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Why do different bacteria have different shapes?
Why do different bacteria have different shapes? Is it only related to their function?

Due to multiple evolutionary forces acting over long periods of time (along with chance events, heterogeneous environments etc)? I really don't see this as a constructive question. You could just as well replace with "Why do birds have different colours?" or "Why do fish have different sizes?"

@fileunderwater: I see it as a very interesting biological question. I would rather compare it to "why do birds have differently shaped beaks?"

@nico I see that question as too broad as well - too many possible answers and reasonable mechanisms to be answerable in less than a book.

Reasons for Bacteria with different shapes as given in Wikipedia/Bacteria:

The wide variety of shapes is determined by the bacterial cell wall and cytoskeleton, and is important because it can influence the
  ability of bacteria to acquire nutrients, attach to surfaces, swim
  through liquids and escape predators.

There is an article based on research by Kevin D. Young Bacterial morphology: Why have different shapes? which highlights 3 main points which defines the shape of Bacteria:

Nutrient uptake: Cell shape, in and of itself, affects nutrient acquisition and argues that other nutritional situations may create conditions that favor one bacterial shape over another.
Motility: Motility imposes a heavy selective pressure on cell shape. Fast cells are better off as rods with a certain length-to-width ratio, chemotactic cells must adopt shape ratios in line with their environments, and cells that forage near surfaces or navigate viscous environments may do best if they are slightly curved or spiral.
Predation: In their struggle against being eaten, bacteria have adopted morphological defenses that may have produced the wealth of shapes we now observe.

These factors play a role in shaping bacteria. Further he explains what in general gives the shape to bacteria:

Bacterial morphology is affected by a combination of selective pressures - access to nutrients, cell division, attachment/dispersal, predation and motility (among others). Among these different factors, our understanding of the relationship between motility and cell shape is most complete; for example, highly motile bacteria are usually rods with a specific (optimal) shape and size, and movement through viscous fluids seems to a favor spiral shape. But since multiple selective forces are always in play, there is at the moment no way to predict cell shape based on the environment or vice versa.

Shape Matters: Why bacteria care how they look - This article highlights Kevin's work explaining why shapes matter for bacteria and they take it seriously for survival.
So adaptations to various environments could be possible but depending upon the environment we can not predict the shape of bacteria because some other factor might have played major role in giving shape to it. But the above mentioned 3 main factors gives some explanation.

As for how certain bacteria achieve their shapes, the cell wall plays an important role. Almost all bacteria have a cell wall made of a substance called peptidoglycan, a mesh of peptides and saccharides that provides rigidity and strength to the bacteria. This wall is produced through a complex series of steps that starts inside the cell, where the peptide and sugar units are attached to a lipid to make a compound called Lipid II. However, Lipid II must be flipped to the outer layer of the cell membrane to deliver the peptides and sugars to the growing cell wall. The proteins responsible for flipping the Lipid II are believed to be FtsW, RodA, and SpoVE. FtsW is considered the main enzyme for most cell growth. RodA is found in rod shaped bacteria and is considered necessary for cell elongation. SpoVE is used to build the thick cell walls of bacterial spores. By controlling how Lipid II is delivered to the growing cell wall, these proteins play a role in controlling cell shape.
References:

Structural similarity among Escherichia coli FtsW and RodA proteins
and Bacillus subtilis SpoVE protein, which function in cell division,
cell elongation, and spore formation, respectively.
Specificity of the transport of Lipid II by FtsW in Escherichia coli


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Alternating Ovulation
I have often heard that right and left ovaries alternate in releasing ovum.
Is it always true? What controls this rhythm? Is it simply because the other ovary is unresponsive to LH or FSH? If so, why?

I am not sure if this alternation occurs. Can you post the reference ?

Nope, not true.  It's a pretty common myth; that paper cites a  reference from 1932 in primates claiming to show that the ovaries alternate.  A few papers before this, in particular this one from 1991 showed that ovulation was not alternating, but this was the first to do so in actually fertile woman.  In particular,

Alternate ovulation occurred in 61 of the 119 succeeding ovulations (51.3%, not significant) which means that there was no consistent tendency to alternation.

Alternation only occurred half the time.  Neither did they find a difference between side preference; right-side ovulation occurred in just over 50% of the cases, not significantly different.
FSH, follicle-stimulating hormone, and LH, luteinizing hormone, stimulate each ovary equally, but one ovary will get slightly ahead.  Ovulation (and indeed pregnancy at times) is a positive-feedback loop, meaning the response will be exponential; if one ovary is even just slightly ahead it will rapidly dominate the other.  The less-developed one quickly senses the other is ahead of the game and ceases to respond.

Can you provide details of the positive feedback loop and the sensing the "lost race" by the less developed ovary as mentioned in your answer?

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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Giving diuretics to insipidus patient
I read in Tortora and Derrickson that giving diuretics to diabetes insipidus patients may in fact alleviate the symptoms of the disease.  How is this possible?

Wikipedia has your answer:

It seems paradoxical to treat an extreme diuresis with a diuretic, but the thiazide diuretics will decrease distal convoluted tubule reabsorption of sodium and water, thereby causing diuresis. This decreases plasma volume, thus lowering GFR [glomerular filtration rate] and enhancing the absorption of sodium and water in the proximal nephron. Less fluid reaches the distal nephron, so overall fluid conservation is obtained.

The source for that is an editorial from 2004 that has some good other sources, including what appears to be the 1959 original paper finding this seemingly-paradoxical result.

Thiazide diuretics inhibit the NaCl co-transporter (NCC/TSC) in the renal distal convoluted tubule (DCT). The DCT is water impermeable and considered to be part of the diluting segment. Therefore, the water-preserving effect of thiazides is unlikely related to a direct effect on the DCT. In fact, the most widely accepted hypothesis suggests that the antidiuretic action of thiazides is secondary to increased renal sodium excretion. The renal sodium loss causes extracellular volume contraction leading to lowered GFR and increased proximal tubular sodium and water reabsorption. Hence, less water and solutes are delivered to the distal tubule and collecting duct and are lost as urine.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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observed luminescence in a piece of plaice
A plaice fish bought for human feed has been cleaned and cooked.
Some parts of the raw body have been left out of the fridge at about 22°C for about 15 hours.
During the following night a luminescence phenomenon has been observed on the meat of the fish.
The second shot has been taken in a dark environment with a professional camera using a high sensitivity and long-time exposure.

What could it be?

It's probably bacteria.
Here's a pdf describing the phenomenon, along with an in-depth history of the reported occurrence, which should tell you everything you might want to know.

These seafood products exhibited luminescence due to the presence of certain bacteria that are capable of emitting light.  Luminescence by bacteria is due to a chemical reaction catalyzed by luciferase, a protein similar to that found in fireflies... Most of these species require salt except for the two nonmarine luminescent bacteria.

There is some link to potential pathogenicity, so I'd recommend not eating it.  That document also requests that you contact the researcher, so why not?  Here is a potentially-relevant paper but 1. is very old, 2. is in Russian, and 3. I have no access to it.  And this supposedly tells you how to isolate them.

thanks, very useful, we find ourselfs in one of the cases that the FDA document describes (the one of the cat). we are not sure about emailing the researcher because we live in europe so probably the fda is not the 'right' authority to report to. i will wait few days then mark your answer as accepted.

I can only second this. There are bacteria growing on the fish. Interesting example though.


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Is there differences in components of saliva among species
Are there differences in the components of saliva among species? Also, do the functions of saliva differ between species?

This question should be narrowed down somewhat. Which species are you asking about?

It could be better answered if you specified which species you were interested in. Broadly from Wikipedia, snakes have venom, some swifts have gummy saliva to help in the building of nests, spiders produce their web from salivary glands etc. This is too broad a topic. The human salivary composition is found on the Wikipedia page I have linked. Salivary compositions can change with habits which have been detailed in this article. To compare, I am also providing the link to an article on the saliva composition of an assassin bug.

@leonardo wikipedia mentioned venomous saliva so i just put it in but u are right. Toxins would be right term to use

I think the answer is not very original or authoritative. Can you try to flesh it out a little? I agree that the question is broad, but I think you could put a little more into the answer.

@jmusser Thank you for your opinion. I will have a look at it as soon as I get some time.


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How much can you learn about species variation from a skeleton?
I just read about the discovery of the 1.8-million-year-old human skull in Georgia, and how it suggests that early humans were all one species instead of distinct ones. Would an archaeologist unearthing dog bones a million years from now know that a Great Dane and a Chihuahua are the same species?

It seems as if this article is purely speculative. They didn't mention any DNA testing, but instead discussed physical features.
There are two "types" of archaeologists: clumpers and splitters. Clumpers (like the author of this article) believe that there is wide variety among members of the same species, and so it is often wrong to categorize every new hominid fossil as being a different species. Splitters like to "split" their findings into new species, even though there is no evidence that speciation had ever occurred; they just decide that since the remains look different, they must have speciated.
In the future, I hope that archaeologists will have more sophisticated means of sequencing the DNA of ancient remains, allowing them to construct an accurate phylogeny


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Attachment of muscles during molting in insects
Normally, insects' muscles are attached to their exoskeleton but what happens to this attachment when they are moulting?
Sorry if this is an extremely silly question but I have wondered about it for a long time and have tried searching it.

You can find a concise answer here in a section from The Insects: Structure and Function  by R. F. Chapman, eds. Stephen J. Simpson, Angela E. Douglas. 5th Edition. Cambridge University Press.
In essence the source says that the muscle attachment to the cuticle is maintained during the moulting process, while the new cuticle is formed under the old cuticle.

As a result the insect is able to continue its activities after apolysis during the development of the new cuticle. The connections to the old cuticle are broken at about the time of ecdysis.

Connections to the new cuticle are formed at the same time as the old ones are broken.

