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Does the testicle's temperature increases with the body temperature during a high fever?
The testes is the male sexual organ. It is positioned outside the abdomen along with the scrotum. I would like to know if its temperature is independent from the body temperature due to its location.

Welcome to health SE:-) Sorry but I'm not actually getting your question correctly. Pls can you make it a bit clearer.

The question is quite vague. Please specify for clear answer.
However, although testicles are out of the body, but a part for sure. Due to pyrogen attack when the body temperature increases, literally the temperature of the testicles should be increased but clear research has not been found yet.
Please specify your question.


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Commensalism with Virus bacteria
Why people die of infection from microorganism, when germs can keep breeding for longer if they dont kill host?
Would not millions of years of evolution make germs evolve to not to kill human but feed on them just enough to not to kill them ?

Great question! In fact, some of the most successful pathogens (Herpes viruses are a excellent examples) have evolved with precisely this strategy. Herpes viruses have very low virulence, but infect nearly every human on the planet, and stick around for life.
But there's an evolutionary trade-off to this strategy. Herpes viruses have giant genomes (for a virus), because they need a ton of genes that counteract the immune system and perform other feats of cellular control so that they can stay dormant for long periods of time. While dormant (the technical term is "latent"), the virus is not transmissible, so while it persists  for a long period of time, they actually don't transmit very often.
Other viruses (influenza is a good counter example), are readily transmissible throughout most of their life cycle, but end up being cleared in a few weeks by most people. And yet influenza also spreads around the globe each year, so this also seems to be a pretty effective strategy.
It's really hard to ask questions like "why doesn't influenza behave like herpes?" When it comes to evolution, there are many successful strategies. Might as well ask, "why don't fish have feathers?" "Why don't sea birds have gills so that they can stay under water?" "Why aren't humans single-celled organisms?"

Some of the information contained in this post requires additional references. Please [edit] to add citations to reliable sources that support the assertions made here. Unsourced material may be disputed or deleted.

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Male Parenting from Evolution point
From evolution point of view can we explain as to why mothers care about child rearing more than fathers? Is it Social phenomenon or genetic phenomenon?
Are mothers hard wired to take care of children more or they are socially forced to do so?

Are you talking about humans only? There are many species (although not the majority) in which males parent more than females.

I think good answers would address multiple species and should also address how common male primary parenting is...

I am focusing more on humans

Because mother invest the most material and time into producing the offspring, so there is a stronger pressure on them to not waste it. Males can go impregnate other females so there is a stronger possible disadvantage for child rearing, few mates thus fewer offspring. Whereas a female can't have more offspring by finding other males while currently carrying offspring so they are forced to sink a lot of time and energy into the offspring. So evolution strongly disfavors females who waste those resources by abandoning the offspring.
Strong K strategists like human tend to override much of this becasue of how much investment the offspring need. So there is a strong pressure for the female to only accept mates that can provide a great deal of resources, including time. And males can seriously hurt the chances of their offspring surviving by abandoning them. But there is still more built in investment on the part of the female.
There is one other factor, A female knows who her offspring are, males do not, so the offspring they invest in might not be theirs, so there is a pressure to not put all their eggs in one basket so to speak, this is also why males tend to be more worried about physical infidelity (cuckolding) while females worry more about risk of abandonment (loss of support).
Now remember this is males an females in general, individual species can have different pressures. And remember that humans have very complex behavior so much of this just amounts to tendencies on average, not hard and fast rules.
More on the ethology of mating here. http://www.tandfonline.com/doi/pdf/10.1080/11250008409439461

John,  you could further strengthen your answer by providing some references.

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What might a supposed “tree enzyme” be — injected into a Morton Bay Fig tree?
I was recently visiting Fremantle in Western Australia and noticed a large Morton Bay Fig tree in Kings square in the centre. Apparently the health of this tree had been declining, but they hope that recent treatment will lead to an improvement.
The notice by the tree said this was by “injection of a tree enzyme”. I also found the following quote on the City of Fremantle FB page:

To improve the tree’s absorption of nutrients which will help it grow stronger, the bioscientist has given it a ‘booster’ enzyme injection. This enzyme naturally occurs in trees and is an additional boost that will hopefully help the fig tree recover and flourish again this spring.

Well trees have enzymes like any other living thing, but I find it difficult to imagine what enzyme injected into a tree would get transported through its system and help it heal. Is there anyone in silviculture (or WA) who has any idea what this was?

Interesting question. Here is the sign, if anyone’s interested.

So eventually I decided to email the City of Fremantle, who put me in contact with their Parks Department, who gave me the name of the company who had handled the tree, who replied with a most informative letter.
And the answer is…

Glutathione

Most animal biochemists, like me, will be more familiar with the importance of glutathione (reducing sulphydryl group highlighted in yellow, above) as a reducing agent in erythrocytes, the constituents of which are subject to oxidation damage.
What was wrong with the tree?

“…the figs in Kings Square… had quite elevated levels of heavy metals Cd, Cr, and metalloids Hg and As.
We traced this back to the colonial past, where in the 1830s – 1840s, when gold had been discovered south east of Fremantle, a battery operated (by the Crown) in Fremantle. In those days, gold was commonly lixiviated using mercury. Kings Square had a pit cut earlier for mining limestone. A good place to dispose of battery mullock is a pit.The earliest gold deposits were mafic ores, so often contained Cd and Cr.”

Why use glutathione to treat the trees?

“Firstly, it stimulates the jasmonate pathway, thereby alters transpiration and root growth.
Secondly, it assists in the isolation and immobilisation of heavy metals.
Thirdly, if assists in the breakdown of triazine herbicides by ring cleavage…”

And my correspondent kindly provided a review by Hossain et al. in the Journal of Botany, which elaborates on the second point.
And why the “tree enzyme” business?
This did not come from the company that handled the treatment, but from someone (unknown or nameless) who was handling the public relations, and who wished to provide reassurance that the treatment was ‘natural’:

“I guess in the world of snake oil, “enzymes” are benign, natural things, rather than usually ephemeral catalytic proteins.”

I admit that, depending on a personal letter, the answer does not totally conform to the criteria of testability. (I did not think it appropriate to name my correspondent.) However the background details and the literature reference do provide strong support. In any case, as there had been some interest in the question, I thought I should do some work myself and then post an answer.

Interesting answer.


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Protein diet composition
I have read that non veg food are better for proteins while veg food is deficient in either one or other protein. If it is so are herbivores protein deficient always in case of animals as well as humans?

http://health.stackexchange.com/questions/9124/is-all-protein-the-same/9130#9130

Link from VonBeche is good.
Proteins vary in amino acid content.  Humans can make some but we need 9 of them in our diets.
from https://www.ncbi.nlm.nih.gov/books/NBK234922/
    Nine amino acids—histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, and valine—are not synthesized by mammals and are therefore dietarily essential or indispensable nutrients.
This guy http://michaelbluejay.com/veg/protein.html
is clearly a vegetable enthusiast but he makes a good point (and provides a nice table): just about any vegetable can provide enough amino acids if you eat enough of it.  Getting your entire caloric requirement from iceberg lettuce would a project, it is true.  But until I did the back reading for this answer I thought it would be impossible to take in the calories it would require to get all necessary amino acids from some of these plant foods.  Thanks michaelbluejay.

I here assert that animal foods have more amino acids per calorie than vegetable foods.  So, if you wanted to limit calories but meet your amino acid requirement it would be easier to do with animal proteins than with vegetable proteins.
But even all calories from potatoes can get you your amino acids.  The people who get into trouble are people who are not getting all the calories they need because they are starving, and the calories they do get are from low protein source foods like yams or bananas.  That is protein-calorie malnutrition.


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Evolution history of virus tracing
How do biologist trace evolutionary history of virus, is there any article on this issue,
e.g. how scientist got to know that coronavirus evolved from bat or camel or pig?

The identification is done by sequencing virus samples and comparing them to reference genomes of viruses. By doing this, you can analyze how closely related an unknown virus is to the references.
For the nCoV this method shows it is 96% identical with a known bat coronavirus (see reference 1 for details).
As viruses accumulate mutations due to errors during replication, this method is also used to generate genetic trees of the virus to analyze how it spreads, map routes of infection and also if the virus has been introduced to humans more than once (reference 2 has a nice overview on this topic).
The problem here is: You need to have some known references for comparision, if you have a completely new virus which has never emerged before, this will not help. For this reason there are projects ongoing which collect samples to identify yet unknown viruses (see reference 3)

Discovery of a novel coronavirus associated with the recent
pneumonia outbreak in humans and its potential bat origin
DNA sleuths read the coronavirus genome, tracing its origins and
looking for dangerous mutations
Virome analysis for identification of novel mammalian viruses in
bats from Southeast China

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Can Anyone Identify This strange cockroach looking bug
I am looking for someone to identify this bug:
location india. It flew from my window in my room, killed it by spraying cockroach killer spray, it could fly like cockroach.

If you were a Jainist, I believe you wouldn't have killed it, right?

That is a mole cricket. Family Gryllotalpidae. They generally live underground, but as you noticed, they can fly. https://en.wikipedia.org/wiki/Mole_cricket

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Need for -70 degree temperature for Corona vaccine
Recent news of Pfizer vaccine for corona needing -70C temperature, made me thinking why such a low temperature is needed for mRNA based vaccine?
Are there other vaccine around which need such a low temperature?
NewsLink

This is the temperature at which RNA is stored for long term storage without the occurance of degradation. It is also standard lab routine to store RNA at this temperature. Conviniently, this temperature can be reached by dry ice (-78°C), which makes shipping a lot easier.
However, there are indications by Biontech themselves that the vaccine will be stable at refrigerator temperatures between 2-8°C for five days and probably even for prolonged times (see here). This is actually being tested, storing below -70°C is simply the safeguard to ensure nothing bad happens. For injection, it will have to be warmed anyways.


