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Large black caterpillar, cocoon, moth - Los Angeles
This is my first visit here, probably the first of many, since I have many species to identify!
The first is a regular resident of my back yard in the Los Angeles neighborhood of Mt. Washington. It's a large black caterpillar that comes out at night to feed on what I assume is native flora. I have seen as many as five or six at a time in a good (wet) year, but the last couple of years have literally seen only one at a time. Note the ant in the lower left for scale:

A couple of years ago, I brought one home and kept it in a terrarium until it pupated and hatched.  I have a picture of the cocoon, but can't post more than 2 links right now. It was dark brownish-red, with strands of silk that looked to anchor it to the ground, with the empty body on top.
It turned into this very pretty moth:

Unfortunately, it beat up its wings a little, as it took me some time to realize it had hatched. It was released at night.
I had a possible ID at one point on another website, but I didn't follow up with them, and have a lot of trouble searching there for my old thread. Found this place, and thought I'd give it a shot. As I say, I have many more species questions, but I'll just start with this one. Many thanks in advance.

Based on the image of the moth, I think this is a Painted Tiger Moth (Arachnis picta). See the image of the moth from the Wikipedia (you can even see the yellow color at the head region):

An image of the caterpillar can be found here, but this is less decisive.
It also fits with the geographic location where you found the moth, see here.

That was fast! Thank you! The location does fit, because that's the same one! Tha'ts the page I couldn't get back to, and couldn't remember the possible species they had mentioned. Thank you very much.

@Chris - You do realize you used the OP's own photograph as a source, right?

@anongoodnurse I see different images in the question and my answer.

@Chris - You linked to the OP's photograph as a source for your answer. Still, it worked out well for the OP sice he had been searching for it.

Yes, it did work out well! They are cropped differently, so it wouldn't be immediately apparent that it's the same picture. Thanks again.

@anongoodnurse Now I got it, strange coincidence.

@Chris - I did upvote you, btw, regardless. Good answers are good answers.


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What is a "noninvasive" biomarker for a disease?
What is a "noninvasive" biomarker for a disease? I know what a biomarker is, but what makes it noninvasive?

The term "non-invasive" probably refer to the sampling method rather than the nature of the biomarker. One would probably need the original paper and citation where you found this term in order to answer the question.

There are tons of papers that use this term, and none that I had a look define this term. All those papers as well as Wikipedia assume the readers already know what it is.

A biomarker, or biological marker, generally refers to a measurable indicator of some biological state or condition. - Wikipedia

The presence of certain 'things' (sorry for being vague) in a tissue obtained invasively - via biopsy, for example - are considered biomarkers for, say, a cancer. It could be histopathological - a particular abnormality seen on staining the tissue - or it could be the presence or absence of a membrane receptor, etc.
A non-invasive biomarker is simply one that can be obtained easily and without "harm" to the (patient?), for example, to identify the potential presence of a cancer without the need for a biopsy. (Obviously, this doesn't eliminate the need for invasive methods. It just adds to the arsenal of detection methods.)
That is the usual meaning of non-invasive biomarker in the many, many papers using the term (at least medically), such as the one cited.
Serum microRNAs as non-invasive biomarkers for cancer

Although one could argue that a blood draw is still invasive. I use the term non-invasive to refer to things like the presence of lumps in a cancerous breast (something that can be palpated) or the yellow-tinged eyes and skin correspondent with various diseases of the liver, that sort of thing.

@MattDMo - There are biomarkers that don't involve venipuncture (like exhaled substances), but the literature doesn't use the term like you do, as evidenced by the thousands (literally) of papers about them.

So a biomarker in the blood is non-invasive? Hmm. I'll have to chat with my colleagues about that...

@MattDMo - Please do. Serum biomarkers are considered non-invasive when the gold standard is an invasive study. Again, I can cite you papers that use it in this way (see the one cited in my answer, for example.)

No, that's fine, I believe you. I just want to make sure the rest of my team and some of my senior colleagues in the department all think the same way (I'm guessing they do), because I've somehow missed picking up on that in my reading. TIL :)

So even something like a leukopak is non-invasive, but a needle/punch biopsy is invasive? I'm just wondering where the line is. I'm guessing it's whether or not solid tissue is removed...