To clarify the issue: muscles do not contact with the cuticle directly. They form junctions with epidermal tendon cells, which pass the tension via microtubules to their outer membrane - to hemidesmosomes. From the side of the cuticle these hemidesmosomes are supported by intracuticular (extracellular) fibres (= tonofibrillae). During pre-molt, when the new cuticle is being synthesized, these fibres run through both the new and the old exoskeleton, thus ensuring maintenance of the mechanical support for muscles: in isopods.


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Termination of translation
What dissociates first - the last tRNA, mRNA and release factors or the subunits of ribosomes?
I tried searching this from Lehninger but couldn't get a clean answer.

Shigeta's got a point: the ribosome is latched onto the mRNA so those two are intrinsically linked.  You're really asking whether the ribosome comes off first or whether the tRNA does, but it's actually the new polypeptide, which makes sense:

The stop codon is recognized by a protein, the polypeptide chain release factor (RF), which triggers the hydrolytic release of the nascent polypeptide chain from the P-site-bound peptidyl-tRNA.

This minireview puts forth a model (see below) where, in E. coli at least, the 50S ribosome subunit is then dissociated from the mRNA/30S subunit/tRNA complex, following which the final tRNA is removed.  An in-depth review from a few years later gives more context.

just off the top of my head... since the ribosome is made of 2 large complexes which assemble and clamp onto the mRNA, I'd say it was the tRNA first, then the ribosome and mRNA would detach simultaneously.


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A possible cause of autoimmunity
I read that

Doherty and Zinkernagel found that MHC- heterozygotes present more
  antigens to the immune system than homozygotes; yet, the infected
  heterozygous mice in their experiment all died, apparently from
  overresponsiveness.

Can MHC-heterozygotes be more susceptible to autoimmune disorders and allergies because there is a tendency of over responsiveness ?

It looks moderately muddled, but perhaps.  This paper1 is a good place to start; it's free and the intro lists a number of more recent studies.  That study found a connection to lifetime reproductive success in sticklebacks (a fish) with intermediate MHC diversity.  This 2007 study in mice2 is a particularly nice one, dealing with a inbred line outbred to wild mice, finding again, no advantage to heterozygotes.  There are others, but most deal with the concept descriptively (self-delighting in their continued refutation of a commonly-held belief) or predictively (such as this from PNAS in 19923 or a 2009 review4) but specific and proven reasons are sparse.
The general feeling is that it may remain unclear what sort of genetic interactions are involved in MHC (additive effects, overdominance, etc.) but it is probably also complicated due to the nature of immunology.  For example, a paper from 20035 points out that in an immunological response, only a few peptides dominate the response; there may be no real advantage to having extra ones if they are unused, and having those others around might dilute the useful response (That paper also takes an interesting view of serial infections, and shows that heterozygotes are indeed advantaged during coinfection).  The above PNAS publication3 gives the idea, which the stickleback paper1 recapitulated, that if more alleles are present, more T-cells will be self-reactive and will therefore be purged, resulting in an overall decreased T-cell availability.
Other hypotheses are present in the review4 I mentioned, such as perhaps positive selection efficiency is not MHC-diversity dependent whereas negative selection is, or indeed increased autoimmune reactions as you guessed.  My guess would be some combination of the above, with selection for heterozygotes being favored in the real world for multiple and repeated infections but certain specifics resulting in a homozygote preference, of which autoimmunity is likely playing a role.


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Are identical twins exactly the same?
http://www.scientificamerican.com/article.cfm?id=identical-twins-genes-are-not-identical
According to this article some identical twins show differences with respect to their copy number variants. How is this possible? If mitosis of an egg can lead to this difference, why can't mitosis of any cell in our body?
If we assume that identical twins are exactly identical, then if we make a clone of a twin will all three be exactly identical?

Errors in division occur all the time and can show up in any dividing cell; this is, of course, important for cancer biology.  If one of my cells replicates oddly right now it likely won't matter since it's only one out of trillions, but if that happened at a very early age in development it could be present in many if not all of my cells.  Identical twins indeed come from the same egg-sperm fusion event but they develop separately from a very early state.  It's trivial to imagine a minor replication error in DNA at an early cell stage that results in different genotypes between so-called identical twins.  Besides, we've known for years that identical twins can have major epigenetic differences, so this isn't particularly ground-breaking.

If we assume that identical twins are exactly identical, then if we make a clone of a twin, will all three be exactly identical?

Depends on your definition of "clone" but how identical is identical?  If you mean exact, then probably not; at the very least they will have different numbers of cells, for example, not to even mention CNV or epigenetics.  If you want some SciFi cloning thing then, well, join the club.

If I make a plant out of a single cell, will it be more appropriate to say that the new plant and the old plant are exactly identical genetically or to say that they are more like "twins" ?

In theory, they should be more like "twins" but in practice you could say identical.  For all intents and purposes there's no difference.

Identical twins do start out identical, but their DNA will quickly diverge. Not in a dramatic way, but in point mutations, at random locations, in different cells.  Think of how there is a certain error rate associated with DNA replication - so even from that very first cell, when it divides to form a second cell, there is a chance there may be mutations in the DNA copy.  It is highly unlikely that both twins will make the same mistake in copying the DNA in exactly the same location.  Now repeat that idea millions and millions of times, as they develop, forming all the cells they need to form their bodies, and throughout their lives.  Mutations are random, and they accumulate.
I made a video about this topic - Are Identical Twins Really Identical?

@ biogirl: Why clone? There are quite a number of monozygotic  quadruplets. One zygote giving rise to four identical beings.

The clarification that I require is whether the identical twins are exactly similar or are they mirror images? That is if there is hair whorl on the left side in one, whether it will be on the right side in the other. Functionally also if one is right handed will the other be left handed etc.

@khhsocratica Loved the video ! You guys are doing a wonderful job :)

@RamManoharM there is nothing in the biology of twins that would cause such mirroring. The parts of hair whorls or handedness that are determined by genes will be the same.

The video was good. But then references to scientific studies on twins would have been better.


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Difference between viral and human genetic material
I have heard that there is a difference between viral and human genetic material. What is that difference?
If I take my cells and take DNA out of them and insert only a small part of it having a sequence, say, AGTTC, and viral DNA with the same sequence, can my body distinguish between the two? If so, how?

It is not at all my subject but here are some differences. bacteria's DNA are circular and does not look like our chromosomes. Bacteria don't have epigenetic variation. They don't have histones (which are proteins aroung which DNA forms 2 loops). Bacteria have no introns (no pre-RNA splicing). Bacteria have almost no non-coding DNA.

In the gene (DNA) there are sequences that are called exons and sequences that are called introns. Exons are those that will code for the protein amino-acid sequence and introns will be spliced (=eliminated). Before splicing the mRNA is called pre-mRNA. You can have a look to the wikipedia page as well, you'll get more information. http://en.wikipedia.org/wiki/RNA_splicing

not having methylated CpG is a big difference, and a red flag for the Tol-like receptors that a certain bit of DNA might be invasive: http://en.wikipedia.org/wiki/CpG_site

Additionally, a virus genome is not necessarily DNA. There are (lots of) RNA viruses. There are viruses with single stranded DNA and double stranded DNA. But your "AGTTC" is just an oligonucleotide and could come from anywhere. At least if the original C in the human sequence was not methylated, replacing it with AGTTC from a virus should not make a difference. (If this is the only thing happening, replacing exactly this sequence with the viral equivalent, and nothing more. Which is unlikely.)

To sum up: If we are not talking about chromosome organization, nucleotide sequences and overall genome architecture (which are incomparably different in eukaryotes and [even their] viruses) the differences in the genetic material are as follows:

viruses are much more diverse in their choice of genetic material, which is in the cornerstone of viral higher systematics. It can be DNA or RNA, single- or double-stranded, circular or linear. Animals, in turn, possess only double stranded DNA as their genetic material: linear dsDNA for the nuclear genome and [usually] circular dsDNA for the their mitochondrial genomes.
DNA termini pose a special problem for the maintenance of the molecule and show very unusual organization in terms of DNA sequence and structure. Repetitive terminal sequences of eukaryotic chromosomes have 3'-overhangs, which form a special quadruplex form of DNA. Termini of viruses are naturally much more diverse and are (nearly?) never of the same structure as in Eukaryotes. [Circularization/decicrularization is one of the mechanisms recruited by viruses]. (Deng et al 2012)
DNA methylation is normally present in varying degrees in animals and in vertebrates most of the cytosines in CpG dinucleotides are methylated. Viruses differ considerably from one another in this respect, but it seems that smaller viral genomes are generally under-methylated and larger genomes do not show under-methylation, although it depends on the stage. This conclusion is based partly on indirect evidence that CpG motifs are considerably much less frequent in smaller viruses. Integrated "genetic parasites" like retroviruses are normally rich in CpG and are highly methylated. (Hoelzer et al 2008)
although I couldn't find relevant literature, I'd hypothesize that the highly packed genetic material in viral particles may potentially exist in more compact forms of the DNA helix (in dsDNA viruses). Most of the dsDNA in cells is present in a so-called B-form, but there are more compact A-form and less compact left-turned Z-form (there are other forms, most of which are biologically not relevant). (cf. Wikipedia for an introduction)


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Skeletal muscles in clam
Although skeletal muscle fatigues fairly rapidly, clams have a protein called paramyosin that allows them to sustain contractions for up to a month. What might be the role of paramyosin at the molecular or cellular level, which results in this peculiarity?

This appears to be a homework question, which is often frowned-upon without prior research. Where have you looked so far?

Without proper background knowledge I'd say that that's for keeping the shell closed.

actually this is an 'Scientific Enquiry'- type question in "Biology By Campbell & Reece"...

Older papers initially presumed that it was part of a mechanism called "catch" in invertebrates like molluscs which is a "sustained contraction."  However, paramyosin was also found in insects.  There is a very detailed review on invertebrate muscle from 2008 that you should read through (or, you know, search through) points out that recent evidence has shown that paramyosin is not involved in catch; that review also has this to say on the subject (emphasis added):

Furthermore, paramyosin’s presence in almost every invertebrate muscle (including those with relatively small thick filaments) suggests that paramyosin should not be considered a ‘special’ molecule whose presence needs explanation. Paramyosin is instead an everyday constituent of invertebrate muscles, similar, for instance, to the giant sarcomere associated proteins (see Hooper and Thuma, 2005). Indeed, a more salient question might be why vertebrates do not have paramyosin.

