a common ancestor). Is this really a notable position?

I think you're probably right, but is there any study to support "The biomagnetism of a virus will be negligible compared to all the surrounding cells, and hardly measurable."?


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What is the function of clot retraction?
I am thinking how clot retraction and fibrinolysis work together.
I think that clot retraction is a process that gets clot towards fibrinolysis process.
Fibrinolysis process then lyses the clot.
However, I am not sure if it is so simple.
Some seems to be discussing about how to differentiate start of fibrinolysis from clot retraction morphologically.
So they probably seem to be at this stage similar processes visually, but not functionally.
What is the function of clot retraction?

The platelets in the clot contain contractile proteins. They bring the edges of the wound together, which also reduces the chance of further bleeding. The contraction process also supports the wound healing process as it brings the ends of the wound together.
For more information see this article: "Mechanics and contraction dynamics of single platelets and implications for clot stiffening"

So these contractile proteins cause the clot retraction. Thank you for your answer!

Is this different type of contraction than vasocontraction? It seems to be so.


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To characterise diameter of capillaries in organs
I know that there exist Continuous capillaries (skeletal muscle, adipose tissue, connective tissue, pulmonary circulation), Fenestrated capillaries (small intestine, renal glomerulus, exocrine glands), and Discontinuous capillaries (sinusoids; liver, spleen, bone marrow and hypophysis).
However, I am not sure how to characterise these.
The diameter of capillaries is different for each.
I have not managed to find any figure which present the relationship of diameter of these capillaries.
I have reviewed books Guyton, Pocock and Lange.
What are the diameters of capillaries in different organs?

This question is dependent on the specific patient at hand.
I think in the normal situation the diameter of the capillaries is about the same in each organ.
Better question would be: how does the diameter changes in relation to the venous and arterial ends of the capillaries?
Then, think about how big portion of the capillaries are in the venous end in the organ.
I cannot say that 50% of capillaries are on the venous end of the organ and 50% on the arterial side.
This is again an open research question.

authors: Иннокентий Жвац


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Saliva test for Toxoplasma gondii?
I am trying to find some reliable gene kit by which you can rapidly test Toxoplasma gondii.
I am not sure if it exists.
I have an intuition that some tests done during 90s-00s on this species had high false negatives.
Which genes should you detect to find Toxoplasma gondii in a gene kit?

rRNA sequence would also be good.

All research on saliva tests I've found involve antibody detection which, as you suspected, can produce false negatives depending on the disease process or the presence of immune disfunction (such as due to AIDS). Thus, if you can isolate T. gondii gDNA from the saliva, a genetic assay may be more sensitive. However, Amato Neto et al. report:

In 26 patients with AIDS, including six with tomographical evidence suggesting cerebral abscess caused by Toxoplasma gondii, no parasites were found in the saliva by the use of the mouse inoculation model. This trial [suggests] that the search for Toxoplasma gondii in the saliva is not an alternative method for the diagnosis of toxoplasmosis in patients with AIDS.

So perhaps the most difficult aspect of generating a gene based saliva test is actually isolating the parasite from the saliva. I was unable to find other isolation attempts, but my research was very brief.
As for which genes to detect, studies involving human blood samples have found that PCR amplification of B1 paralogs provides a sensitive and selective method for detecting T. gondii. Burg et al found that there are about 35 copies of the B1 gene in T. gondii and also state that:

Because of its repetitive nature, the B1 gene is an attractive target for detecting T. gondii parasites through amplification of B1-specific DNA.

They were able to amplify and detect the gene from crude cell lysate as well as from purified DNA samples containing a 1:10 000 ratio of parasite to leukocyte. Furthermore, they could not detect the gene when assaying other organisms. Ho-Yen et al. later attempted PCR amplification of the same genes in human blood from patients with suspected toxoplasmosis and found that:

PCR can be reliably used on human blood samples. For a reference laboratory, this is a valuable addition to its array of diagnostic tests, and provides a more rapid assay than animal culture.

Jones et al. compared detection of the B1 genes with P30 and 18S rRNA genes in aqueous humour. They were able to detect 50 fg of gDNA using the B1 assay, which is equivalent to a single parasite. They concluded that:

The B1 PCR protocol appears to be the most sensitive protocol in the detection of T. gondii DNA and has been successful in identification of T. gondii DNA in ocular fluids and retinal sections.

Good and clear meta-analysis about the current situation for the saliva test of Toxoplasma gondii!


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Does the Heart Require Gold?
I distinctly remember an episode of NOVA from the early 1980’s that concerned itself with gold. One of the points that was made was that there are trace amounts of gold in the human body, specifically in the heart, and without this gold our hearts wouldn't beat. I've never been able to find another citation of this. Is this true?

According to this source, gold is not a necessary trace element for living organisms.
Would have been cool, though...


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How do the quantities of ATP formed during aerobic and anaerobic respiration compare?
How do the quantities of ATP formed during aerobic and anaerobic respiration compare?

What do you mean by compare? The amount of ATP made in each process? Is this a homework question?

@Aly I guess you are referring to glycolysis and its switch to lactic fermentation in anaerobic conditions?

You means fermentation and respiration?
In aerobic,1 mol glucose trough respiration and get about 38 ATP
In anaerobic, 1 mol glucose through fermentaion and get 2 ATP

I think you mean 1 molecule, not 1 mol.

Yes! I means that.


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mVenus fluorecent protein, life time? luminosity?
If fluorescence proteins get excited by radiation, how long does it usually take for the excitation to decay (at room temperature)?
I guess, if the life time is too long, the luminosity will be very low. Do you know something about how luminous the fluorescence can be?

what exactly you wanna know? Life-time of fluorescence is on the order of nano seconds


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Can HIV be transmitted via breastfeeding?
If a pregnant women is HIV positive and she is treated with medicines to deliver a normal child,can she transfer the HIV virus back to her normal HIV free child by colostrum?

possible duplicate of How does a person get AIDS?

The other thread doesn't cover the post-natal infection by breast milk.

Note that is seems that sexually sucking an infected woman's breasts is not considered a dangerous activity.

Yes, it is possible and the chances are pretty high. According to the WHO paper linked below, the rate of partially or completely breastfed children which get infected by this route is about 20-35%, while the rate of children which are not infected and doesn't get breatfed is zero (no surprise here).
The mechanism by which this infection occurs is currently unknown, but it is hypothesized that the virus enters via the mucosa. See these two articles below for more information:

A review of HIV transmission through breastfeeding.
HIV transmission through breastfeeding : a review.