@MattDMo - Needle biopsy is considered an invasive study. I think the difference is that an invasive study obtains a tissue sample. A buccal swab, however, is considered by many - but not all - as non-invasive, even though tissue is obtained (others call it "minimally invasive".) So, TIL, as well. Thanks. :)

source: Stack Exchange

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

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Why do some men have patchy beards?
Why do some men have patchy beards? Or more specifically, why would some hair follicles lack sufficient 5-alpha reductase while others nearby don't when their genetic code is identical and they are both the same type of cell? (See below.)
(Though my actual question is more broad in nature, the answer to this particular example should give me what I'm looking for.)
On this website (http://beardcoach.com/2009/11/why-you-have-a-patchy-beard/) explaining why some men grow patchy beards it says:

"When the dermal papillae of your beard follicles utilize testosterone, they actually metabolize it and create another androgen as a byproduct called dihydrotestosterone...To utilize testosterone and create dihydrotestosterone, your beard follicles need yet another substance, an enzyme called 5-alpha-reductase.  This enzyme is necessary for this conversion, and if you have low levels of it, then you have low levels of dihydrotestosterone.  More importantly to the topic at hand, if you don’t have enough 5-alpha-reductase, the dermal papillae of your beard follicles can’t properly use testosterone to tell your hair matrices to make hair.  And if your beard hair matrices aren’t making hair, you aren’t growing a beard."

What it doesn't explain is why certain hair follicles have sufficient hormone (or enzyme to utilize it) and others don't.

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


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What is the Cordil that Edward Topsell describes?
In his "History of four-footed beasts and serpents", Edward Topsell describes a "serpent" called Cordil. Since he lists everything that crawls on the ground as a serpent, regardless of being a reptile, amphibian or even insect, there seems to be a wide array of possibilities.
So far, I couldn't find anything about what the cordil described here seems to be. Does anybody know more?

Your link says:

[...] whereof the Latines derive or rather borrow their Cordulus, and
  Cordyla [...].

Wikipedia says about this:

The genus Cordylus (Sauria: Cordylidae) includes a wide variety of small- to medium-sized spiny lizards from Africa, collectively called girdle-tailed or girdled lizards.

Tropical girdled lizard (Cordylus tropidosternum)
Source: Wikipedia


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What will happen to a neuron if I suddenly remove the pump but not the leaky Na+ and K+ channels?
K+ is more abundant inside the cell and thus has a propensity to move outwards. It has an equilibrium potential of -80 mV. Na+ is more abundant extracellularly and thus has a propensity to move inwards. It has an equilibrium potential of 58 mV. The resting membrane potential of a cell is about -70 mV. So, K+ moves out (more towards its equilibrium potential) and Na+ moves in (more towards its equilibrium potential). The pumps throw out the Na+ and bring back in K+ thus maintaining their concentration and hence the membrane potential.
Now if I suddenly remove the pump from the cell, what would happen? Will the cell moves towards K+'s equilibrium potential or towards Na+'s equilibrium potential? I know that the answer is that the cell will discharge and have a membrane potential of 0 mv, but I don't understand why.

Both Na+ and K+ will move according to the electrochemical gradient. Given that K+ leaky channels are ever present, the cell is already around its K+ equilibrium. If you introduce leaky Na+ channel and remove the pumps, eventually the cell will be nothing more than a passive membrane and it will adopt the same concentrations of ions as the extracellular space, i.e., Na+ will pour in along its electrochemical gradient, after which K+ (formerly already at equilibrium) will start pouring out alongside its chemical gradient, due to the reduced electrical gradient because of Na+ coming in.

Why will K+'s electrical gradient reduce due to Na+ coming in? And say, if I remove the pump but do not introduce Na+ leaky channels, then what will happen? Will the K+ still pour out?

@BlackDagger -  1) inside less negative 2) more slowly - eventually every battery discharges

Why will it discharge eventually --- I'm asking from a theoretical point of view.

@BlackDagger stochastics; channels are never fully closed. A cell is not a sealed container. Even batteries discharge spontaneously.

No I mean, why will the cell discharge? The K+ will pour out but as soon as it reaches the equilibrium potential of K+, it should stop pouring out and reach a steady state. Why will it further discharge and go to 0 mv.

cause Na+ goes in


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How does the brain immediately know when one's thirst has been quenched?
The question struck me the other day when I drank a glass of water. I understand that there are at least two conditions under which the brain signals thirst: extracellular thirst, when there's not enough fluid in the blood, and intracellular thirst, when the cells need more water to lower the concentration of osmolites.
However, it takes time for water to enter the bloodstream after it has been ingested, and it spends at least a little while in the stomach.
Why does the sensation of thirst disappear despite the water having not yet made it into my bloodstream?