Following through; OP's questions seems poorly posed. Indeed, sustained contraction is nothing special. That's what muscle tone is.

From an anthropocentric position, though, it's a fair question, although as I point out the better question is why we can't contract consistently but many invertebrates can.

Yeah I'm confused by your point. Paramyosin is not involved in catch. Contracting consistently isn't difficult if you think about rigor tonus.


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Can replication occur if DNA is methylated?
Can a methylated strand of DNA be replicated without removing methylation? Does it make any difference if the strand is methylated or not (during replication)?

Don't have sources at the moment, but as far as I know: Yes. Methylated DNA cannot only be replicated, but it can also be passed on to subsequent generations as part of the Epigenetic info inherited by the offspring.

Absolutely.  It's a pretty cool process, actually.  Most (well...) DNA methylation occurs in the context of what are called CpG; that is, a C (Cytosine) followed by a G (Guanine).  Because C and G are the Watson-Crick pair for each other, the sequence on the opposite strand will also be CG.  Usually, both Cs are methylated, which turns out to be rather critical for maintenance of methylation.
DNA replication occurs through a semi-conservative mechanism, which means each old, original strand is copied and paired with a new strand.  The new strand has no methylation on it, however; it is at this point that the enzyme DNA methyltransferase (DNMT1, specifically) comes into play.  DNMT1 finds the CpGs methylated on one strand ("hemimethylated") and methylates the other strand, providing complete inheritance.  Here is a nice summary, and this is a review that (briefly) summarizes the evidence that CpGs may play a role in irigins of replication (the jury's still out).

Thanks for the answer !In PCR ,do we always use methyated dna ?

@biogirl I dunno, do you?  Theoretically your input sequence, if it's straight genomic DNA from an organism, could/should be methylated, but DNA polymerase does no methylation at all; that is done by DNMT1 and others, and is much slower than replication.  After PCR, none of your product will be methylated.

I have never done a PCR :) If I take DNA from an organism like human(whose DNA is naturally methylated) and then deliberately demethylate it, can it get replicated in PCR or in a cell ?

Sorry, that's what I was trying to say above, you can't.  PCR is pretty straightforward, it's basically just DNA polymerase.  Each strand of DNA is split and copied, over and over.  As I said above, DNMT1 adds methylation, not DNA polymerase, so none of your PCR product would be methylated.  Adding in DNMT1 after each cycle would be prohibitively time consuming.


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Function of papain in papaya
I know that papain is a proteolytic enzyme present in papaya. It is often used to tenderise meat.  What is the function of papain in papaya?  Is papain sweet? Does it function as an antibiotic?

Papain is a cysteine protease, for which Wikipedia should be sufficient:

Cysteine proteases play multi-faceted roles, virtually in every aspect of physiology and development in plants such as in growth and development, in senescence and apoptosis (programmed cell death), in accumulation and mobilization of storage proteins such as in seeds. In addition, they are involved in signalling pathways and in the response to biotic and abiotic stresses. In humans they are responsible for apoptosis, MHC class II immune responses, prohormone processing, and extracellular matrix remodeling important to bone development.


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Transfer of antibodies in breast milk of humans
Why isn't the IgA secreted in breast milk digested due to proteases of the digestive system in the baby?
Wikipedia says:

The secretory component of sIgA protects the immunoglobulin from being
  degraded by proteolytic enzymes, thus sIgA can survive in the harsh
  gastrointestinal tract environment and provide protection against
  microbes that multiply in body secretions.

But what exactly does the secretory component do?  What is the secretory component?  Is IgA absorbed in the circulation of fetus? I remember reading it somewhere that it is not absorbed, at least in humans. Please answer these questions focusing more on humans. Though, information about other animals will be appreciated as well.

I haven't read it through, but maybe this might help: http://www.ncbi.nlm.nih.gov/pubmed/8292260

It is!  Here is an amazing review from 2011 that literally has all the answers.  I'm not kidding, all of them.  I would marry this review if I could.1  It also includes information on other animals.
The main takeaway is that IgA from milk is not readily absorbed by the infant body.  Secreted IgA is mainly to provide a protective coating for the mucosa while the infant is developing its own nascent immune system.  IgG passed along from the placenta (your other question) provides the main source of absorbed antibodies.  As it says in the review:

Milk sIgA is not taken up by the infant’s intestinal mucosa. In fact, gut closure in humans occurs before birth and little immunoglobulin is absorbed intact in the intestine after birth. However, the presence of sIgA in the intestinal lumen is part of the protective function of the epithelial barrier in the intestine... Secretory IgA is considered to be the primary immunoglobulin responsible for immune protection of mucosal surfaces such as the intestine.

In terms of enzymatic activity, the digestive system will in indeed chomp up the antibodies; that's part of the reason breast feeding should continue as needed.  That's okay, because there's plenty to go around:

Much of the immunoglobulin consumed in an immune milk can be expected to be partially or completely digested, however some portion of the immunoglobulin will remain intact or at least partially intact and capable of binding to an antigen.

It turns out that immunoglobulins are moderately resistant to digestion, at least more so than other milk proteins.  There's a section in there detailing some experiments where Ab was given to individuals:

In adult humans consuming a bovine whey protein concentrate, approximately 59% of IgG and IgM was detected by radial immunodiffusion from effluents from the jejunum, while 19% was detected in the ileum. These estimates of digestion of immunoglobulin compare with estimates of digestion of milk proteins in adult humans which are approximately 42% complete at the end of the jejunum and 93% complete by the end of the ileum, again underscoring the relative resistance of immunoglobulins to digestion in the gastrointestinal tract.

Digestive enzymes vary as to which antibody they prefer to digest, but at least some of them will technically digest the antibody, but still leave functional Fab fragments, which are still immunologically active and useful to the infant immune system.

1: Did I mention I love this review?  I love it.


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How long human can survive with just drinking water everyday
Can humans live without eating food, just by drinking water?  How long can we survive just by drinking water everyday?

116 "Singh finally heeded a resolution of the Congress party and the request of his father, ending ended his 116-day hunger strike on 5 October 1929"
You can see this on: link: http://en.wikipedia.org/wiki/Bhagat_Singh In section: "Hunger strike and Lahore conspiracy case" last paragraph

About 52 to 74 days according to hunger strike wiki page.
This wiki page bases its data on 8 persons who died due to hunger strike:
Days survived by each person: 66, 59, 61, 61, 61, 46, 71, 73, 62, 60.

@RhysW: Last line of Medical View says: There are examples of hunger strikers dying after 52 to 74 days of strike.

nice find... I imagine the average is a bit lower than this, but the record kind of tells you how long we can endure without food if we're well hydrated and not otherwise stressed.

This timeframe is similar to one mentioned in malnutrition lectures I've had

This would vary a LOT depending on the amount of stored fat, previous diet, the weather and even the water drunk.  Weeks though there is a good chance that a loss of electrolytes can cause health problems.  (that's why I mention the water you drink, because many bottled water brands and wells have a bit of salt in them.)
Its hard to say from anecdotal experience. There are claims of 3 weeks being easy, but a medical study would be unethical because of the risks posed to the subjects.

You can remember this easily as the rule of threes:
You can survive:

3 minutes without air. (death by asphyxiation)
3 hours without shelter (death by hypothermia, heatstroke).
3 days without water. (death by dehydration)
3 weeks without food. (death by starvation)

Going beyond those guidelines will generally do you permanent damage.
Further reading: http://www.wildernesscollege.com/basic-survival-skills.html

Hi cpendlebury, here at Biology.SE we like answers to reference the claims they make.  For more information on this, see meta.

Noted and fixed.

1 year and 17 days only on water and electrolytes.
Actually, he went water only for about 75 days (read that elsewhere, can't remember) and then they supplemented his water only diet with electrolytes. He's done it under medical supervision and gained 7 KG in 5 years after the fast. So the weight does stay off (obviously, if you go and stay into a healthier diet).

"He did not eat any food, but the staff gave him yeast for the first 10 months and multi-vitamins every day. Potassium is essential for the proper working of the heart, and when his potassium levels got a little low around the 100-day mark, he was given potassium tablets for about 70 days."  Certainly not just water.

@Amory Well, if it's any consolation, he pushed further than anyone mentioned here on water alone. I've also read this in a research PDF and they mention at least 75 days on water alone. If I'll find it again, I'll link it here.


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Difference between mutation and DNA damage
What is the strict difference between mutation and DNA damage?  As far as I understand it, a mutation is an alteration in the genetic sequence, having "tricked" the repairing machinery and thus getting replicated in the future.  DNA damage, on the other hand, is any alteration of the DNA molecule including breaks, chemical alterations of the molecule, etc.
Then, are mutations considered a type of DNA damage?  I would thank the strict definition of both concepts.

Have you read the DNA repair article on Wikipedia?  The DNA damage and mutation section answers exactly what you're asking:

DNA damages and mutation are fundamentally different. Damages are physical abnormalities in the DNA... [and] can be recognized by enzymes, and, thus, they can be correctly repaired if redundant information, such as the undamaged sequence in the complementary DNA strand or in a homologous chromosome, is available for copying.... In contrast to DNA damage, a mutation is a change in the base sequence of the DNA. A mutation cannot be recognized by enzymes once the base change is present in both DNA strands, and, thus, a mutation cannot be repaired.

Here's the entry from the NCBI MeSH Glossary saying the same thing:

Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION... They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR).

And for mutation:

Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.

Usually a mutation occur when one strand got a modified base and the enzyme correct it by choosing the "wrong" strand as a template, therefore both strands are modified and there is nothing to repair anymore. Is it correct?