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Identify species of snake in India
image

Is this snake poisonous, found wrapped around a tree in middle of hot summer of 40 degrees celcius, in himachal, Northern INDIA, Himalayan foothills?

This appears to be a bronzeback tree snake, which is a common species of tree snake in India. It is a slender snake with characteristic bronze body and a pale stripe down the sides. It usually has a white spot on top of its head, which I think you can see in the second picture. It should also have blue inter-scale areas if you pull the scales apart.
It is non-venomous, but like all snakes may bite if attacked.


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Insect crawling Identification

What kind of insect is this, and is this venomous, or dangerous? Don't need full species name just common name will do, color is red. Grandma always warned me of this, they usually are seen in monsoon season during heavy rains. They coil upwhen disturb .
Location: Country: India, lower himalayas
Google Map :Exact location
A miniature version of this also exist in my area don't have pic though.

Given the shape and the number of legs. That most definitely is not an insect. An insect has exactly 6 legs. No more, no less.
That critter in your picture is some kind of millipede (“a thousand feet”; not literally a thousand, of course; https://en.m.wikipedia.org/wiki/Millipede), not to be confused with a centipede (“a hundred feet”; also not literally a hundred).
Millepedes are mostly harmless to humans. They eat things like dead plant matter or fungi. They sometimes also eat seedlings so they can be considered pests in gardens.
And given the colour, that’s possibly a rusty millipede (https://en.m.wikipedia.org/wiki/Trigoniulus_corallinus). They have a very wide distribution around the Indo-Malayan region. Although there seems to be no recorded observation of it on iNaturalist around your region (https://www.inaturalist.org/observations?place_id=9248&taxon_id=123010).


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What is the evolutionary advantage to a lifespan limit?
How/Why
Do Koi have a lifespan of hundreds of years?
Do humans have a lifespan of decades?
Do dogs have such a short lifespan?
Within these questions I pose further questions.  How does size relate to lifespan. Elephants?
If dogs were to evolve independent of humans (at this point) would they rule the world?

This question is far too broad, because you are asking too many questions. Please limit yourself to one focused question per post.

An interesting question and @Wesley has answered it quite nicely. Apart from this, I would like to direct you to a neat article published by Yaneer Bar-Yam in PRL last year on when does natural selection favour limited lifespans. A detailed explanation was given in Gizmodo website last year.


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How do I score differential activity of cellular pathways in microarray data (not enrichment)?
I would like to identify cellular pathways (KEGG) with discriminative changes in the average activity (expression levels) of their gene members in a two-condition microarray dataset. The goal is to use the average pathway activity for machine learning (sample classification), not to identify pathways enriched in differentially expressed genes (i.e. not performing a classical gene set enrichment analysis).

How do I score differential activity of cellular pathways in microarray data (not enrichment)?

You would look at downstream genes, which are selective for individual pathways - or genes which have binding sites for transcription factors that sit at the end of your pathway. Depending on the existing literature, and your experiment, and the specific pathway, this can include genes, which are themselves part of the pathway (if feedback). For interpretability you would prefer genes, which have previously been established as makers of a pathway in preceding literature.

I would like to identify cellular pathways (KEGG) with discriminative changes in the average activity (expression levels) of their gene members in a two-condition microarray dataset.

This might be tricky, since the taking the average introduces several assumptions such as: little impact of technical background (expression of most genes of pathway above background), average being representative of the KEGG pathway of interest (and not only of the most abundant pathway members), and enforcing a somewhat arbitrary decision of whether to average log-transformed data (which is justified for many genes, but not genes that don't scale multiplicatively, such as many stress genes), or not log-transforming.

The goal is to use the average pathway activity for machine learning (sample classification),

You can use this to your advantage, and create multiple features per pathway (e.g.: median, mean, variance, non/log-transformed etc..., manually -curated signature genes of pathways), and then having machine learning choose the best features for your classification (e.g.: as would happen if using Random Forest Classifiers)

use the GSVA R package to collapse gene expression data to pathway activity scores. https://bmcbioinformatics.biomedcentral.com/articles/10.1186/1471-2105-14-7

You can use the PathVar software available here: www.pathvar.embl.de
See also the corresponding publication:
http://bioinformatics.oxfordjournals.org/content/28/3/446.long


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What is the energy consumption of an insect quantified?
Allegedly humans have an average power consumption of 97.2 watts, but what about something smaller like a housefly or an ant? What is their energy consumption measured in watt?


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dbSNP clarification
I am currently going through this paper - link.
In their methods section the authors have described they have used dbSNP for checking biallelic expression of genes. I would like to know if dbSNP contains SNPs for intergenic regions i.e. for non coding RNA regions.

Yes, dbSNP is in no way limited to coding SNPs.  One example, an intergenic SNP I found in ensembl.org:
https://www.ncbi.nlm.nih.gov/SNP/snp_ref.cgi?searchType=adhoc_search&type=rs&rs=rs542978047

Thanks a lot. I am currently trying to learn as much as possible on the topic.


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Role of processing bodies in mammalian development
I am currently writing a project proposal for university admissions regarding the duration till which maternal mRNA is required for mammalian development. Till now all the literature I have read has data on P-bodies during oogenesis:-
1) https://www.ncbi.nlm.nih.gov/pubmed/22918798/
2) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2785738/
It will be very helpful if anyone can provide a link for research articles showing p-bodies during embryogenesis in mammals.

These papers might be helpful.
http://www.molbiolcell.org/content/19/10/4383.short
https://www.sciencedirect.com/science/article/pii/S1874939913000047

@Divyanshumishra Thanks. I will go through them.


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What kind of microorganism is this?
It moves like a worm pretty much. I found it in a pretty big pond with brackish water. The water temperature was around 10 celsius.

Here's a video of it moving

Could you add some more details? Where you found it, what kind of environment it lives in, size, etc?

Now  I cannot really tell the name of it without knowing more of its properties and characteristic features, e.g. size. (I am afraid I am not very good with faces, especially of microorganism :D)
But I am 90% sure it might be an
Oligochaete

Please do not post guesses as answers and always provide references to your claims. I recommended deletion for your post as it does not fulfill standards for good answers. Please feel free to edit accordingly to avoid deletion or - after possible deletion - give a new, well-researched and comprehensive answer. Thanks!

This does not provide an answer to the question. Once you have sufficient reputation you will be able to comment on any post; instead, provide answers that don't require clarification from the asker. - From Review

@AlexDeLarge ok


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VCF files - examples for haploid organisms
I am trying to self-learn some aspects of bioinformatics (coming from a stats background), and i am trying to find / download some VCF files for haploid organisms as an input to some statistical analyses. I have seen a few sites where one can download example VCF files for human populations, but there are any sites where i can download some example haploid VCF files from e.g. bacteria as well? I have tried to look at http://bacteria.ensembl.org/info/website/ftp/index.html - but i was not successful yet. That said, as a newbie, i might very much be looking in the wrong location.


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DNA quantification in a high school bio lab
I'm working on a project in a high school bio lab (so limited resources), and I need a way to quantify the concentration of DNA in a PCR product. I can't use spectrophotometry (cheap spectrophotometers at school can't measure absorbance at 260nm), and any fluorescent dyes are out of the question as we don't have a transilluminator. Right now I'm looking at measuring absorbance change in a visible-light dye like crystal violet or methylene blue, but there isn't enough data on quantification using these dyes. Can anyone suggest anything?
Thanks.

Can you run a gel?

Yes, although gel extractions might be a little difficult.

If you are lucky, and you don't need many repeated measurements, and there is a university in your town, you can contact the administrative staff (note: not professors) of a fitting department (e.g.: genetics), who will usually put you in contact with a grad student of an experimental lab. Usually people are happy to help with "minor issues" like those - and having someone from a high school briefly visiting a lab will be good for any involved party, as it is a nice sign of community outreach.

I do know a guy at a nearby uni who might be willing to help, but because the project is officially graded I'd need a pretty good set of data with replicates so it would mean basically doing everything at the uni, which I'm trying to avoid for now. I'll keep it in mind for a backup option, though.

You can quantify DNA in a gel by comparing band intensity of the unknown sample to that of a known mass. I can elaborate if this seems like a reasonable strategy for you.

That sounds interesting, can you elaborate?

Within some linear range, the intensity of stained DNA bands in a gel is directly proportional to their mass. By making a standard curve from bands of known mass, the mass of unknown bands can be estimated. This process is called densitometry. I wrote briefly about its use in quantifying protein bands after SDS-PAGE in this answer, but I'll go into more detail on how this is done using the following ethidium bromide stained gel:

On the right is a molecular weight marker (BstEII digest of λ DNA) with bands of known mass. On the left are two bands of unknown mass (actually a double-cut plasmid).
I use a free program called ImageJ to estimate band intensities. They have a tutorial on measuring band intensity here. You can also get ImageJ packaged with Java (and bunch of other stuff) in the software Fiji.
Open the image in ImageJ and use the Rectangle tool to draw a box around the marker, then select Analyze > Gels > Select First Lane (or shortcut Ctrl+1). Next, drag the box over to surround the other lane and select Analyze > Gels > Select Next Lane (Ctrl+2). Now select Analyze > Gels > Plot Lanes (Ctrl+3) to plot image intensity as a function of position on the gel:

The area under each peak (minus the background noise) represents the some total of intensity for each band. To measure this area, use the line (Straight) tool to draw bounds on the base of each peak:

I've done it somewhat haphazardly here, but you get the idea. Now, using the wand tool, click inside each peak and ImageJ will tabulate the integrated intensity of each. Shown below are the intensities of the marker bands (with the top band being Band 1) as well as their masses (which are known):
          Mass (ng)    Intensity
Band 1    45           5319.891
Band 2    28           3816.234
Band 3    24           3256.406
Band 4    16           2298.749
Band 5    15           2074.749
Band 6    8            1084.991

Take this data into Excel (or similar) and plot intensity as a function of mass. Band 1 looks like it is outside the linear range and is underestimating the mass. This was actually expected since, if you look closely at the band in the gel image, there are red pixels indicating that it is oversaturated. Ignore this band and perform a linear regression on the rest.