There are two different aspects to or drivers of thirst, osmolality and hypovolemia, with plasma osmolality elevation being the more potent stimulus of thirst.
As stated by @arboviral (and supported by his link), not a lot is known about the mechanisms of immediate thirst satiety. Much more is known about the mechanisms causing thirst, and the mechanisms of return to normal serum osmolality over 120-180 minutes after rehydration than those immediately satisfying it.
Most of the research on this is old (pre-2000). In one often-cited very small study 1, swallowing and esophageal reflexes (or as the authors termed it, “oropharyngeal metering”) had a significant effect on relief of thirst, that is,

the act of swallowing helps to regulate the volume of fluid ingested by providing an integrated signal proportional to the cumulative ingested volume.2

Study participants were all mildly dehydrated. One (control) group was allowed to drink ad lib. Another was allowed to drink ad lib but as they did so, the fluid was simultaneous extracted from the stomach by a nasogastric (ng) tube already in place. Interestingly, the difference in the amount of fluid ingested between these two groups (N.B. ad lib) was only 15% (the latter group drank a bit more.) The third group was given fluid by ng tube only.
The very act of swallowing fluid boluses induced satiety. However, plasma arginine vasopressin levels (involved in the regulation of fluid intake) dropped rapidly during the first 5 minutes of drinking in both ad lib groups, but not in those given fluids via ng tube, so it is not only mechanical receptors that are involved in quenching of thirst.
This confirmed an older study which demonstrated the importance of the rapid drop in plasma vasopressin in hydration before major changes in plasma osmolality occurred.3
Given the lack of extensive research and the relative immediacy of thirst suppression, The most likely explanation is a combination of sensory modalities and reflexes (mucosal wetness, temperature of rehydration fluid, mechanicoreceptors in the oropharynx, esophagus, etc.), and some rapid hormonal changes - e.g. in AVP - are responsible for limiting the amount we drink when thirsty.
1 Regulation of fluid intake in dehydrated humans: Role of oropharyngeal stimulation
2 Influence of age on thirst and fluid intake
3 Acute suppression of plasma vasopressin and thirst after drinking in hypernatremic humans

Satiety is divided into pre-absorption and post-absorption - the mechanism you're asking about is preabsorption satiety, which as you point out occurs long before the water can be absorbed into the bloodstream and appears to be remarkably accurate. The receptors and underlying mechanisms of pre-absorption satiety are not fully known but are thought likely to include moistening of the mucosa of the mouth and stretch receptors of the stomach and intestine.
I'll try to fill this out later but there's a longer description with diagrams on p309 of Schmidt & Thews (2013) "Human Physiology" (published by Springer).

Interesting. I considered the possibility of stretch receptors in the stomach, but I don't see how they could distinguish between water and food, since eating doesn't make you any less thirsty. And it seems to me, from a layman's perspective, that moistening of the mucosa could signal that some fluid has passed recently, but not the amount or the composition of the fluid.

I'd say the answer is easy.

Since the whole body is one body all you need is the change of of water saturation in a part of you to determine / extrapolate how much water has been ingested.
We all came from the water and are mostly made out of water. So it's not like water is a foreign substance and we needs special receptors in order to determine water content.
We are water. And the system has evolved over time to be built in. I.e. the ones with a broken system have died of dehydration and anybody else survived.
Of course you might be looking for one singular mechanism that says stop, that's enough. But it's a mixture of body temperature, what you have eaten, how much energy you have, etc. (water requires energy in order to be heated to your body temperature)
That reminds me that apparently in hot regions you are supposed to drink tea or warm water because that allows you to drink more / be better hydrated. Based on that I'd guess it's just a temperature gradient? I.e. the water cools you down, and when it becomes too cold in your insides, you stop until you are hot enough again.

It would be most helpful if you could provide links for these assertions.

I could post a link to my own answer. Would that help?


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Respiration of an animal cell media
I want to do respiration process of an animal cell media in laboratory environment.
I don't entirely sure how to supply it with Oxygen to the process because it is a gas, but not a liquid.

You want to grow animal cells in cell culture flasks?

@Chris I wanted to grow them in petri dishes, but I'll check it out!

That's basically the same.

@Chris so yes, I consider it as laboratory environment. I just look for a technique of supply.

Does this answer your question?

@Chris So are you basically saying I can just put Oxygen into container with a cell and it will absorb it by diffusion? I ask just to clarify.

@CubaQ it sounds as if you have little or no experience with growing animal cells in culture.  Be aware that there is a lot to know, and if you do things wrong (even slightly wrong) the cells will die very rapidly.  This isn't something you can improvise off the top of your head.

@CubaQ Yes, that's how it is done in the lab. If you have special requirements (higher or lower oxygen content) you will have to adapt this.