Basically, yeah.  Errors in the DNA repair enzymes themselves will allow a whole mess of trouble.

i did read the article, but i wanted a more reliable answer as sometimes wikipedia might lack precission

@JunkDNA I won't argue with you there, but for definitions it's usually spot on.  Still, I added the appropriate definitions from NCBI.


text:
Do T-cells express MHC molecules?
T-cells recognize the MHC molecules and body's own peptides. When it doesn't, it alarms the immune system. But do T-cells express MHC molecules ? If so, how are they using it? If not, what happens when a virus infects T-cells? (Yes, I am confused about HIV infection mechanism too. They escape from immune response by altering their genes and disrupting the MHC-peptide bonding. I can see that this can work in macrophages. But what is the situation in T-cells ?)

They express MHC1.

They do not express MHC II molecules.

It is incorrect to say that T-cells do not express MHC class II molecules. Please see: https://www.ncbi.nlm.nih.gov/pubmed/15120183

There are two types of MHC molecules:
All nucleated cells express MHC class 1 proteins.  A sample of all proteins produced within the cell are 'sliced' into their constituents which are then presented by MHC-I receptors.  This means that if a virus infects a cell, the foreign proteins the cell is induced to make are expressed on the cell membrane by MHC-I.  This is important as antibodies can not cross cell membranes, therefore this is the method by which a cell signals that it is infected by a virus.
MHC II are the special molecules that are only expressed in antigen-presenting cells, which I think is what you are referring to.  As neither CD4 or CD8 T-cells present antigens, they do not express MHC-II themselves.  Instead CD4 have receptors for MHCII  (while CD8 have receptors for MHCI), allowing them to interact with antigens presented by other immune cells.
If a virus infects T-cells, the viral proteins are sampled by the MHC-I pathway and presented via MHC-I on the surface of the infected T-Cell.  The immune response then progresses as for any other virally infected cell, destruction by CD8 T-Killers that destroy the cell by non-phagocytic means.

Are you positive CD4 cells don't present antigens? I could have sworn they had the capability to.

@MCM that was off the top of my head, I'll have a read of my notes tomorrow.  Happy New Year!

Are antigen-presenting cells a specific type of cells? I've always been confused about this because the label seems so general.

@shigeta I would say they're a class of cell, defined by their expression of MHC-II.

I would expect that they do something else besides only presenting antigen - is that their only function?

Antigen-presenting cells include dendritic cells, and B-cells, but there are more: http://en.wikipedia.org/wiki/Antigen_presenting_cells

"All nucleated cells express MHC class 1 proteins." - This is a pretty bold statement... :D At least I would add "human cells"...

I believe this is the better answer, though I recall this being a debated issue. Some MHC class II molecules are found on at least some subtypes of T cells, though it is (at least was) unclear whether they acquire them through expression or from other cells.
http://www.jleukbio.org/content/63/6/707,
http://www.bloodjournal.org/content/101/7/2704,
http://www.ncbi.nlm.nih.gov/pubmed/7522009,
http://www.sciencedirect.com/science/article/pii/S1074761305003006


text:
What are the differences between G+ and G- bacteria?
The distinction between Gram-positive and Gram-negative bacteria is based upon the Gram staining method, that reflects the bacterial wall physical properties.
However, this classification involves also a large number of differences between them. For example, the endospore formation usually occurs in Gram-positive bacteria and also the quorum sensing mechanism is different.
So what are those differences? Which of them are due to the cell wall thickness and membrane(s) composition and which instead to evolutionary divergences?

here's a partial answer... http://biology.stackexchange.com/questions/7118/what-are-gram-negative-and-positive-bacteria

I didn't know there were distinct differences between gram-positive and gram-negative bacteria when it came to quorum sensing, but it seems as though there are:

In gram negative bacteria, acyl-homoserine lactone type molecules serve as the main signalling molecules while lipid, peptide, and amino acid based signalling molecules infrequently serve as signalling molecules. Furthermore, in gram-negative bacteria, there is one well conserved mechanism for controlling quorum response. Gram-positive bacteria, on the other hand, use peptides or modified peptides as the primary means of signaling; and also differing from gram-negative bacteria, there are several different mechanisms found within the class which are used to gain quorum responses.

Source.
In G+ bacteria, the two main quorum sensing mechanisms are apparently as follows:

Two-component signal transduction, in which the peptide signal works by binding to a sensor protein, histidine kinase, located in the cell membrane of the bacterium. The activation of the histidine kinase leads to phosphorylation of response-regulating protein, and interaction with another regulatory protein facilitates transcriptional activation.
Internalization, in which the signal molecules are transported into the responder cell to interact with intracellular effectors.

G- bacteria on the other hand, synthesize autoinducers, effector molecules that can diffuse freely through the cell membrane and trigger cell response when a certain concentration threshold is reached. I do not know how or if these differences are related to cell wall structure.
When it comes to endospore formation, all I know of the difference between the two is that this is by far most common in gram-positive bacteria.


text:
How to understand influenza strain designations?
What do the strain designations for flu mean?
For example avian flu is classified as H5N1, what do the letters H, N and numbers 5, 1 mean? Is it more than a simple string-identifier?

The sub-type is named for the broad classes of the hemagglutinin (HA) or neuraminidase (NA) surface proteins sticking through the viral envelope. There are 16 HA sub-types (designated H1 - H16) and 9 NA sub-types (designated N1 - N9). All of the possible combinations of these influenza A subtypes infect birds, but only those containing the H1, H2, H3, H5, H7 and H9 and the N1, N2 and N7 surface proteins infect humans, and of these, so far, only H1, H2, H3 and N1 and N2 do so to any extent.
Read more: http://www.fluwiki.info/pmwiki.php?n=Science.NamingInfluenzaViruses

Subtype is denoted using the HxNy notation for the variant of hemagglutinin and neuraminidase.
Strain names are specified as: [virus type]/[location of origin]/[sequential number of isolation]/[year of isolation] ([subtype]), such as "A/Alabama/AF2070/2010(H1N1)"

Virus type would be A, B, or C for the various forms of influenza (influenza A being the most common among humans)
Location can be a country, state or city (e.g. Laos, Alabama, or Moscow)
The number of isolation can be a simple number, but sometimes it goes beyond; e.g. "AF2060" or "UR06-0455", possibly due to the tremendous number sequenced nowadays.
Year, obvious.
The subtype refers to the aforementioned HA/NA subtype.

Many more strains can be found on the Influenza Research Database.

The two letters represent the type of hemagglutinin (H) and neuraminidase (N) present on the viral surface. Those are the major surface proteins of the influenza virus and therefore crucial for the immune response.
From Immunology and Evolution of Infectious Disease

HA and NA reactivities with antibodies define the subtypes of
  influenza A (Cox and Subbarao 2000). Fifteen different HA antigenic
  subtypes occur, each subtype cross-reacting relatively little with the
  other subtypes. Nine distinct NA subtypes are known. The designation
  HxNy describes an influenza subtype with HA antigenic subtype x =
  1,...,15 and NA antigenic subtype y = 1,...,9.

The numbers represent different subtypes of the hemagglutinin and neuraminidase proteins.

Adding to the other answers posted:
Hemagglutinin  (HA or H) -  Helps the virus enter the cell by binding to sialic acid receptors on cell membrane. It then unfolds in a lysosome and fuses the viral and lysosome membranes.
Neuraminidase (NA or N) - Helps the virus exit the cell by cleaving the terminal sialic acid residues at the progeny virus release.


text:
Would Bubling Oxygen Through "Dead Zones" Like A Fish-Tank Make Much Difference?
I am a dilettante when it comes to dead zones. I realize that they vary from fleeting algal blooms to continuous dead zones. For the continuous dead zones it would seem to me that adding a "bubbler" like for fish tanks might help restore the depleted oxygen content, which would increase microbial activity and thereby increase the quantity of nitrogen removed from the water (hopefully) before it reaches the open ocean where the fleeting algal blooms occur. Has this been investigated or could it at least be assessed from a scientific perspective?

algal blooms consume all the oxygen in the water to make it anoxic.  You'd have to bubble a lot of oxygen into the water.  It probably depends on the nutrient mix in the water.  If the algae can continue to grow and consume the oxygen as you bubble it in, then it won't help.

@shigeta If the algae continue to grow and consume oxygen, they they are also consuming nutrients that would otherwise contribute to algal blooms and/or dead zones. The idea is essentially to exhaust the runoff nitrogen through speeding algae growth - not necessarily to instantaneously solve the problem of dead zones. This should reduce the extent of dead zones.

i see.  it would take some work to figure this out - it might end faster but in any case i'd be surprised if all the other living things aren't dead by then.  is the goal just to end up with a little nitrogen in the water?

@shigeta The goal is to remove nitrogen from the river water, since in the open ocean nitrogen is the limiting  reagent for algal growth.

Actually, if you could get the oxygen in there, you would probably turn the dead zone into a "feast zone," because all that algae would be food.  But I think it would be prohibitively expensive.  Fish tanks aren't deep, so it doesn't take much pressure to force air bubbles into the bottom.  And they're not large in volume, so you don't need huge amounts of air bubbling.  Oceans, or even rivers or harbors, would be another matter.
Also, some of the algal blooms are poisonous "red tides."

Going from our comment train I thought I'd put this into an answer.
This is similar to the proposal to dump iron into the sea as that's also supposed to be a limiting reagent for growth.  There the goal was to sequester carbon from carbon dioxide as dead plankton which would sink into the depths of the ocean.  I'm assuming they did their home work and the cost of producing iron metal, which uses a lot of oxygen is actually worth it.
Its interesting to observe here that oxygen depletion was not a concern here.  Assuming they have done enough work to show that iron is the only reagent needed to induce the algal blooms, that's a different angle on the problem than you propose.
In any case the critiques are many because of the scale proposed are likely to create other unanticipated side effects, not the least of which is the massive release of the powerful greenhouse gas nitrous oxide.
The iron dumping experiment was mostly rejected because it was too simplistic.  So, this proposal would require a model - there's no simple back of the envelope calculation that would give a thumbs up/down on this proposal.  The question is - what's the next limiting factor after oxygen/nitrogen?  I'd be surprised if that was not dependent upon location climate and local water chemistry.
A lot of red tides are caused by fertilizer and sewage dumps so you may be on to something here. If the goal is to remove nitrogen from the water, not only would it work, but would the cost be reasonable for what you're hoping to get?
Unless someone has already built the model I'd guess it would be up to you.