The regression gives the equation $I = 134.74M + 53.988$ with $R^2 = 0.9975$. Rearranging for mass, we have $M = \frac{I - 53.988}{134.74}$. Get the intensity of the unknown bands as described above and calculate their mass with the preceding equation:
          Mass (ng)    Intensity
Band 1    27           3736.991
Band 2    15           2125.284

My experience is that this is a much safer method than using (for example) Nanodrop. I have to admit though, that I rarely ever did the quantification in ImageJ/FIJI; estimating by eye was usually close enough for most applications :)


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How does the age of a parent affect the chances of occurrence of certain genetically transmitted diseases?
Do genetically transmitted age-related diseases (like hypertension, arthritis etc.)have the probability of occurring at an earlier(younger) age in the offspring if they are born at a later age to their parent(s)?

Are you asking if an increased age of the parents at the time they have children, increases the risk of developing symptoms of genetically predisposed diseases in the offsprings at an earlier age?

Yes. And  I am asking about the diseases like diabetes, heart disease etc. which usually appear after a certain age.

In some studies, they have observed either positive or negative association between maternal or paternal age (the age of mother or father at the time of delivery) and earlier development of genetically predisposed diseases, such as diabetes type 1 and certain cancers, in offspring.
Diabetes type 1
Maternal age and diabetes in childhood (BMJ, 2010):

...the risk of childhood onset diabetes [type 1] increases with
  maternal age: 5% for each five years of age...the main explanations
  are that biological programming of the child is in some way affected
  by the age of the mother, or perhaps the father...

Cancer
Parental age and risk of sporadic and familial cancer in offspring: implications for germ cell mutagenesis (Epidemiology, 1999)

We used the nationwide Swedish Family-Cancer Database to analyze the
  effect of parental age on cancer in offspring at ages 15-53
  years...Maternal age was associated with sporadic melanoma and
  leukemia, causing a 30% excess if mothers were more than 40 years vs.
  less than 20 years of age. A marginal effect of about 10% of both
  maternal and paternal age was observed for sporadic breast cancer.
Paternal age increased the RR of sporadic nervous system cancer by about 15%. Accumulation of chromosomal aberrations and mutations
  during the maturation of germ cells may be a mechanism for these
  findings. In familial cancers of colon, melanoma, and thyroid, higher
  age showed an apparent protective effect, which was also noted for
  sporadic cervical cancer and melanoma.

Rheumatoid arthritis
Ages of onset suggestive of genetic anticipation in rheumatoid arthritis multicase sibships can be explained by observational bias (Rheumatology, 2007)

There was no significant correlation between the age of RA onset and
  the maternal or paternal ages of conception.

Cardiovascular disease
In one study, they have found no significant association between maternal age and blood pressure in children. There seem to be no studies about the effect of maternal/paternal age on early-onset heart disease.
On the other hand, offsprings are at increased risk of developing a cardiovascular disease early if their parents had it early (PLoS One, 2016).

In another study, they have observed that maternal ages <25 and >45 have been associated with increased frailty index: a sum of 8 conditions (cancer, lung disease, mental health problems, diabetes, heart disease, stroke, blood pressure and arthritis)
Maternal Age and Offspring Adult Health: Evidence From the Health and Retirement Study (Demography, 2012)

In summary, net of some obvious confounders, only maternal ages below
  25 and above 45 are associated with negative offspring health
  outcomes. (see Fig 1 and Table 2)
The mechanisms thought to be responsible for the young maternal
  age–offspring health link are related to the physiological immaturity
  and sociodemographic disadvantage that often accompany young
  parenthood... On the other hand, the negative association between advanced
  maternal age and adult health is thought to be driven by the
  physiological reproductive aging of the mother.

In this study, they have not checked for the age of onset of diseases in offspring, though.


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Where and how is information about pathogen immunity stored in a cell?
If all of the DNA is being used, then how would the cell be able to store new information about pathogens in DNA? It's like a full hard drive that can't hold any more. So does the cell just compress the information about the pathogens and then just adjust the existing information about pathogens?

All the body does is produce a ton of cells that can recognize single antigens. Each time you encounter pathogens, some of these naïve cells contact antigen that can activate them. The activated clone replicates itself, forming effector cells that can deal with pathogens.
As the infection is cleared and the population of effector cells begins to contract (i.e. many die off or become anergic), some of them undergo changes which alter their migratory pattern and longevity. Some can stay in the tissue that was originally infected as tissue-resident memory cells. Some home back to the lymph node and hang there as central memory cells. The lineage is affected largely by chemical signals being produced by the tissue and other immune cells in the vicinity.
Upon re-encounter of the same pathogen, if it has some of the same antigenic determinants as the original infection, these memory cells are already known to be specific to them. Encountering the same antigen will cause these memory cells to undergo another round of clonal expansion, producing more effector cells and additional memory cells so the process can repeat. These events can be limited by telomere length or inhibitory molecules, as a caveat.
The key understanding is that the immunologic memory is actually stored in the repertoire of long-lived memory cells, and in part results from recombination events at the T or B-cell receptor locus during their maturation before they're released as naïve cells.
See: Abbas (2014). Cellular and Molecular Immunology, 8th ED., many different chapters.

There is also 'intrinsic' and 'innate' immunity. Immune cells can recognize common patterns on pathogens, such as lipopolysaccharides, double stranded RNA and flagella and respond to these shared patterns. These common responses are more ancient. 'Adaptive' immunity is relatively new.

That makes a lot of sense. Like I said to the other person, I'm just taking AP Biology at school, so I'm not very knowledgable of this field. So if you get an infection on your foot, and your lymph node with those memory cells is around your neck, will it send those memory cells to the foot, or does the lymph node just protect its immediate surroundings? Also, you mentioned the textbook. Do you recommend that book for further research at my level of knowledge, or should I start out with less advanced material?

There are pathogen sensing cells called Antigen Presenting Cells which nibble on bacteria and proteins in different environments, these cells then migrate back to lymph nodes where memory cells are 'present' the antigens they picked up. If there's a match then you initiate the so called 'adaptive immune response'.

So in that case, would the Antigen Presenting Cells only make it to the local lymph nodes? In that case, memory cells in the neck would not be helpful to an infection in the foot.

Central memory T cells are considered a circulating subset. They home to lymph nodes temporally (time-dependent) through the expression of the receptors CD62L and CCR7. There's actually a neat paper in immunity about how T cells circulate on a circadian clock of sorts, and so they come out of the lymph nodes and circulate every now and then. This basically means your central memory T cells aren't always in the neck, and it's how a DC in the draining lymph node in the foot can find a naïve or memory cell to prime.

Also note that while im quoting T cells, many things are the same for B cells in terms of trafficking, just not for function/activation.

You're asking for a course in immunology, which is far too long to include here.You have several misconceptions. Short and oversimplified answer, the information is not stored in one cell, but in trillions, each with a single piece of pathogen information. Within each cell, the information is stored in DNA, which in these particular cell types can be modified. Your hard drive analogy, like most such analogies, is completely misleading and you should abandon it. There are several introductions to adaptive immunity online; you might find one (such as here, here, or here) helpful.

Sorry, I'm just taking AP Biology, and it was a topic that we're learning about. I definitely want to get more into it, so I'll probably try to find some resources to learn more. Do you have any recommendations aside from waiting until college?

The IMGT writeup is probably a good starting point -- I think if you're taking AP Bio you should be able to follow it pretty well.  You might jump to the "Mounting an Immune Response" section for a quick overview. The Wikipedia article on the Adaptive immune system goes into more detail; you might want to follow some of the links in the introduction.


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Solute potential of sucrose relative to NaCl
Does 1M NaCl or 1M sucrose solution have a more negative solute potential?
I was thinking that for the same volume of solution, (eg 1 dm^3) there will be 2 mol of ions in NaCl solution and 1 mol of sucrose.
However, there are more OH groups in sucrose that water can form hydration shells around.
So which solution has the more negative solute potential?

I would say 1 M NaCl has lower solute potential. By the equation, solute potential is proportional to solute concentration.

Yes, but how do we account for the fact that sucrose has more OH groups that water can form hydration shells around? Wouldn't that lower the solute potential to a greater extent than NaCl? There are more OH groups per mole of sucrose than there are ions per mole of NaCl.

You are right. NaCl has a van't Hoff factor of 2. For simplicity you can assume sucrose as a simple solute and ignore macromolecular interactions. BTW, even sodium and chloride ions will have a hydration shell and its size depends on the surface charge density.

So, we assume that the hydration shells formed around Na+ and Cl- ions are bigger than those formed around sucrose (which we assume to have only one hydration shell formed around it)?

Hydration shell is a totally different concept. I don't think it is a major factor in osmolarity. Osmolarity is a bulk property.


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Negative Oxygen Consumption Rate
Oxygen consumption rate (OCR) is defined as the rate at which cells consume oxygen. I reason that for cells not capable of photosynthesis, OCR is strictly non-negative.
That was until I read this article which provides a graph with negative OCR values. Could someone enlighten me as to how this might be possible? If the cells are consuming no oxygen, I would expect OCR to be zero, not negative.

Scientific Paper:
http://www.pnas.org/content/108/33/13829.full

Start by asking if the zero in the scale actually zero, an arbitrary baseline, or a proxy measurement? in this case it appears to be a proxy so zero might not represent actual zero.

The diagram is not clear. They should write "change of oxygen consumption rate".
The caption of the diagram makes it clearer what they are describing:
" In A, a time course for measurement of oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) is shown under basal conditions, [...] ".