Supply of cells growing in adherent culture is unproblematic, as long as you don't fill too much media in the petri dish/cell culture flask.
Oxygen supply here work by diffusion which is getting more problematic if the layer of media covering the cells gets to thick. I usually follow the recommendations of Corning for the amount of media to be used in the flasks/dishes:

The complete information can be found here, other companies have similar data sheets available. With these amounts I do a lot of cell culture work and I have no growth problems.

I used to put 4ml of media in t-25 and 9ml in t-75, and change it in ~2 days. I mostly handled HeLa, HEK, Neuro2a and U87 cells. Worked fine for me.


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A question regarding trichomes in plants
Trichomes in general are features of xerophytic leaves, which reduce water loss by evaporation by trapping water vapor and increasing humidity (as a result lowering the water potential gradient).
BUT I wanted to know whether trichomes also reduce water loss by decreasing "surface area" of the leaf, so that less water loss occurs (considering they occur as finger-like projected structures that occur in large numbers)?

Trichomes can serve the purpose you ask about, but certainly not only that. They also appear on a great many other, some very delicate, plants from many different habitats. Decreasing water loss is only one of a number of different functions they might serve.
But with respect to xerophytic plants, trichomes are still a projection from the leaf surface and so, by definition, increase the surface area of a leaf by a significant amount.  However, it's not the surface area per sé that leads to water loss, it's increased evapotranspiration which can be caused by and mitigated by many different factors, one of which is, indeed, trichomes.
Some trichomes, such as those on Tillandsia species, occlude or reflect light.  This reduction in incident light is primarily what protects the leaf tissue from damage and helps reduce water loss due to heat. Such trichomes may also function, as you mention in your question, by creating a insulating layer of still air around the leaf, thereby reducing diffusion of water vapor away from the leaf and creating a smaller gradient, though this is usually not their primary function.


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What is the most up-to-date CRISPR/Cas9 protocol?
I am collecting literature to start a new project on CRISPR/Cas9 gene editing. I must put together a protocol to start and am intending to use the following paper as guidance:
"Genome engineering using the CRISPR-Cas9 system". Nature Protocol 8(11):2281-308 · November 2013
Could you please indicate whether this is the most reliable and recent published general protocol for the CRISPR/Cas9 system.

A PubMed search will tell you that.

Dear  MattDMo, I am aware of that. There are many papers to choose from and go through all will take large amounts of time. What I am aiming for is to collect information from experienced people and optimize my time. Thanks

Sergio - the way to do this is to search pubmed, and sort by date. Alternatively, email somebody from a lab who is currently performing CRISPR and ask them, usually people are happy enough to help with simple questions like that.

You can easily find out if it is most recent, if it is most reliable is an opinion-based question and as such out of the scope of this platform.

It really depends on what you want to do with it. Sticking to genome engineering in Human cells, Nature Protocol 8(11):2281-308 · November 2013 is the de-facto standard. One improvement I suggest is to replace the "Surveyor Assay" with deconvolution analysis of sequencing traces using TIDE.


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Are there genes in sex chromosomes that determine facial features?
My friends and I were bored enough to try out this activity.

Picture a teenage boy in your mind.
From this picture, remove any accessories (glasses, piercings, etc.), moustache or beard, then replace the hairstyle with that of a stereotypical teenage girl.
Are you possibly convinced if someone tells you that, this picture was originally of a teenage girl?

I tried it by picturing a few boys who are my friends, but still, I was never convinced because I feel that there's something inherent about the facial features of these boys that made them appear boyish rather than girlish.
If this is not some psychological effect caused by my acquaintance with the boys I pictured (as I know them well so I cannot accept the mapping of their faces to the opposite gender), then are there really biological factors, genes in sex chromosomes in particular, that result in differences in the development of facial features between males and females?
Apparently, "facial hair" isn't an acceptable answer...

Yes, having a Y chromosome does cause specific alterations to facial structure.
The Y chromosome doesn't contain much actual genetic information. Most of the information needed to activate the male developmental program (the female one is the default) is in just one gene 'SRT', the other genes on the Y chromosome aren't super important, such that you can get a normal looking (but infertile) man if this gene is transferred onto an X chromosome.
This SRT acts as a switch causing various changes, but one of the most important ones is the higher production of testosterone. Testosterone (and some other hormones called  'androgens' cause changes to a lot of things, and one of them is facial morphology. In fact weirdly, the bones in the face retain the capacity to grow in adults, so you can give someone hormone treatment and their facial structure will change (google this and you'll clearly see the difference in people's facial shape after hormone therapy for sex change procedures - especially around the jaw). There is also some correlation, in both sexes, between the amount of testosterone in someones blood and the 'manliness' of their face.
Your teenage friends are currently undergoing a natural process similar to artificial hormone treatment, and their faces will get more and more male looking as puberty goes on.