The iron dumping was shown to be quickly removed from the seawater through its incorporation into some component of the algae that then sank: much like nitrogen. I think the iron might have been incorporated into a shell of some sort as part of the algae--possibly mixed in with CaCO3 or something. That was the reason Iron dumping was abandoned: it was hoped the iron would remain in the ocean ecosystem for longer.

My point is just that your proposal is probably deserving of more thought - similar sorts of questions would have to be answered before the proposition would be considered valid.  I myself couldn't find any preliminary work on this. and it does seem to be the case that they might have already considered oxygen. best of luck.

Bubbles have actually been tried as described on Wikipedia. Usually the issue is layer stratification where the top layer has oxygen but the bottom layer where the decomposition of algae takes place lacks oxygen. Therefore mixers have been employed to bring the de-oxygenated water to the surface where it naturally re-oxygenates. It is interesting to note that one proposed and highly experimental idea is to use mixers to bring cold water from below to reduce the surface temperature to prevent or weaken hurricanes.

During heavy rain, London's sewage storm pipes overflow into the River Thames, sending dissolved oxygen levels plummeting and threatening the species it supports.[14] Two dedicated McTay Marine vessels, oxygenation barges Thames Bubbler and Thames Vitality are used to replenish oxygen levels, as part of an ongoing battle to clean up the river, which now supports 115 species of fish and hundreds more invertebrates, plants and birds.[14]
The dissolved oxygen concentration within Cardiff Bay are maintained at or above 5 mg/L. Compressed air is pumped, from five sites around the Bay, through a series of steel reinforced rubber pipelines, laid on the beds of the Bay and Rivers Taff and Ely. These are connected to approximately 800 diffusers. At times this is insufficient and the Harbour Authority is using a mobile oxygenation barge built by McTay Marine with liquid oxygen stored in a tank. Liquid oxygen is passed through an electrically heated vapouriser and the gas is injected into a stream of water which is pumped from, and returned to, the bay. The barge is capable of dissolving up to 5 tonnes of oxygen in 24 hours.[15]

Water Aeration


text:
Do you know of any disease where HLA / MHC association discovery has led to better treatment or management?
If we discover an association between a disease and a particular HLA type (MHC class I or class II molecule) then it may provide us with some insight into the disease in a very basic way. However, will it provide us with a therapeutic target? Or second best, will it provide us with information that is useful for diagnosis or management? I am looking for examples. Do you know of any?
The most obvious is in transplantation where one would use HLA typing to match donor to recipient but that is not the same as using knowledge of an HLA type to target, treat, diagnose, prognosticate.

I don't know any true disease associations, but since this question still has no answers, I'll offer one...
One class of associations you might be missing is difference in drug response. Patients with HLA-B*5701 are known to be hypersensitive to abacavir. Genetic screens are available to screen for this allele, and this information is used clinically.

Actually it can help by curing specific types of cancer e.g. Chimeric Antigen Receptor–Modified T Cells in Chronic Lymphoid Leukemia. But ofc. it does not help in every case. You can live without B-cells, but you cannot live without liver...
So yes it can be used by designing a therapy for a disease, if that's the question.

Bone marrow transplant for leukemia and multiple myeloma.
Uses extensive HLA typing like you said are you looking for additional diseases?

That is just a matching process so that the graft does not attack the host. I am seeking an association between some form of a HLA which makes for a therapeutic target.


text:
What is the evidence that australopithecines were bipedal?
Before the discovery of Australopithecus afarensis in the 1970s, most anthropologists believed that an increase in brain capacity had preceded bipedal locomotion. However, this reconstruction of the Lucy skeleton shows that the A. afarensis was bipedal even with a brain size of around 400 cc.
But the actual Lucy skeleton does not include feet, and only has two partial leg bones.
How do anthropologists determine, based on the bones preserved, that A. afarensis was bipedal?

Lucy does however have knees, which are more informative than feet, her knees are locking straight knees like ours.

Mainly because of the characteristics of the pelvic joint with the femur and the foramen magnum (the hole the spinal cord uses to connect with the encephalon). Also, there are more specimens other than Lucy, and there also exist fossil footprints (for instance the Laetoli footprints). All this evidence points to a bipedal walking.

Source: http://www.talkorigins.org/faqs/homs/pelvis.html
As you can see, the Asutralopithecus pelvis resembles human pelvis more than chimpanzee's (wich is adapted to a primarily quadrupedal movement).

Source: https://web.archive.org/web/20160817080843/http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/P/Primates.html
In this image you can see the position of the foramen magnum in a typical pure quadrupedal mammalian, such as a dog. The foramen inserts in the posterior part of the cranium. In the human, the foramen inserts in the base of the skull, due to de erected position. In chimpanzees, which have quadrupedal march, but can also display some bipedal movements, the foramen is slightly displaced towards the basis of the cranium, in an intermediate position between both.

Source: http://www.fcnym.unlp.edu.ar/museo/educativa/serypertenecer/principal/australopitecinos.html (Spanish)
In this image it shows the foramen in chimpanzees, Australopithecus and modern humans, and you can see that the position in the second is at the base of the skull, just like in Homo.
It is assumed that the bipedal locomotion is an adaptation to the savanna environment, where trees were rare. Bipedalism also allows a better visual field and it has more energetic efficiency.

It would be great if you could add citations for where the information and figures come from.

This is a great question and one we should all be asking. Given that our closest relatives the great apes are all quadrupedal, our ancestors at one point must have also been quadrupedal. In fact we as humans are mainly quadrupedal between our first nine to fifteen months of postnatal life. As adults we still engage in quadrupedal behaviors from time to time. For instance, humans often copulate, climb steep hills and walk through thick underbrush on all fours. Because all great apes also engage in bipedal behaviors the difference between us and them is one of frequency. As adults we are much more likely to be bipedal while great apes are much more likely to be on all fours. Because changes in behavior precede changes in structure, to diagnose fossil behaviors we use characters that change during the individual's lifetime in response to practiced behaviors (i.e if we used characters that are mainly inherited to diagnose behaviors we would not know if it is the fossil in question that practiced these behaviors or an ancestor of the fossil that did). In the case of Lucy we can use the x-sectional area of the arm bone vs the x-sectional area of the lumbar vertebra. Bone x-sections change during our lifetime in response to the loads placed on them.  Because bipeds place all their upper body weight on their lower back vertebrae and none on their arms, while quadrupeds distribute their upper body weight on their arms, it would be expected that a biped have a much larger lumbar and smaller arm x-sectional area than a quadruped. This expectation is confirmed in comparisons of humans to great apes, or to baboons and other large monkeys. Notably, Lucy shows ratios that are most similar to baboons (a small lower back and large arms) suggesting it wasn't mainly a biped but often practiced quadrupedal behaviors. Lucy does not preserve a foramen magnum and shows no pelvic characters that are exclusive to bipeds. As you note it only preserves a thigh bone, a leg bone, a single foot bone and two toe bones, none of which show exclusively bipedal characters. The foot bones of the first family fossils which are ~200,000 yrs older than Lucy and have been assumed to be the same as Lucy(but may not be) show a gorilla-like foot.
Unfortunately, paleontologist would not gain as much fame or money if they found a possible ape ancestor.  As such to be able to claim it is human they claim these fossils are bipeds using whatever human-like characters they exhibit to associate the fossil to bipedality. More than likely Lucy represents an African great ape that diverged from the common human African ape group around the time of the chimpanzees/gorilla/human split. Lucy is thus a human ancestor and a biped for convenience sake and not based on facts.

It would be great if you added some references to support your response!

it is not just a matter of frequency the way humans stand and the way chimps stand is completely different. humans and lucy can both straighten our knees for instance. you have to break a chimps knees to get them in that posture.

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


text:
Can an influenza virus carry other infectors with it?
This idea came to my mind when thinking about how many people become ill in many locations with similar symptoms (fever and rough cough) from Influenza.
There are of course different types of influenza virus.
Can Influenza A virus work as a vector for other upper respiratory infections?
That is, much the same as the mosquito being a vector of malaria, can an influenza virus carry other infections with it?
If so, how? If not, why do some people get so sick from viral influenza, and not others?

What do you mean by vector? That it can cause other respiratory infections?

@Chris No. That it can help transport other respiratory infections which cause other respiratory infections.

Transport in the way that it helps a secondary infection to get into the upper respiratory pathways because the immune system is already dealing with influenza?

I think the meaning is much the same as the mosquito being a vector of malaria, "can an influenza virus carry other infectors with it?" @chris

I don't think there is a reason to close this question. I think it's better to ask for clarification first.

I agree with @Chris - it should get a chance to get clarified first.

@Masi - please feel free to roll back. I tried to keep it in the spirit in which it was asked.

@anongoodnurse Thank you for edits which make the body clearer! No need to rollback.

I wouldn't call influenza a vector here, but yes, an infection with the flu virus which results in a full infection can have secondary infections as complications. There are often caused by bacteria which usually live in the respiratory pathway and kept under control by the immune system.
This includes pneumonia (either viral or bacterial), inflammation of muscles and the heart muscle (myositis and myocarditis) as well as pericarditis. Less severe complications include infections like ear infections and sinusitis.
See the references for more details:
References:

Complications of Viral Influenza
Double trouble: Bacterial super-infection after the flu
A Mouse Model of Lethal Synergism Between Influenza Virus and
Haemophilus influenzae

Does this help answering the question? If not, you need to be more specific and I will work on it later today.