So basically they are measuring oxygen consumption rate under basal conditions and apply some chemicals and depict the change in oxygen consumption rate in a diagram, given in percentage.

Hi there, thank you for your answer. Will your answer still hold if the OCR was measured in units of pmol/min? (i.e. moles of oxygen per unit time)


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Cell cycle arrest and apoptosis
Is cell cycle arrest needed for apoptosis to occur? I note that some of the factors that mediate cell cycle arrest induction (e.g. DNA damage) happen to be responsible for initiating apoptosis as well. However can apoptosis occur without first arresting the cell cycle?

As I remember, apoptosis is generally triggered by mitochondrial membrane being destroyed. I don't think cell cycle arrest is necessary to trigger this process.

@RoniSaiba not necessarily... that would generally be the pathway for the intrinsic pathway of apoptosis (release of cytochrome C from mitochondrial IM space), but it doesn't necessarily apply for the extrinsic pathway.

For context, realize that a large proportion of cells in complex multicellular organisms (for which apoptosis is relevant) are in G0 for most of their life. Cell cycle arrest is the norm.

Apoptosis can occur without cell cycle already being arrested.  For instance, in the case of extrinsic apoptosis, which could be induced by T lymphocytes, for example, a trimeric receptor such as TNF-R or TRAIL-R's containing a DD can be bound at any time by the death ligand secreted by (TNF, TRAIL) or bound to the immune cell membrane (FasL, TRAIL).
The DD (death domain), independent of where cell cycle is, recruits adaptor proteins with DED domains (ie., FADD), which in turn recruit procaspase 8.  Procaspase 8 is cross-activated (becoming caspase 8) when two of them are recruited, then released.  It then begins activating procaspases 3, which begins the actual work of killing the cell (cutting cytoskeleton => blebbing, etc.), activating CAD.
It bears mentioning, however, that once it's kicked in, cell cycle will inevitably stop, since CAD will start fragmenting the DNA...  It also bears mentioning that caspase 8 also activates the intrinsic pathway via Bid => tBid => Bax => Bak => mitochondrial leakage, cytochrome C activating caspase 9...

Sources:

Sayers, Thomas J. 2011. Targeting the extrinsic apoptosis signaling pathway for cancer therapy. Cancer Immunology, Immunotherapy 60 (8): 1173-80.

Eimon, P. M., E. Kratz, E. Varfolomeev, S. G. Hymowitz, H. Stern, J. Zha, and A. Ashkenazi. 2006. Delineation of the cell-extrinsic apoptosis pathway in the zebrafish. Cell Death and Differentiation 13 (10): 1619-30.


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Purpose of intensive protein synthesis in G1 phase of mitosis
What is the purpose of intensive protein synthesis in G1 phase of mitosis, and what purposes do these synthesized proteins serve? Why are lipids and carbohydrates not synthesized intensively as well?

The G1 phase of eukaryotic cell cycle is part of interphase, which is when the cell is replicating its DNA ready for division. To understand the need for intense protein synthesis, we first need to understand how DNA is organised during mitosis.
Before DNA is condensed into chromosomes ready for nuclear division it is in the form of chromatin, a long fiber-like structure inside the nucleus. In order to condense into chromosomes, this chromatin must undergo a process of coiling and folding in order to create the chromosome 'X' structure we are familiar with.
A major part of this DNA 'miniaturization' is the folding of the double helix around proteins called Histones - this creates new structures called nucleosomes.
In order to fully condense the roughly 3 meters of DNA in the average human cell down to a singular chromosome, millions upon millions of these Histone proteins are required.
And that answers your question; intense protein synthesis during the G1 phase is required in order to produce the extremely large amount of Histone proteins that are needed for packaging DNA into chromosomes ready for cellular division.
As for carbohydrates, these are constantly being processed by the body in order for the production of ATP for use as energy. The use of said energy for mitosis is a just another constantly required use of ATP within the body. Therefore there isn't any noticeable increase in carbohydrate processing/production, as it is happening regardless of the cell's stage in its cycle.
-See the image below (from shmoop.com) that explains the process of getting DNA into a chromosome.


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Sugar as a defence against bacteria?
An answer on another SE site mentions that sugar "at a certain level acts as a preservative". I've always been taught that microorganisms eat sugar and expel acids, that is why sugary food are damaging to teeth. How is it that sugar acts as a preservative, then?
Googling the question I've found conflicting answers though I don't credit the sources as being especially reputable. What is the real reason that sugar can act as a preservative?

Sugar in high concentrations acts osmotic. This means that the water available in the cells is drawn towards the high concentration of a solutant (sugar), like in the image below (this is demonstrated with a plant cell, but the principle is the same for bacteria and other microorganisms):

Since microorganisms can not survive without water, they are not able to grow or reproduce. This effectively safes food. The same mechanism works when salt is used to conserve meat or fish.

This is also why quite large amounts of sugar (or salt) is needed in order for it to work as a preservative. With too little sugar there will be no osmotic effect (or too little) killing of the microorganisms spoiling what you're trying to preserve. Which in turn is why e.g. jam always is so sugary.

Sugar participate in food preservation only at high concentrations. When microbes are introduced to high sugar concentrated environment, water inside the microbial cell diffuses out to the high sugar concentrated solute due to the phenomenon called osmosis. As water is very much needed for cell functioning and metabolism the dehydrated cells fail to perform its function and eventually die. This is called sugar curing, a food preservation technique. Also hard sugary sweet is less susceptible to microbes than soft sugar sweet because of its high sugar content that makes it intolerant for microbial growth and also the absence of moisture (important factor for microbial growth) in the hard sweet as compared to soft sweet makes it less susceptible to microbial attack.


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How does one experimentally obtain a hemoglobin-oxygen dissociation curve?
I've always wanted to do comparative eco-physiology studies looking at Hemoglobin-Oxygen affinity of populations in different environments, but I can't find a protocol to experimentally measure the relationship. Does anyone know where I can find a protocol, or know a protocol themselves?
I'm assuming an answer would include what the necessary instrumentation would be, what condition the blood needs to be in (fresh?), if the heme is isolated (and if so, how), and what an appropriate sampling scheme would look like.

There are existing instruments commercially available to measure hemoglobin-oxygen saturation curves. Whole blood or lysed blood can be used; I would expect the instrumentation to come with specific directions for sample preparation because it may depend on the exact equipment.
These devices use a spectrophotometer to measure saturation, taking advantage of the same color difference between arterial and venous blood that is visible to the human eye.
To collect a curve, you start with the sample saturated in room air or oxygen, and the instrument gradually introduces nitrogen to replace the oxygen, while also monitoring oxygen concentrations using a Clarke electrode.
Here is an example paper that uses one of these devices. Their precise methods may or may not be appropriate to your research approach.
References

Head, C. A., Brugnara, C., Martinez-Ruiz, R., Kacmarek, R. M., Bridges, K. R., Kuter, D., ... & Zapol, W. M. (1997). Low concentrations of nitric oxide increase oxygen affinity of sickle erythrocytes in vitro and in vivo. Journal of Clinical Investigation, 100(5), 1193.

Thanks! This sounds not terribly difficult, given the right equipment. Something for me to think about if I ever have my own lab/startup funds.


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Why are ammonium ions reabsorbed in the thick ascending limb during acid secretion?
In order to produce HCO3- from glutamine and to subsequently reabsorb it,
H+ ions need to be secreted. The kidney does this by via ammonium ions
in the PCT. But why are the ammonium ions then reabsorbed in the TAL before
being put back into the collecting duct? Wouldn't it be more efficient if
they were just left in the tubule fluid where they would reach the
collecting duct eventually? The first method seems to be a longer way of
achieving the same result.

Why reabsorb $NH_4^+$ in the thick ascending limb if you're just going secrete it in the collecting duct

This is an excellent question. When you find an odd, seemingly inefficient aspect of physiology, it's an opportunity to learn something new.
This alternating secretion, reabsorption, and secretion starts to make sense when you look at the anatomy of the nephron.

There is no appreciable ammonia in the filtrate at Bowman's capsule (free ammonia is efficiently converted to urea in the liver by the urea cycle, so it's in very low concentrations in the blood).  As you say, it is produced in the proximal convoluted tubule. The amount that is produced is regulated by the acid load (more acid, more ammonia production). The proximal tubule is in the cortex (top of the photo).
$NH_4^+$ is in equilibrium with $NH_3$ in the tubule, and renal tubular cells and junctions are relatively permeable to $NH_3$ here, so the more $NH_4^+$ is produced and actively pumped into the lumen, the more $NH_3$ backflow leaves the tubule and enters the ECF. Because of this, the primary work of the PCT in acid base homeostasis by the kidney is not secretion (though $NH_4^+$ is actively secreted here), but rather in the production of new $NH_4^+$ and new $HCO_3^-$.
The bulk of the work of secretion happens in the collecting duct. There are a number of passive and active transport mechanisms for the secretion of $NH_4^+$ here, especially in the medullary collecting duct. These mechanisms are aided by a high concentration of $NH_4^+$ and $NH_3$ in the medulla (at the bottom of the picture).
So where does this high concentration of ammonia come from? It's from the reabsorption of $NH_4^+$ in the thick ascending limb. This is reabsorption (the tubular cells take $NH_4^+$ from the lumen and send it to the ECF), but you can think of it more as taking it from the cortex and putting it in the medulla. The filtrate flows along the lumen of the tubule, toward the collecting duct. Much of it is in equilibrium between the lumen and the ECF before it gets to the thick ascending limb. At the thick ascending limb, the permeability of the tight junctions and the tubular cell membrane changes. Solutes (the one we're interested in right now is $NH_4^+$) are taken out of the lumen and left behind in the ECF. Because the filtrate flows but not the ECF, and because the tubular cells are permeable before the thick ascending limb, and impermeable after, this substantially concentrates these solutes in the medulla, and dilutes the solutes in the cortex.
This is a process known as the countercurrent multiplier. The same principle is used to create a hyperosmotic ECF (and consequently, allow for a hyperosmotic urine if you've been wandering in the desert for hours).
Here's a diagram of the nephron from a decent review article that illustrates each of these processes for ammonia handling:

Isn't it all to do with the reabsorption of water, i.e. everything gets flushed out in the Bowman's capsule and then some stuff is reabsorbed to lower the water potential of blood, so water is reabsorbed as well.
I guess I figured it was easier to have a leakier sieve at the Bowman's capsule than try to only release the waste products via facilitated diffusion.

but ammonium ions are secreted in proximal tubule before being reabsorbed in the thick ascending limb. From here they're pumped into the collecting duct to be excreted. But if they were just left in the tubule fluid (without being taken up in the TAL), they would've also reached the collecting duct.