It helps. Is it possible that influenza is asymptomatic but it causes opportunistic diseases? This can be one explanation - influenza triggering some infections of upper respiratory tract without itself causing any symptoms. This could explain why influenza is felt differently by different people too.

I don't know right at the moment, but I will look into it. The other problem is the use of the word flu - most people which talk about having a "flu" in fact have something else. Most likely an influenzal infect (which is not caused the the influenza virus). This one feels bad as well but is not as severe and clears much faster (usually within a week, from what I know from my MD colleagues).

A vector transmits a disease or parasite from one animal or plant to another. Fruit bats are vectors for Ebola. They are a host to the virus, which can then be passed on to humans.
Influenza A, the virus responsible for human seasonal epidemics, is not a vector for other pathogens, although co-infection with two different strains of influenza can give rise to progeny viruses with mixtures of genes derived from the parental strains. If anything, that would make humans, other mammals and birds the vectors for Influenza A.[1]
Influenza A doesn't carry plasmids, and it does not insert it's genes into cell DNA as does a retrovirus.
The most frequent serious complications of influenza are pulmonary and fall into 4 categories or groups:

primary influenza pneumonia
secondary bacterial pneumonia (also called co-infection, but from different sources)
pneumonia due to unusual pathogens or in immunocompromised hosts
exacerbations of chronic pulmonary diseases

Typically, the first group is smaller than the second (except for Avian Influenza A). No additional infection is necessary in this group to cause pneumonia or death.[2]
In the second (and largest) group, typically viral influenza infection is followed by near resolution of symptoms, subsequently complicated 4 to 14 days later by a recurrence of fever, dyspnea, productive cough, and pulmonary consolidation. Common pathogens are S. pneumoniae, S. aureus (methicillin-sensitive [MSSA] or methicillin-resistant [MSSA]), S. pyogenes, H. influenzae, and some others.
The pathogenetic mechanisms of viral-bacterial co-infections result from virus induced alteration in pulmonary epithelial cells (e.g. reduced ciliary function, cell death/decreased epithelial barrier function, etc.), virus-mediated inhibition of innate immune cells (e.g., suppressed phagocytosis, impaired microbial killing, etc.), dysregulated inflammation (e.g. increased inflammation due to chemokines) and other mechanisms.[2][3]
Pneumonia due to unusual pathogens or in immunocompromised hosts, and exacerbations of chronic pulmonary diseases are less common than the second group but carry a high mortality.
The second reference is an exhaustive review which you might find quite helpful.
1 FluGenome: a web tool for genotyping influenza A virus
2 Complications of Viral Influenza
3 The co-pathogenesis of influenza viruses with bacteria in the lung

Yes, I like the second source most: Better use of influenza vaccines and antivirals
may decrease risks of pulmonary complications, but
novel prevention and treatment strategies are needed to
improve outcomes for those at highest risk. This proposes me that all coinfections caused by influenza A virus are not known or cannot be protected by the usual influenza vaccine. Meta-analysis of the development of influenza vaccine would be great. I have the general idea that newer vaccines include just recent developed strains. I am not sure if this is best approach, since some do not have old ones.

While a viral infection such as influenza can lead to secondary infections, it is inappropriate to call it a vector for those other infections. It is not the means by which those other infections are acquired. If a bacterial sinus infection follows upon a bout with the flu, that bacteria was not carried to the patient by the influenza virus. A single bacterium is immense compared to any virus. No, the bacteria most likely resided within the host before the infection, but it was under control. Or it might be introduced during the infection and find a foothold it would not have likely found in a healthy host. In a situation like this, the immune system is distracted and weakened enough to present an opportunity for this bacteria to grow out of control into an infection.
The bacteria in this scenario are a little bit like the annoying hordes of roofing contractors that recently swarmed my neighborhood after a hail storm. These guys are always around, looking for the occasional roof that might be getting old and need repair. But right after a hail storm, they find a lot more of the opportunities they are looking for. So suddenly they are all over the place. They didn't literally fall from the sky with the hail. But the hail presented the opportunity they needed to thrive.
Malaria is a microscopic germ which hitches a ride inside a comparably enormous mosquito to find it's way eventually into a human blood stream. An influenza virus is too small for anything infectious to hitch a ride inside it.

love the roofers analogy

Except the roofers are symbiotic.

@vajra78 OK. Most of these roofers are symbiotic. But let's say some are parasitic. They are extremely crooked, unlicensed fly-by-night businesses that take advantage of the home owner. They use substandard materials, and then disappear after collecting initial payment without even finishing the job. Symptoms may include drained funds, uncovered roofs, and water-damaged homes. They cannot thrive in an ordinary environment as reports of their misdeeds and lawsuits catch up with them. But after a big hail storm, the volume of need allows them a temporary foothold.

Contrarily to the main opinion expressed so far, I would say that, in theory, it is possible that an Influenza virus can be a vector for another virus.
Here is a paper about using influenza virus as vector for a variety of genes.
The same method can be leveraged to engineer an Influenza virus particle that contains, for example, genes coming from another virus. Upon infection, the Influenza virus will infect the host cells with both genomes.
In this way you will end up with an Influenza virus that act as vector for another virus.
However, such a hybrid looks very unlikely to occur in nature.
But it can be certainly made in lab.

Excellent article! Thank you for your answer! Please, add further articles and/or books if there are some which could be useful to understand this case better.

There are tons of similar articles for many different viruses. In molecular biology they are called viral vectors. Its a virus used to transfer DNA to a target cell. Just google viral vectors and you will have a nice overview.

In bacteriophage, the viral capsules serve as vectors for other DNA so frequently that there is a common name for this: transduction. The image below, from the Wikipedia, illustrates the basic process. Here a phage, with pink DNA, accidentally packages up other DNA -- in this case, from the bacterium -- in one of the capsules and thereby serves as a vector for this DNA.

Something a bit like this happens any time we have recombinational assortment in the influenza virus. The influenza virus genome segmented, with 8 "chromosomes". When an individual is multiply infected with different strains, new combinations of the 8 chromosomes can be packaged up within an given viral particle. This process is often responsible for new epizootic strains.
In principle, genetic material from another virus could be packaged up accidentally into an influenza virus particle. If it happened to enter the right kind of cell, the influenza capsule could in that way act as a vector for the other virus's DNA. In practice, I would imagine that this would require remarkable coincidence and thus would be extremely uncommon in nature.

+1 for picture and new proposal! Is this method of bacteriohpage the one of most likely methods how influenza could act as a carrier? Can you relate it to alec_djinn's answer?


text:
What hair color will result in someone inheriting both blond and ginger genes?
Both the genes for blond hair and ginger hair are recessive, so they need both parents to give the same gene for it to take affect. What happens when a person has 1 copy of a recessive gene and another copy of a different recessive gene.
They don't have enough of the recessive genes to have either blond or ginger hair, but they don't have a dominant gene to "take charge"?

Hair color is not so simple as that.  Most traits, especially those as complex as color, are controlled by many alleles at many loci.  That's why there are different kinds of brown, blond, and red hair in the population.  There is no "hair color gene."  A fascinating paper came out a few years ago, identifying dozens of SNPs playing a role in hair and eye color.  It's a deep, deep rabbit hole that we have only begun to plunge into.
EDIT: To summarize, it's very complex.  This paper performed genome-wide association scans looking at two comparisons each for eyes (Blue and green, blue and brown), hair (red or not, blond or brown), and skin (freckles, sun-sensitivity).  The researchers looked in a group of Icelandic and Dutch individuals, which means they only looked at a small portion of human variability (i.e., very few African or Asian genomes, for example).  Still, just from those simple comparisons, their scans:

revealed 104 associations that reached genome-wide significance, accounted for by 60 distinct SNPs, of which 32 showed genome-wide association with only one pigmentation trait, 12 with two traits and 16 with three traits.

That is to say, they found 60 DNA bases that explained their data.  Roughly half of those only affected one thing (eye, or hair, or skin, but only one), a fifth of those single base changes contributed to two different traits, and a full 25% of those SNPs were related with three traits.
That's still pretty hefty.  Basically, they found 60 things that can affect hair, eye, or skin color, and some of those can affect some or all of those at the same time.  And they only looked at people from two countries.  Here's a figure where they summarize the seven strongest SNPs; you can see how tricky it can be to explain colors.

Wait, so Game of Thrones gets its genetics wrong!?

Yeah, that always bugged me.  Also, there are dragons.

I don't have access to the paper. And I doubt that I have the knowledge to understand it. Could you please explain shortly how hair (and eye) color is determined.

@IlyaMelamed Hopefully that helped!

Thanks. just 1 last question. What is the meaning of the stars on the figure?

@IlyaMelamed Asterisks mean highly significant.  In this case, it means there is a less than a 1 in 100 million chance that those findings occurred due to chance.


text:
Does the human body convert water?
I just read Andy Weir's "The Martian" (which was very good) and one line made me wonder:

[...] a human body only borrows water.

Is that true? Does all water "that goes in, go out"?

Water is "created" and "destroyed" in biochemical reactions in the body all the time. The overall water balance, as described below, stays at a relatively steady state, but any one water molecule entering the body may be used as a proton (Hydrogen) donor, to make a hydroxyl (-OH) group, etc.

Yes, the human body "converts" water.
Out of the hundreds of chemical reactions going on in the human body, there are reactions which take water as an input and "react it away" into something else. There are also reactions which create water out of other molecules.
Example 1: Hydrolase reactions. They have the form of

A–B + H2O → A–OH + B–H

You get water as input, and something else as output.
Example 2: Peroxidases "defuse" the highly reactive hydrogen peroxide, producing water. For example, look at the L-ascorbate peroxidase, which catalyzes

L-ascorbate + H2O2 → dehydroascorbate + 2 H2O

Beside these reaction, there is also a lot of water which doesn't react and is simply excreted after having served its purpose. So, while some water is "converted", some other part "passes through".
The reactions are balanced in such a way that normally, you excrete the same amount of water as you drink, as explained in Amory's answer. But despite this balance of the amount, you cannot claim that the water just passes the body unchanged. Some molecules of it are used up, and others are created de novo.

Yes, essentially, but in practice you need to consider the context of the novel.[1]
Your body needs water every day - somewhere around 3 liters is sufficient for baseline activity - in order to maintain balance due to obligatory losses.  Here's a figure that sums it up (it has a few errors, see below):

That whole online textbook chapter might be of interest, but that figure has a few errors.  If you look, the numbers at the bottom for output aren't summed up correctly, and the value for transpiration is repeated.  Doing the math on the correct numbers gives 2500 ml output for the 2500 ml input.
So yes, input and output are roughly equivalent.  You and I need new sources of water every day since our urine isn't something we'd like to drink, but Watney has a "water reclaimer" and lives in a sealed environment[2]; his entire world is one small, well-balanced water cycle.

[1]: For the uninitiated, "The Martian" is a novel and soon-to-be-movie about Mark Watney, an astronaut stranded on Mars who must use his ingenuity to survive as long as he can.  The context of that quote is the need for hydrogen, which Watney will get by hydrolyzing his urine.
[2]: Well, most of the time anyway.

So all the $H_2O$ that goes in, comes out as $H_2O$?

Actually, more comes out than goes in: metabolic water is synthesized by the organism.

@NickRussler no, that's wrong. There are several metabolic reactions which require water as input, for example the esterase activity comes to mind. So, when looking at a specific water molecule, it is very much possible that it is consumed, and then reacts to something else, without being excreted as water. What this answer says is that the amount of water going in and out is balanced, not that all water passes through the body unchanged.

@NickRussler As rumtscho said here and in the other answer, it's not the same water molecules, but it's the same amount.  If you look at the diagram, you'll see that plenty of the input water is from food that we eat, not just liquid water.


text:
Why does flu vaccination only work against specific strains?
I was wondering why the flu vaccination doesn't protect us from all different types of flu. I know there are 3 major groups A, B and C and they mutate really fast. For example Influenza A virus has 2 different proteins on the surface hemagglutinin (H) and the neuraminidase (N). There are 18 different hemagglutinin subtypes and 11 different neuraminidase subtypes. So if they produce a vaccination which covers 187 of the virus (from H1N1 to H18N11) wouldn't it mean that the Influenza Type A could be eradicated from the world ? And wouldn't it work the same way for Type B and C?

I'm going to try and focus on the latter part of your question; if you want to know why the tri- or quadrivalent flu vaccine doesn't provide protection like many other vaccines, that's already been answered.
Anyway, the main reason we can't is because there are simply too many.  You say 187 (not sure why, 18*11=198) but the truth is that not all H1s are the same.  The different subtypes constantly mutate, so one H1N1 may not be the same as another H1N1.  There are hundreds upon hundreds of flu types, constantly changing.  And that's not even accounting for type B viruses.
When you make a vaccine, you need a certain amount of protein.  The major quadrivalent vaccine study used 15µg of protein of each strain.  The more protein you put in, the bigger the vaccine, the more it hurts, and the more likely the body is to have a significant negative reaction.  You'd have to test all of them as well - the FDA doesn't usually work on a "three is safe, four is safe, so hundreds is safe" principle.
Plus, you have to MAKE all that protein.  We're not very good at making enough for the tri- or quadrivalent vaccines now, much less hundreds or thousands of times more.  We simply don't have the capacity for that level of production.  Even if we could, it's not likely that immunity to all strains would take.  Besides, erradication is unlikely because there are large animal flu reservoirs (avian and swine, most famously) that can and will jump over to humans.  That's the piece everyone forgets about smallpox - with no animal reservoir, it was easy to eradicate.
That's not to say the cause is lost.  Intense research has begun on universal flu antibodies, and it looks somewhat promising.

There is a number of different multivalent vaccines available on the market. This is not really a problem.

There are 18 different hemagglutinin subtypes and 11 different neuraminidase subtypes that have been reported! The point is that many more are present in the overall viral population and some variant will escape the effect of the vaccination. In general however, to cover multiple variants with the same vaccination sounds a good idea.


text:
Does vitamin D affect melanin concentration?
I am aware of the affect on vitamin D production by melanin (in sunlight) but I can not find any information regarding a reverse connection.

Darker skin, as opposed to common belief, probably did not develop as cancer protection. Cancer is usually something that attacks the body in a subsequent life. Even pale individuals under the sun are likely to survive far beyond their reproductive era before they are wiped off by skin cancer.
Instead, it is believed that folic acid manufacturing is the highest selection pressure causing darker skin. Folic acid (vitamin B9) which is used all over the flesh, especially during pregnancy and childhood, will decompose in sunlight.
So the skin tone tries to discover the ideal equilibrium between vitamin D and minimal folic acid breakdown.
As a consequence, if you genuinely have enough vitamin D in your diet, there is no need for lighter skin (and further proof for the vitamin-d hypothesis). That is why the Inuit have lighter skin than expected for their extreme location: the intake of vitamin D is large, so the folic acid part of the equation "wins" and pale skin is not preferable. This is why Inuit individuals do not need so much sun.
Source:
scienceline.org/2007/06/ask-dricoll-inuiteskimos/
pnas.org/content/107/Supplement_2/8962

This is not true. Skin color is highly correlated with UV-radiation, with the highest pigmentation present in areas where the radiation is the highest. This is said in both references, we also know that the skin cancer rates are much lower in people with high pigmentation. Melanin is a very effective protection for your skin. Folic acid is not mentioned in your sources, so please edit them.

@Chris I don't claim to be expert in this area (hence the question) but nowhere did I claimed the absence of correlation of skin color and UV, quite the contrary. Also, nowhere did I dispute, "skin cancer rates are much lower in people with high pigmentation." or "Melanin is a very effective protection for your skin. (regarding cancer)."

@Chris Ctrl+F yields following two paragraphs from each source:

@Chris "The possibility that photolysis of folate by sunlight was a determining factor in the evolution of dark pigmentation was first explored (24) before the full importance of folate in DNA biosynthesis, repair, DNA methylation, amino acid metabolism, and melanin production was recognized. In 2000, we advanced the theory that dark skin pigmentation in humans had evolved primarily to prevent reduction of fertility due to the photolysis of folate present in cutaneous blood vessels (7). We ..."

@Chris "Ultraviolet, or UV rays, from the sun are responsible for activating the melanin. As melanin levels rise and our body’s natural pigment darkens, protection against the sun’s rays increases. Too much UV exposure can deplete vitamin B folate –used by the cells to create DNA. On a smaller scale, the rays can also cause painful sunburns, with too much exposure leading to cancer."

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


text:
In marine DNA viral diversity studies, what would "paradigm of rampant mosaicism" refer to?
The recent paper in Cell Marine DNA Viral Macro- and Microdiversity from Pole to Pole describes the (huge) new Global Ocean Viromes 2.0 (GOV 2.0) dataset.
In the Results and Discussion section, the subsection Validating Viral “Population” Boundaries begins with the paragraph:

Defining species is controversial for eukaryotes and prokaryotes (Kunz, 2013, Cohan, 2002, Fraser et al., 2009) and even more so for viruses (Bobay and Ochman, 2018), largely because of the paradigm of rampant mosaicism stemming from rapidly evolving ssDNA and RNA viruses, whose evolutionary rates are much higher than dsDNA viruses (for review, see Duffy et al., 2008). The biological species concept, often referred to as the gold standard for defining species, defines species as interbreeding individuals that remain reproductively isolated from other such groups. To adapt this to prokaryotes and viruses, studies have explored patterns of gene flow to determine whether they might maintain discrete lineages as reproductive isolation does in eukaryotes. Indeed, gene flow and selection define clear boundaries between groups of bacteria, archaea, and viruses, although the required scale of data are only available for cyanophages and mycophages among viruses (Shapiro et al., 2012, Cadillo-Quiroz et al., 2012, Gregory et al., 2016, Bobay and Ochman, 2018).

I know what "rampant" means in the colloquial sense, and the colloquial form of "paradigm" is familliar as well. Mosaicism usually relates to genetic differences between groups of cells within an individual multicellular organism. I am not sure how it applies to virus populations.
Is it possible to explain the meaning of "paradigm of rampant mosaicism" in this particular context, and give it some background?

If you check definitions of the words you arrive a the logical meaning: "... the standard model of uncontrolled, widespread, pervasive mosaicism ... "

@com.prehensible consider writing that up as an answer and letting people vote on it then?

It could possibly be related to packaging of different viral genomes in the same capsid. Not sure about it. I'll read the paper and get back.

As I understand it from skimming the Cell paper and that by Bobay and Ochman, 2018, which it cites, the concern is the validity of the established method of defining viral species. Quoting from this latter paper:

Members of a biological species are defined by their ability to exchange genetic material…

The problem would appear to be that ssDNA and RNA viruses evolve rapidly (rampant is probably meant to convey this idea), but most importantly, not just by acquiring point mutations or deletions, but by horizontal gene transfer from other viruses (and from bacteria).
The net result of this is that such viruses are made up of segments from different sources, some evolved by conventional mutation and others ‘hijacked wholesale’ (my own hyperbole) from other organisms. Another way of putting this is that their genome is a mosaic of genes from different organisms. An example of this is in the diagram below, taken from a paper by Juhala et al. entitled “Genomic Sequences of Bacteriophages HK97 and HK022: Pervasive Genetic Mosaicism in the Lambdoid Bacteriophages”.

For anyone unfamiliar with the word ‘mosaic’ (or its applicability in relation to genomes) I reproduce below a Roman mosaic from Pompeii. The idea is that what appears as an integrated organism is composed of disparate pieces with distinct boundaries.