I don't know the specifics of this pathway, it does seem convoluted, but it could be something along the lines of ammonium ions are reabsorbed during non-selective cation reabsorption, then selectively secreted. Again it's easier to take everything up then get rid of what you want to than try and take up just the things you want to. Edit, try looking at the transporters (ion channels/pumps etc.) involved.


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What does "local folding" means in secondary structure?
I'm new to biology field, so I'm learning all kinds of biochemistry knowledge for a bioinformatics project. I've found a few definitions of secondary structure online. For example, I found this brief definition here:

A structure of a biological molecule characterized by the local
  folding within the biopolymer as a result of hydrogen bonding (within
  the biopolymer).

What does "local folding" mean here? More specifically, what does "local" in this context refer to? Thanks in advanced.

Please provide a link to your quote. We need to be able to see it in context.

The most common examples of secondary structure in proteins are alpha helices and beta sheets, and the most important distinction between secondary and tertiary structure is that a single protein can have multiple "local structures", alpha helices and beta sheets, within its complete global structure. In contrast, a protein cannot have multiple "global structures" by definition.
In other words, a local structure can occur multiple times within a protein, while a global structure by definition can only occur once, and describes the complete shape of the protein.

Ok, so it means a local segment of the global structure? And because secondary structure do not specify the exact position of an atom, it is just a general template to represent what it is? And therefore, secondary structure do not specify the function of that segment?

Secondary structures don't have specified positions in a protein, they can occur almost anywhere depending on the protein. However, secondary structures often do have important functions. For example, alpha helices are useful for proteins binding to DNA and for proteins crossing cell membranes.

It's interesting to know that the secondary structure has such a generic function. Could you also briefly explain why the secondary structures can occur almost anywhere?

There are likely a few structural constraints for where secondary structures can occur, to allow for energetically stable folding and bending, but I'm not too familiar with them. Secondary structures are very common though - why? probably no better answer than simply evolution found them useful. It's fairly straightforward to construct secondary structures, you just need to ensure that your linear sequence of amino acids has certain bioechmical properties, like a lot of MALEK: https://en.wikipedia.org/wiki/Alpha_helix#Amino-acid_propensities

This is very helpful for me to understand what's going on because I've been reading some papers using these parameters to predict the secondary structure.

No problem! Glad to help.


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What is Oncogene, and how do you get it?
I was looking at my family tree and it said that one of my family members died by Oncogene. What is it and how do you get it?

An oncogene is a gene that has the potential to cause cancer. If an oncogene is activated, it will contribute towards cancer, though there are typically many other factors necessary before cancer becomes noticeable and potentially lethal.
In short, your family member presumably died of cancer, though writing the cause of death as "oncogene" is highly abnormal.
Many normal and healthy genes can cause cancer when they are overly active. For example, PDGF produces a growth factor required for normal health, but if too much growth factor is produced it can cancer like breast cancer.

Oh. Thank you. Well now I know why she died. Have a good life, live it to the fullest (but not by smoking or drugs) and have fun. I hope I get to talk to you again.


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When is really necessary to visit field to observe sample collection process?
I know this could be a bit generic question, but for the sake of providing context this applies to a Transcriptomics Thesis.
Yesterday I've seen two researchers discussing about if it was really necessary for a post-doc geneticist to visit the place where the blood, weight, height, hair (and other) samples are taken.
From your experience, it is really necessary for a post-doc to travel and visit the field? Does that add real value to a Thesis? Shouldn't the sample collectors report everything like their name, how they measured a sample, etc?

This may be better on Academia.SE

After being a lab tech, just because they should report everything, doesn't mean that they are doing exactly what you think/wish. I would say it is important so you can see if the process of sample collection and processing is exactly what you need for your thesis. I had to follow a written report on how to feed a certain insect, after a few nights the post doc came in and realized there was something missing from the report and we were feeding the insects one the wrong side of the leaf. May not happen to you, but I think its always good to verify.


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Difference between Classic Satellite DNA and Microsatellites/Minisatellites
I am very new to this community and have a basic question about repetitive DNA sequences.
How is different (classic) satellite DNA from microsatellites/minisatellites?
All textbooks give concrete examples of microsatellites and/or minisatellites like --(AC)2--- or ---TACA(TAG)3--TACA----.
Are Classic Satellite DNA just sharing the same properties (perfect, imperfect, compound, complex, di-nucleotides, tri-nucleotides, etc.) as STRs or Minisatellites but the only difference is Classic Satellite DNA are longer?


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What is this spider? Two black stripes

When I opened my front door, there were five of this type of spider sitting on the door. I can't quite find anything online matching the two black stripes on it's back.
I vacummed them up before I realized I should identify them, so the above picture is the only one I have available. (I like spiders, but there were too many.) I'd feel more comfortable if someone could identify the spider and determine it's threat level.
Details:

Inch or so longer
Brown
North East Wisconsin
Wooded Area with little to no grass
Mile away from lake Michigan
Jumpers
Party of about 5
Door was in direct sunlight

It musb be a Lycosa erythrognatha

Judging by the stripes, it's most likely a wolf spider.

If they didn't have a web I would say they're almost certainly wolf spiders, since they don't build webs. Like most spiders in North America, they are harmless to humans.

The stripes in your specimen are drastically different from the OP's spider. This is not a good answer. Please consider updating with more evidence.

The family of Lycosidae (wolf spiders) is correct, but it is hard to justify with evidence aside from the general shape/proportions and colour and the geography of the observation. The most telling attribute to ID wolf spiders is the eye arrangement but they can't be seen in the quality of the pic provided in the question.

The spider in the original post is probably genus Gladicosa.

I think the spider you have found must be https://en.wikipedia.org/wiki/Tegenaria_domestica
In europe this is called the Domestic house spider,It can bite humans and pets the bite is painless.
This spider is common in Europe-USA-Canada.

No, the pictured specimen is not T.domestica or any funnel weaver. It does not have the abdominal markings or leg annulations or spinnerets. The spider in question is most likely a wolf spider.

@JimN thank you for the feedback,if it is a wolf spider you should upvote the other answer it is how our site works ,good answers should be upvoted and bad answers like mine should not.you might consider making an answer to the question yourself.


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Open access datasets for QTL analysis?
I'm just getting started out learning how to use the QTL package in R studio, and I'm trying to find additional datasets to practice with. I've already worked through the datasets here on the Rqtl website. Is there anywhere I can find similar datasets to work with? I'm specifically looking to work with autosomal data.


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What Is This Tactic Called? (Banishing Adolescent Females)
I was watching a documentary about Meerkats the other day and one thing that stuck out to me was how the Mother of a family will banish her daughters once they reach adolescence. If the daughters try to return to the family then the mother will viciously attack said daughter, it's quite sad.
Anyway, the reason for this makes sense (in terms of evolution) because if the adolescent Meerkat were to fall pregnant, she would need more food & support from the clan, thus jeopardizing the original Mother's chance of survival.
I think this is an example of animal behavior/population control where there can only be 1 mature female in the group, like there is with bees. Am I correct in assuming this? Do all animals show this behavior for the same reasons? Also is there a general term that can be applied to this phenomenon?

The reason the dominant female doesn't want her daughter to breed is that she would prefer her own children survive, rather than her grandchildren (the children of her daughter).
I wouldn't call this population control - the dominant female isn't thinking to control the group size, rather, to monopolise the group composition.
The difference with bees is that the genetic relationship between the individuals is more complex (haplodiploid), so the female bees are more closely related to their sisters than to their own offspring!
The general term for the fact that only some animals are taking part in breeding is "reproductive skew".


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Are (muscle) satellite cells the same as muscle stem cells?
In terms of muscle: are the terms 'satellite cell' and 'muscle stem cell' interchangeable? That is, are there muscle stem cells that are not satellite cells, or vice versa?

Well, there is some level of ambiguity here. The distinction at terminology level between "muscle satellite cells" and "muscle stem cells" is generally made by those researchers who insist/emphasize that muscle satellites are not a homogeneous population, e.g. Kuang et al., 2007

we conclude that satellite cells are a heterogeneous population composed of stem cells and committed progenitors.

Or from a review  summarizing that paper:

Due to their position on the surface of the muscle fiber beneath the basement membrane and their characteristic expression of the marker Pax7, satellite cells can easily be analyzed by standard immunofluorescence technologies. [...]
Recent studies have provided more evidence that satellite cells are actually a heterogeneous population where all cells express Pax7 but only a fraction also expresses the myogenic transcription factor Myf5 (Kuang et al., 2007). In vitro lineage analysis shows that the Myf5-positive satellite cells arise from the Myf5-negative cells. Upon transplantation, only the Myf5-negative cells contribute significantly to the satellite cell compartment whereas the Myf5+ cells preferentially undergo terminal differentiation. Thus, the Pax7+ Myf5- cells are true stem cells whereas the Pax7+ Myf5+ cells are more committed progenitors.