(The protagonists in the mosaic are about to exchange blows, rather than genes. There are also mosaics at Pompeii depicting the latter type of exchange, but these are a little too ‘rampant’ to present here.)
The implications of ‘mosaicism’ for defining viral species is — I imagine — that viruses which could be regarded as distinct species from examining the sequences of the majority of their genes might still be able to exchange genetic material by crossing-over at genes they have acquired by horizontal transfer.
Oh, and what about paradigm? It would clearly be unfair of me to suggest that this is a fancy word that the authors have used to sound important. The Oxford Dictionary online defines it as:

A typical example or pattern of something; a pattern or model.

I think that the authors mean that the viruses provide a good example of horizontal gene transfer.

Okay, this is really helpful. I've absorbed as much as I can; it's too unsettling to try to really imagine the extent of gene flow in these huge systems, though I'm sure it's quite exciting to the molecular geneticists. I'm going to keep it simple and just remember the anecdote that Sputnik was found in a Paris water-cooling tower in 2008.

I don't think this is an answer, but I have been told to write it as an answer by a mod:
it means
" ...the standard model of uncontrolled, widespread, pervasive mosaicism..."
Mosaicism mechanisms are probably for another topic, Wiki states that:
Genetic mosaicism can result from many different mechanisms including endoreplication, anaphase lag, and chromosome nondisjunction.


text:
Radial Basis Function Network (RBF Network)
In the Wikipedia article on radial basis function network, I didn't understand what was meant by "center vector for neuron i", in other words "center of the RBF units called also prototype".

In RBF networks each neuron in the hidden layer applies a computation that is related to its "center vector".
First consider the set of input neurons as a vector $\mathbf{x}$, and that each hidden layer neuron receives the complete input vector as its own input.
Second, each hidden layer neuron $i$ is parametrised through a vector (center vector) $\mathbf{c_i}$ of equal dimension than $\mathbf{x}$.
The computation of each hidden layer neuron $i$ consists of:

Evaluate the distance (according to a metric, which may or may not be Euclidean) between the input $\mathbf{x}$ and the center vector $\mathbf{c_i}$. When the input is equal to the center vector, the output for that neuron will be maximal (see 2).
Evaluate a Gaussian function that decays with increasing distance between the vectors. That's the output of each hidden layer neuron. In the following equation, $\beta$ is a parameter that specifies the decay rate of the Gaussian (converse to the standard deviation in a regular Gaussian distribution).

\begin{equation}
\rho_i(\mathbf{x})=\exp{[-\beta\Vert\mathbf{x}-\mathbf{c_i}\Vert^2]}
\end{equation}
Now combine linearly the output of all hidden layer neurons to obtain the total neural network output. For that, you need an additional set of parameters or weights $a_i$ (one $a_i$ for each hidden layer neuron, but the $a_i$ values are scalars while each $\mathbf{c_i}$ is a vector).
The final equation, that yields the total network output (a scalar value), is:
\begin{equation}
\varphi(\mathbf{x}) = \sum_{i=1}^N a_i \rho(||\mathbf{x}-\mathbf{c}_i||)
\end{equation}
And that's it.

I have all the honor if you can response me to the question "ventral stream architecture" asked now in this site :):)


text:
Colorado potato beetle diet
The Colorado potato beetle is best known for being a potato pest. However, I've just learned that it originates from Northern America and the potato itself comes from South America.
So the question is, what did potato beetles eat before they were introduced to potatoes?

Other Solanacae, in particular buffalo-bur — http://entomology.ifas.ufl.edu/creatures/veg/leaf/potato_beetles.htm#hosts — although the time period between discovery and potato was quite short.

I see, so the hosts were likely other members of the same family and not some completely different plant?

Basically, yeah.  This is a wolves-to-dogs thing, not a wolves-to-humans (bad analogy).

Please convert your first comment to answer

They ate other Solanaceae species.  This University of Florida info page gives an excellent overview of the species, including its hosts (emphasis mine):

Potatoes are the preferred host for the Colorado potato beetle, but it may feed and survive on a number of other plants in the family Solanacae, including belladonna, common nightshade, eggplant, ground cherry, henbane, horse-nettle, pepper (rarely), tobacco, thorn apple, tomato, and its first recorded host plant: buffalo-bur.

The naming history is a bit weird — being neither originally from Colorado or associated with potatoes — but hey, that's science.

That for the fun fact about the name :)


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There are linear and rotary molecular motors in the cells. Do any of them have a fixed or stable frequency or speed?
Are there any linear, rotary or oscillatory molecular motors in the cells which can have fixed frequeny and which can be used as a reference for elapsed time timer? This question is with relevence to my earlier question 'Is there a realtime molecular clock within the genome to co-ordinate the developmental sequences in an embryo?'

There are molecular motors but the frequency is a function of energy input (ATP); similar to the angular velocity dependence on amount of current in electrical motors.
The concept of molecular motor may not be suitable for a clock like device. There are clocks based on genetic circuits, which produce stable oscillations. Examples include the circadian clock, cell division, menstrual cycle etc.
Developmental events involve checkpoints and the timing is regulated by several factors such as number of cells, concentration of some protein etc. However, I haven't come across a master clock that integrates and synchronizes all these signals for precise developmental timing. That makes it an interesting area of research.

These molecular motors' response maybe dynamic and nonlinear. But it entirely dependent on the external influence and also the characteristics of the motor itself including number of active motors involved in operation. As it is microscopic, it will not possible to analyse by assumptions and say they have some random frequency. They do have certain frequency of operation (I do not know whether they are controlled by biological clock or some master clock but they are controlled by nucleus of the cell) and "Modeling molecular motors" explains how motors act on the filament inside the cell. It mainly talks about the influence of external force on the operation of motor and also speed(v) of the motor. The following excerpt from that paper talks about the external force on motor.

The action  of  the  motor is induced by generalized forces, which for
  the motor/filament system may be identified  as the mechanical force
  fext  applied  to the  motor, and  the chemical potential difference
  Dm, which measures the free-energy change per consumed ‘‘fuel’’
  molecule. The force fext describes external forces, for example of
  optical tweezers,  microneedles, or the viscous load of an object that
  is carried. fext could also include viscous friction forces between
  the motor and the surrounding solvent if the latter  is considered as
  ‘‘external.’’ The chemical  potential  difference Dm is for the
  process of the hydrolysis of Adenosinetriphosphate (ATP) to
  Adenosinediphosphate(ADP) and phosphate (P).

The frequency of molecular motor according to "Biophysics of Molecular Motor" has been classified into two categories:

Density controlled: In the density-controlled model, it is assumed that the depolymerization rate is proportional to the motor density at the terminal site of the microtubule. Here the frequency of motor is dependent on density of the motor.
Flux controlled: Filament depolymerization is determined by the flux of motors
to the end. Here the frequency is dependent on the flux of the motor.

In both the above cases the length of the filament on which motor is acting is also important. These models have been analysed and plotted on a graph to give a clear picture of it.

The paper explains the catastrophe frequency, the frequency at which the filament shrinks. Shrinking of of a filament is due to motor. So the paper concludes saying the catastrophe frequency is 0.5 per min for a 8um length of filament.

(Catastrophe = the transition from growing to shrinking of dynamic microtubules).
To summarize, these motors do have speed and frequency of operation but they are not fixed. They vary in a non linear fashion due dynamic environment. But the motor tries to be as much stable and resistant as possible.


text:
Is it possible to suffer from hyperthermia by spending too much of time in the hot springs?
People may tend to spend time in a hot water spring. Is it possible to get hyperthermia (like a sun stroke) due to this?

You betcha!

We report a case of acute hepatic failure combined with disseminated
  intravascular coagulopathy, acute renal failure, and neurological
  deficit caused by heat stroke after bathing in a hot spring.

Generically, the term you're looking for is non-exertional heat stroke.


text:
How far into a pregnancy is it before visible signs of it is apparent and risk of physical trauma increases
I'm doing research for a series I'm writing. in it the main character is pregnant however goes off to fight a criminal organization who have been killing her friends and i want her appearance to show that she may not be pregnant however she fights and defends as if she is mindful of heavy impacts could cause a miscarriage
I am wondering how far into a pregnancy is it before visible signs of it is apparent and risk of physical trauma causing miscarriage increases, if there is also a point during the pregnancy where the fetus could mutate via outside interference then that would be good to know too however I can go without that information.
NOTE: I want to know this information so that even though the world in this series I'm writing is totally fictional, one can begin to question how fictional it really is when some parts are based off actual science and logic of real life.

You should consider cutting down the largely irrelevant background for your specific application, and go directly to the biologically interesting question. Many will ignore your question simply because of the long introduction. Remeber that Stackexchange sites are not general chat forums.

@fileunderwater i'll cut it down given no other option, i included it so that people don't think this question is about trying to hide pregnancy

As far as "mutations" go, I think the term you're looking for is teratogenesis. Birth defects are most likely to form early in the pregnancy, but different toxins can have different windows. As an embryo develops, different tissues are growing and differentiating. If it is exposed to the right toxin at that time, that tissue may be damaged and not develop properly. If the tissue gets past that stage, exposure to the same toxin might have no affect at all.
Wikipedia may be a decent starting point: http://en.wikipedia.org/wiki/Teratogen
Studying birth defects is hard because it's tissue specific, toxin specific, and time specific. For some reason pregnant women just don't like to volunteer for studies on potentially dangerous chemicals.

Around the second trimester.  That's an article from WedMD, which says quite a few things.  To summarize, by the end of the first trimester:

You may be noticing some of the first physical signs of pregnancy: breasts that are sore or tingle at the slightest touch, skin that's drier or oilier than usual, and "morning sickness" -- which may or may not restrict itself to the morning hours. As many as 70% to 80% of pregnant women have it, but not feeling morning sickness doesn't mean there's anything wrong with the baby.

In the second trimester:

Most pregnant women begin to "show" during the second trimester. You likely gained less than 5 pounds during your first trimester, but now the number on the scale is edging relentlessly upward. As your second trimester proceeds, you'll gain an average of 1 to 2 pounds per week.

The exact time and rate of "showing" can vary, including whether or not this is your first pregnancy.  By the third trimester, the infant is rapidly becoming more and more capable of surviving on its own.