However, one has to keep some perspective that these "committed progenitors" are just the offspring of stem cells following a fairly usual asymmetric division strategy broadly used by stem cells in other contexts

Stem cells self-renew but also give rise to daughter cells that are committed to lineage-specific differentiation. To achieve this remarkable task, they can undergo an intrinsically asymmetric cell division whereby they segregate cell fate determinants into only one of the two daughter cells.

Muscle stem cells live in a niche, and the niche mechanism of asymmetric division appears proximity/orientation based, as Kuang et al. found:

Planar divisions were observed to give rise almost exclusively (92%, n = 89 pairs) to identical daughter cells that were either both Pax7+/Myf5- or both Pax7+/Myf5+ [...]
Strikingly, we observed apical-basal oriented doublets where the sister cells assumed asymmetric cell fates (82%, n = 38 pairs). The majority of apical-basal oriented doublets contained a Pax7+/Myf5- cell against the basal surface and a Pax7+/Myf5+ cell located on the apical side against the muscle fiber [...]. In addition, we observed rare events where the basal cell expressed Pax7 and Myf5 and the apical cell had downregulated Pax7 and was presumably undergoing terminal differentiation.

Again, this is a fairly common process, observed elsewhere/before, per the review:

the stem cell is in close contact with the stem cell niche and depends on this contact for maintaining the potential to self-renew (Li and Xie, 2005). By orienting its mitotic spindle perpendicularly to the niche surface, it ensures that only one daughter cell can maintain contact with the stem cell niche and retain the ability to self-renew. In contrast to intrinsically asymmetric cell divisions, which usually follow a predefined developmental program, niche-controlled stem cell divisions offer a high degree of flexibility. Occasionally, the stem cell can divide parallel to the niche, thereby generating two stem cells to increase stem cell number or to compensate for occasional stem cell loss. For this reason, niche mechanisms are more common in adult stem cells, whereas intrinsically asymmetric divisions predominate during development.

However, in contexts when one isn't so interested in the sub-populations of satellite cells during their division process, just their overall contribution to muscle repairs, the terms "muscle satellite cells" and "muscle stem cells" are used (more) interchangeably, e.g. Snijders et al. (2015) write in their review:

Adaptation in the context of skeletal muscle is often discussed as a change in structure and function in response to an exercise stimulus. [...]
Skeletal muscle stem cells, also known as satellite cells, are now thought to play a significant role in the adaptive process.

Interestingly perhaps (from terminology standpoint), Nguyen et al. (2019) avoid using "satellite cell" altogether in their review and talk just of "muscle stem cells" vs "committed myogenic precursor".

To maintain this population, MuSCs may undergo symmetric or asymmetric division, respectively, producing either two identical daughter cells or both a single undifferentiated daughter cell and a committed myogenic precursor.

However this last approach kinda obscures (at terminology level) the anatomical location aspect/angle that gave rise to "satellite muscle cell" in the first place (see Snijders for a mini-history.)

Based on this review, satellite cells can replenish injured muscles, but among satellite cells there are satellite stem cells to maintain the pool of satellite cells.


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What is the name of this plant with 4-5 lobed leaves?
Location is India, It has 4-5 lobed leaves with flowers & pointy seed pods.

I am thinking it is Wild raddish.

50 mins still no answers, what more else details to ID this plant?. Image is not blur very clear.

please include the location of the plant and preferably some info about the surrounding habitat. Also, what are the sizes of the leaves and petals?  Do you have any closeup photos of the leaves or flowers? (Include this info by editing the question directly, do  not add it in the comments). Thanks.

Also, be patient. We're not some  sort of service -- we all have busy lives. But don't worry, when  you get your answer, it should be well supported

Looks like Asian spiderflower.

Thank You. It is Asian spiderflower


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Are there medical imaging devices to look inside artery?
Are there medical imaging devices to look inside artery? If yes, what is there sensitivity i.e. smallest object they can detect?

Smallest object really depends on the size of the vessel and type of object. i.e., it is much easier to detect a small object that occludes a vessel than one that does not; it is much easier to detect a small, dense object with IVUS than one that is similar in density to the artery wall; it can be easier to detect an object on the inner lumen of a vessel rather than deep in the adventitia, etc.


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Do all RNA polymerase in Eukaryotes share the same transcription factors?
I know that TFII proteins bind to cis elements in DNA and help initiate transcription for RNA polymerase II. But do RNA polymerase I and III also use these proteins when transcribing genes? Also, do all genes require promoters/cis elements? Do all genes put in a vector require promoter regions/cis elements?

TBP is common to all three polymerases, even though RNAP I and III promoters don't contain the TATA box. I believe all other core transcription factors are unique to their respective polymerase, though some may be paralogous to TFs for other RNAPs. If I have time, I'll find some references and post an answer later.

Except for the TATA-binding protein (TBP), there are no common transcription factors for each RNA polymerase. However, there are homologies between many of the factors used by the different enzymes.
The paper Conservation between the RNA Polymerase I, II, and III Transcription Initiation Machineriesa gives a good overview over the different initiation factors of each RNA polymerase enzyme. It contains a comparison of various transcription factors in yeast.
Here is an excerpt form the paper showing the homologies between some of the initiation factors of the TFII group and their homologous counterparts. (The first schematic is RNA poly II, the second RNA poly I, and the third RNA poly III):

Source:
a Alessandro Vannini, Patrick Cramer, Conservation between the RNA Polymerase I, II, and III Transcription Initiation Machineries, Molecular Cell, Volume 45, Issue 4, 24 February 2012, Pages 439-446, ISSN 1097-2765, https://doi.org/10.1016/j.molcel.2012.01.023.

Probably.
https://en.m.wikipedia.org/wiki/Conserved_sequence
Here you can find a variety of conserved sequences, not just in eukarayotes but across all organisms. RNA polymerase has only been extensively studied in e coli, where about 100 RNAP related genes have been found. All bacteria seem to share a set of genes such as rpob, terminal domains, and omega subunit. In eukarayotes you furthermore have the 5 polymerase proteins, which closely correspond to archea RNAP. Poxvriuses have their own similar RNAP.
As for retroviruses, the entire science behind them is rather vague so we cannot say exactly what RNAP genes they employ. It is claimed (without much evidence) that they employ a few genes labeled "pol" to achieve a similar functionality.
The promoter regions are not thought to be strictly necessary although they do greatly speed transcription if most genes. They are usually conserved as well.


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What types of plants are Gibberellin used on?
On what type of plant (monocot/ eudicot? family? species?) is Gibberellin used on?
I searched through many sources but could not find whether Gibberellin works for all plants or just a specific type or family. I read that it works well for biennials, but what are some of the other plant families that it is useful for?

I don't know what you mean with 'used on' but gibberellins are plant hormones in ferns, monocots and dicots. All of these plants will react to the application of gibberellin but the effect will depend on the dose, type of molecule and tissue where it is applied. All plant hormones have multiple effects but the classic one for gibberellic acid is stem elongation.
Too much of this can kill the plant though as is the case with Bakanae fungus infection which forces the plant to overproduce gibberellic acid which kills it (reference).
One common agricultural use is boosting the growth of seedless grapes as the seed is an important site of gibberellin production for maturing fruits.
This pdf gives you a reasonable overview of what gibberellins do

Your reference link seems to be broken unfortunately.

@skymningen both links seem to be working for me. One of them is a pdf though, is that the one with the issue?

No, the reference was not working, now it is. Probably got edited.


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Can you identify this tree?

This was photographed near Budapest, Hungary, though my friend said she'd only ever seen these in the USA before.

A question about the same plant: Viburnum.

Yes this is definitely another example of a Viburnum like the one in this post. Without additional pictures, I'm not sure we'll be able to identify it accurately to species/cultivar. As such, -- even though it appears to be a different species/cultivar -- I'm going to vote to close this as a duplicate of the linked post.


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Which ICs can I use to amplify electrical signals from plants?
I wanted to record variation potential and action potential generated in plants due to some stimulus. So which are the ICs that I can use for the amplifying the signals and what kind of experimental setup would be best. I was thinking of using Ag/AgCl microelectrodes with 0.1M KCl solution for measuring the electrical impulses in tomato plants.


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Inheritance of mitochondria
Imagine an isolated population in which each adult female has a distinct mitochondrial genome. In each generation, every adult female has two children (with a 50% chance of being male or female). After each generation, we will assume that all the adults die out, and all the children become adults.
After four generations, what is the expected percentage of mitochondria from the original population of females that will still exist in the population’s children? Express your answer as a decimal between 0 and 1, rounded to three decimal places.
Note: after one generation, there will be 100% of the mitochondria from the original population present in the population’s children since male children receive the mitochondria from their mothers (but do not pass them on to their own children.)

Welcome to Biology.SE. Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. Also, the question has nothing to do with bioinformatics (unlike suggested by your tag).

I don't really get the question. Is it asking what fraction of the unique mitochondrial copies will remain after 3 generations. If it the case, it is impossible to answer without knowing the population size. I guess the question is weirdly formulated and it actually ask whether the allele frequency for this specific mitochondrial haplotype (that is 1 after the first reproductive event) will vary in the successive generations (and I suppose we assume, no mutation and no migration) but that sounds like a too simple  and too unrelated to the special inheritance type of mitochondria

@Remi.b no, AFAICS the answer is independent of population size, and is equivalent to the asking "what is the probability that a female from the initial population has a daughter who has a daughter who has a daughter?" (which, aside from that realization, has nothing to do with bio at all).

@adjan I removed my comment as it contained a math mistake. I tried to write an answer but realized the math are even a little more complex than I first thought (so I have deleted my wrong answer). I think the wording make the question more complex than it seems. What kind a course is it? Also, You are still suppose to show your effort at answering the question

@Remi.b I'm not the OP though

Oops sorry! Wrong name!

This is a question that is not as straightforward as it may seem.
One could make arguments, some better than others perhaps, for several different answers. The way it is worded, one could defend answers from 0.000 and 1.000 and many of the intermediate numbers as well.

After four generations, what is the expected percentage of mitochondria from the original population of females that will still exist in the population’s children?

0.000; the original women died; THEIR mitochondria died as well. None of the original mitochondria still exist.
That may seem, and it largely is, a matter of semantics, but in some ways, it is true without word games.  Every time the mitochondria split, the copies are not EXACTLY the same.  The changes may be so minute they are not always detectable with the current technology, but that does not mean they do not exist.
Some changes occur to the underlying genome; they are rare and may not be readily observed, but that does not mean they do not exist as well. When one of these changes occur, all subsequent mitochondria will have the new genome assuming, of course, that the genome is viable.
If the change will not allow the cell to function properly, this will undoubtedly affect whether the child, as a whole organism, is able to survive.  Depending on the severity of the malfunction that results from the new genome, it may make it more difficult, perhaps impossible, for the offspring to thrive, to mate, and to produce their own offspring which can accomplish the same.
It is also likely that some of these genetic mutations will result in change that is too minute to have an effect on the mitochondria or how it functions. By the same token, it is likely that eventually there will be a mutation in the mitochondrial genome that will have a marked effect on cell function. The change may even improve the overall function of the organism to an extent that will enable the offspring to thrive, to mate, and to produce their own offspring at a greater rate than organisms that do not have this change. Needless to say, the 'improved offspring' will pass on their 'improved genome' to the lucky offspring that will be more likely to thrive and pass it on to the next ..... etc.
There are many factors influencing how well the new genome is going to spread. The population in this particular question was somewhat isolated; this will encourage the genomic change to spread through the general population more quickly. The rate of the spread, however, is affected by many variables.
So in a world with no mutations or any other factors that can result in changed mitochondrial DNA, it would be 1.000 as every offspring gets its mothers, who got it from hers, who got it from hers, so the four types, on an isolated island, would remain four types.
However, in reality, changes do happen. An error(s) in transcription would be one of the most common, but certainly not the only, process that could result in any DNA being changed in a heritable manner.
There is an average rate of mutations. In fact, one can look at the mitochondrial DNA of two individuals and calculate how long ago the genomes were essentially the same. In other words, one could look at a mitochondrial genome from some ancient fossil and tell how many generations it likely took for it to evolve in to the genome of a particular modern individual.  However, as these changes start as mistakes, it can take several generations for a change that is adaptive and will spread to occur.
The only way humans can observe these changes are in animals with very short life spans, such as fruit flies.
There would be very little change likely in only four generations; therefore, unless you had a very large sample size, any prediction would have little more than a theoretical chance to be correct.

Please cite your source.

I think there is an error in the following piece of reasoning: "So in a world with no mutations or any other factors that can result in changed mitochondrial DNA, it would be 1.000 as every offspring gets its mothers, who got it from hers, who got it from hers, so the four types, on an isolated island, would remain four types."
There could be female that have 2 male offspring and others that have 2 female offspring. This phenomenon, called "drift" will cause some genotypes to increase their frequency, and others to decrease theirs, even in absence of selection.


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Alternative conditions for Liquifactive Necrosis
A person is beaten on the head hard enough to swell the whole front part of the head. The body is thrown into the river and recovered after about 36 hours. Is this condition enough for liquifactive necrosis to occur? If not, what could have caused it?


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what are the ethical considerations when preparing a bacterial culture for testing antibiotic resistance?
I cannot think of any ethical issues associated with preparing a bacterial culture to test antibiotic resistance. The bacteria I am using is Bacillus Megaterium so its not pathogenic.
Thanks in advance for your help!

I'm voting to close this question as off-topic because ethics (incl. ethics in biology) is a field of philosophy, not biology. You should give it a try on Philosophy.SE.

While I think the question is off-topic, I could not help but trying to answer it! It is easy to find ethical issues in every activity.
Potential ethical issues

You are killing bacteria
Your research has an environmental cost. You consume loads of plastic thingies for example.
Your research costs money as well. You consume tax payer money (depending on your source of funds)
You are selecting for anti-biotic resistance and might, by mistake, release them in nature (of even they are not pathogens, they might become, they might transfer their resistance to pathogenic bacteria as well or your experience may have all sorts of unexpected consequences)
Are you sure it is not pathogenic? We are never sure of anything, so just don't take risks.
Don't play with nature, you are not God!
Are you helping those nasty big pharmaceutical companies, huh?
You are a clever person. There are so many other things you could do for the world that would be so much more beneficial. Your time could be used for better purposes. You could work on improving sanitation conditions in India, or improve women's right around the world, or help children involved in the current civil war in Somalia for examples.

Basics of philosophy of ethics
For any question of ethics, one has to define his/her own values and from this point this person can formulate an opinion on a particular case. Of course, I personally do not feel bad about killing bacteria and consider antibiotic resistance a very important field of study to improve our everyday well-being but other people may disagree based on their own values.
I am not formally trained as a philosopher. So, please read the wikipedia articles on ethics and values I linked above and if you have any other question of Philosophy, you can ask them on Philosophy.SE

You don't think studying antibiotic resistance is a pressing concern, or is less worthy than the other pursuits you listed?

I did not express my personal opinion. I just listed possible ethical issues. It is up to someone's values to define what is ethical or not. I feel perfectly fine with killing bacteria for example. And of course, I consider antibiotic resistance a very important field of study that has high impact on our everyday well being.

Fair enough....

@canadianer I have now edited the post to try to clarify that I am not expressing my personal opinion. Thanks


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What does 'proper' mean in the anatomical context?
I've seen the word 'proper' in websites, lectures, etc., in the context of human anatomy. But I'm unsure as to what its definition is. For example, the 'oral cavity proper'.

This use of proper is simply using one of the normal English meanings of the adjective proper: "In the very strictest sense of the word or phrase".  Thus, while 'oral cavity' generally might be taken to include, in part, the space between the cheeks and the teeth, the term 'oral cavity proper' refers to a stricter definition which excludes that space.


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Is there a non-bacterial source of lipopolysacchrides
I am wondering if there are any other non-bacterial sources of LPS. To my understanding, lipopolysacchrides (LPS) are components of the outer leaflet of gram-negative bacteria, but are there any other sources of LPS such as fungi?.


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an umbrella term for homeolog and ohnolog?
Is there a word that refer to homologous chromosomes within a polyploid species? If I have AABB species, what is A to B?
The words "homeolog" and "ohnolog" are reserved for the cases if the homologous chromosomes have diverged via speciation or whole genome duplication event. But what if we just don't know?
I hesitate to use word "homologous chromosomes" since they do not for a choromosome pair anymore, they are homologous in sense of an recent common chromosome ancestor.

I think homolog is as good a term as you'll get, though I'm certainly not an expert in this area.

In the case of (A+A'+B+B'), A and A' are homologous chromosomes. In canonically sexual species, one is inherited from each parent. "Homeology" applies to chromosomes that are related by ancestral duplication, yet segregate independently at meiosis.
https://en.wikipedia.org/wiki/Homologous_chromosome

@canadianer Hope is the last to die...
@J It's the same with ohnologs - they are also expected to segregate independently at meiosis. However "homologous chromosomes" are quite tightly linked to meiosis.

@J-- i think that this comment should be an answer. It is more appropriate IMO than Kamil S Jaron's answer.

@MaximilianPress The main problem of J's comment is that the provided reference doesn't say that homologous chromosomes are defined by shared ancestry, contrary it does say they must pair/segregate in meiosis.

@KamilSJaron I haven't looked at the paper I admit- I personally find "homologous chromosomes" to be the least confusing term (none of them are non-confusing, unfortunately), though it's possible that the rest of the world disagrees with me.

Unfortunately, there is no such term. Look at Glover et al. 2016 for a proposal how to unify the ploidy related homology terms, none of the words describes exactly what I searched for, so I at least compiled the relevant vocabulary

homoeolog/homeolog - homologous chromosomal sets in an organism diverged in isolated populations/subspecies and broght back by a hybridization event; note that the two spellings with exactly the same meaning are possible
ohnolog - homologous chromosomal sets originated from a whole-genome duplication (WGD) event; however usually this is used for ancient WGD events (like the R1 and R2 at the base of vertebrates, or the WGD at the base of bony fishes). It is not really possible to distinguish between WGD and hybridization in these ancient cases and therefome ohnologs perhaps suit "unknown" category better.
homologous chromosomes - chromosomes that pair during meiosis (does not strictly correspond to the homology in the context of molecular evolution)
homologous sequences/homologs - any sequences that have a common ancestor (as used in molecular evolution; but does not have to be on a genome-scale or within a genome; tandem duplicates or orthologs in two species are also homologous sequences)

2020 update:
I asked when I was writing this paper. I needed the term to describe the heterozygosity structure of some polyploids and I ended up calling them homolog (A <-> A' divergence) and homoeolog heterozygosity (AA' <-> BB' divergence) or composite when I was unable to set them apart (the majority of cases in fact).


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Why our arms stop growing if mitosis never stops?
I wonder if there's a balance between cell death a new mitosis .

where have you looked for the answer to this question? do you have any ideas?


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Northern Europe tree identification
I've seen it in Nordic countries (Sweden, Latvia). It's a tree that reaches maybe 5 or more meters high and its flowers have a beautiful scent.

Looks like maybe a kind of dogwood, anyone?

Not a dogwood, they have 4 large petals.  I would put in the genus Prunus from the general appearance of the flowers and leaves (https://en.wikipedia.org/wiki/Prunus).  Could be any of a large number of domesticates, maybe the list is shorter that far north.

It's the common Prunus padus, which flowers with its strong scent now in many parts of Sweden (including my yard). At least if you are referring to the common species found in the wild (there are planted domesticated varieties as well). It is common across many parts of Europe though, and not only the Nordic countries, and can be found in Asia as well.


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T-Cell Motility: does motility require direction specific actin polymerization?
T-cells have been shown to migrate inside concentration gradients - both in the direction of the source or away. Even under shallow gradients, t-cells move. I argue that, to be able to move in a directed manner, a cell must be able to have a differential response of actin polymerization and philipodia. But I find it hard to believe that it is a differential response unless the sensor resolution not only communicates centrally, but is also extremely sensitive. How does this work?

I don't have a direct answer to your question, mainly because I'm not an expert on T cell motility. There are, however, some fine resources that help me make sense of it. Video of T cells moving within a lymph node. A paper from the same group talking about T cell motility.

Yes! I have read this fantastic paper, but it simply does not answer the mechanism of action of motility. The video shows clear evidence of philipodia→move, but i wonder how the philipodia is requested to be built in the first place. Perhaps a more direct question would be: is it possible that cytoplasm concentration gradients of phosphatidylserine are creating differential actin polymerization zones based on cell membrane signaling from extrinsic stimuli? I am just not sure if that is even the right question, better to keep it broad... I am just an engineer though, not a biologist.

Okay so you've had some readings, I tried very hard to come up with something sensible. It's a tough one because I work with T cells quite a bit, but mostly in commercialization and manufacturing of T cell-based therapies. So we don't really have to care how they move about.

It's understood at least that leukocyte motility is dependent on cytoskeleton remodeling and actin dynamics. In the blood, as the T cells tumble past the activated endothelium of an affected site, they're grabbed by selectins and integrins expressed on the endothelial surface. These are often illustrated as the adhesion and rolling phases of T cell migration.
Chemokines, which normally form a gradient for T cell chemotaxis, induce changes in the cellular morphology that promote migration into the surround tissues. The cells polarize into a force-generating lamellopodium with a leading edge in the front, and a uropod in the back. It appears as though actin polymerizes in the lamellopodium and juts the cell out toward the direction of the signal, and the uropod contracts in a myosin-dependent manner, releasing molecules bound there, thereby allowing the cell to tug in the direction of the lamellopodia (1, 2).
The mechanism has in fact been characterized by leading-edge redistribution of chemokine receptors such as CCR5 and CXCR4, which may have to do with actin/myosin dynamics and lipid rafts. This makes the receptor distribution asymmetric as well, and so a weaker response to the chemoattractant in the back end of the cell. The best way I could describe it is using the formation of the cSMAC in T cell receptor biology (Figure 1) (3). The SMAC is basically a synapse formed during T cell activation where receptors are concentrated to a particular area where the T cell is meeting the APC.

Figure 1. TCR-mediated cytoskeletal remodeling
The way the authors describe it is the downstream signals from the TCR localize actin pathway molecules to the site of signaling, and causes cytoskeletal remodeling at that particular site.
Studies in neutrophils have shown that polarization leads to a frontness and backness to the cell, regulated by different proteins and inhibit the formation of one another. This is a good paper to read through on that matter, though it's a tougher read in my opinion: https://www.researchgate.net/publication/8957894_Cytoskeletal_remodeling_in_leukocyte_function


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Are there differences in cell membrane cholesterol levels between cell types?
With different cell types, and cell functions, are there distinct levels of cholesterol in each cell type's cell membrane, or do all cell types have a similar amount of cholesterol?
I am assuming certain cell types require different levels of cell membrane stability, and as such, different levels of cholesterol in that cell membrane.

You're right, different cells have different quantities of cholesterol within the membrane. For example a red blood cell will have more cholesterol in it's membrane compared to an epithelial cell in the small intestine. This would be because the blood cell is free floating within the body rather than being physically adhered to something, so a greater level of stability is needed. It is solely dependent on the cells function.

Thank you for the answer! can you provide any links to literature that provide evidence of this?


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How does Line Integrate work on a laser scanning confocal microscope?
Most microscope software provides options for line average or line integrate as a function that helps the signal to noise ratio when taking an image. The math behind line average seems straight forward, but not so much for line integrate.
Line average takes X number of scans per pixel and averages the scans into a final pixel intensity. The same principal of multiple scans for a single pixel is taken for line integrate, but the math involved in the integration of the intensity is not clear to me. I assume it involves summing pixel intensity and operating on that somehow, but it simultaneously is able to reduce noise in the system so I am not sure what else it is doing.

Most microscope software provides options for line average or line integrate as a function that helps the signal to noise ratio when taking an image.

Averaging sums the lines and then divides by the average number. Integration sums the lines without dividing.  They're functionally the same thing just with different scales.

I assume it involves summing pixel intensity and operating on that somehow, but it simultaneously is able to reduce noise in the system so I am not sure what else it is doing.

In terms of shot noise, both have an equal reduction.  If you are averaging over extremely dim signals at low gain (particularly those averaging less than 1 DN per pixel), integration can save you signal from being rounded down to zero.


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Why do turtles ride on alligators?
I often see pictures of turtles riding alligators, I even saw that in a zoo once, but why do they do that?
Is it some sort of camouflage technique for the turtles? And why doesn't the alligator get it off?

turtles will crawl onto anything to get out of the water and bask, fallen logs are common and they likely cannot tell the difference between a still alligator and a log.  It might also be possible that the turtles do know what the gator is and are hoping to tag along and pick up scraps after it strikes.
I image that for the gators thrashing around to dislodge the turtle has to high a risk of scaring off prey so they just put up with it.


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How quickly do bacteria lose genes after selection has been removed?
If bacteria are subject to a biocide and then that biocide is removed from the population, how quickly will they lose that gene that encodes for resistance?


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Bug ID? Lower New York
Found it on the floor of my basement laundry room in a mostly wooden house in the woods in Westchester County, NY. However I had done a mountain hike (same general area) and I may have brought it from there on my pants or something, but I'm not sure.
When it noticed me it stopped moving, but it was still alive because when I put it in this cup for a pic I accidentally flipped it upside down and it started squirming to get itself upright.

That's not an insect but a crustacean (it has more than 6 legs).
It is a woodlouse (plural woodlice). A woodlouse is one of the few terrestrial isopode crustacean. There are about 5000 known species of woodlice. I have no idea which one is the one you captured!

Woodlice are generally appreciated in gardens as they control pests. They sometimes get inside searching for moisture. While it may not be pleasant to have woodlice at home (just because they look disgusting to many, me including), they do not spread disease or cause much damage.


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What is the best way to make a phylogeny from a list of genera?
All I have is a list of about 500 eukaryotic genera, and I need a neighbor-joining tree to show their relationship.  I want to cast on top of this tree the loss of a particular enzyme.  Is the best way to do this to make a 16S phylogeny?

Do you have any information besides their names? Like 16S sequence data?

16S phylogeny would only work for bacteria and archaea unless you are talking about mitochondrial or chloroplast 16S rRNA. Your phylogenetic marker choice should depend on which phyla you are looking at. I suggest you try using Ef-tu if your genera are highly diverse
http://www.scs.illinois.edu/schulten/tutorials/ef-tu/eftu_tutorial.pdf
Once you have a tree in Newick format, iTOL has some nice web tools for overlaying data on trees
http://itol.embl.de/itol.cgi


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Text Book Recommendation: Organic Evolution
I was wondering if anyone could point me in the direction of any text books on organic evolution? I have recently become interested in the subject and would like to know more. I think an undergrad level book would be a good place to start, but if you would like to recommend any graduate level books it could also be helpful.
I have a background in mathematics and modeling using mathematics. I have also taken a genetics class and an intro to cell biology class as well as read some papers on both subjects. Any help would be nice.
update
I was looking for a higher level discussion on the mechanisms of evolution. A better term to use might be evolutionary biology.
Sorry for the confusion I was under the impression that "organic evolution" was a common term.
Thank you for your time.

Do you mean 'evolution of organs' or 'natural evoltion', or something else with organic evolution ?

Please clarify what you mean by "organic evolution".

Thank you for the help Remi.b I will look in to the books you have recommended.

Organic Evolution - Definition
'Organic evolution' was a common term. It is just rarely used today. Today, we just say 'evolution' or 'evolutionary biology' when referring to the field of study of 'evolution' (or of study of 'evolutionary processes').
Book recommendation
Math oriented
As you are used to work in applied mathematics, you'll definitely be interested in an intro book to population / evolutionary genetics. Population genetics is the mathematical basis of evolutionary theory. You will find recommendations at the post Books on population or evolutionary genetics?.
For you, I'd recommend Population Genetics: A Concise Guide as a start (or another one presented in the first section of the top answer to the post I referred to above). If then, you like coalescent theory (branching process), you might want to look at Coalescent Theory: an Introduction or some other more specialized books.
Not Math Oriented
Maybe you'll want something more introductory with much less math such as the Evolution: Making sense of life by Zimmer and Emlen or Evolution by Futuyma. These books are classic textbooks for intro class to evolutionary biology in Bachelor. These books will have the advantage to present you some other subfields of evolutionary biology such as the diversity of life, reading phylogenetic trees, ecological relationships and many other things that the books of population genetics don't go over.
Most common fields of math used in evolutionary biology
The most common fields of mathematics used in evolutionary biology are system dynamics, game theory, approximation theory, probability theory, branching processes and diffusion equations.


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what chromatin factors are the most potent supressors of meiotic crossover?
I think linker histone H1 is probably involved, but the literature is scant.  What else prevents crossovers from becoming hyper-frequent during meiosis?


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law of laplace and pressure developed in arteries
in arterioles the pressure depends on
the impedance of the vessel(elasticity and youngs modulus)
cardiac output
pre arteriolar resistance
what i want to ask is will the pressure also depend on law of laplace
for eg.
if a there is peripheral vasodilation( the muscles of the artery wall are relaxed) so the tension is less
the radius is high
and hence using the equation( pressure=2*tension/r)
the pressure in the arteriole is low
is this arguememt valid??