Any reference ?

For which claim? Most of that is pretty basic. For the association with T and male facial characteristics see e.g. this

@DermotHarnett - +1 for this answer. Usually when someone requests a source, it's good to edit it into your answer (per site guidelines). There are lots of papers to support this answer even more strongly, and even starting with testosterone exposure in utero (e.g. Whitehouse et al, Prenatal testosterone exposure is related to sexually dimorphic facial morphology in adulthood).

@DermotHarnett I'd be wary of claiming the "default" is female, considering (among other things) a single X chromosome will result in Turner's syndrome, not a characteristically distinct female or male.

The answer is a bit of a 'yes and no', though mostly 'no.
The Y chromosome has very few genes, but arguably the most pivotal is the sex-determining region Y or SRY gene, also known as TDF or testis determining factor.  The protein this gene codes for acts essentially as a master switch for male phenotypes by triggering the development of testes in the developing fetus.
One of the primary function of the testes themselves (aside from sperm production), is the production and release of testosterone.  It is the testosterone itself that causes masculinization/male phenotypes. Among these masculine phenotypic changes are a modified subcutaneous fat distribution and a thickening and widening of the jaw bone.
So in this respect, yes, the Y chromosome contains genes that influence facial structure.  However, the influence really occurs at a regulatory level, and there are no 'facial structure genes' per sé on that chromosome. In fact, having a deleted on nonfunctional SRY gene, among other potential causes), leads to a person having an XY karyotype, but often being phenotypically female (a lack of a second X chromosome in this case, however, usually leads to other functional problems including infertility).
Further, there is also a condition known as Androgen Insensitivity Syndrome, wherein a person's cells lack functional receptors for testosterone.  It is possible in this case, for a person to have an otherwise fully functional Y chromosome (including a working SRY gene), but be otherwise biologically female, as it is only the androgen hormones, to which the person's body does not react, that lead to any masculinization in the first place.


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Does reproduction cause aging ? Is aging just a strategy to increase reproductive success in all organisms?
Background for why I am asking this:
I read a book—modern biological theory and experiments on celibacy— which uses life history theory to imply that reproduction is the reason why organisms grow old. Can this really happen?
The book uses several arguments in support of this argument:

Even if an organism does not age, it would still die from accidents.
Therefore, reproduction becomes a higher priority for the organism than repairing and maintaining its body in order to survive over generations.
Consider two organisms, one that ages and one that does not. Now, if the one that ages can 'tune' its rate of aging so that its life expectancy is more or less the same as that of its non aging peer, it will suffer little loss of lifespan and gain a lot of reproductive success in return, giving it a selective advantage.
The book argues that by aging, organisms reduce the cost of dead bodies. For example, if we don't age, all the people dying would be healthy and robust, implying all the energy gone into maintaining health would be wasted. But if, strategically, we start 'spending' health to gain extra reproductive success, we end up gaining what we would otherwise waste. All the really old people in an aging world like ours become corpses even before dying, implying less loss involved.

So, here is my question:
Is reproduction one of the major causes for ageing? Is ageing a strategy to increase reproductive success, as described in the theory above? Does life history theory imply that a 'well fed' individual will strategically age itself to gain a selective advantage? Is that it? Is that why we age?
Some experiments that favour the above theory:

It has been shown in 'hundreds of dietary restriction experiments' done on animals that a decreased rate of reproduction and of aging go hand in hand.
An increase in the lifespan of eunuchs and castrated animals has been confirmed in many experiments.
It has been observed that if a lactating female lacks calcium, the bones in her body are demineralized to nourish her offspring, implying a higher priority towards the child than her own body, which makes sense because the child would outlive her.
Experiments have confirmed that the cost of ejaculate in male adders and Japanese macaques is non-trivial.

It should be noted that this theory assumes life history theory to be correct, and is therefore supported by all experiments that support life history theory.

After reading disposal soma theory, as suggested by rg255 in the comments, I can see that the theory discussed in this book is disposal soma theory with an extra assertion that the best life strategy of any organism is not to have 0 aging, but to have a species specific rate of aging, in order to reduce waste of resources through dead bodies and increase reproductive success.

Comments are not for extended discussion; this conversation has been moved to chat.

Possible duplicate http://biology.stackexchange.com/questions/17077/why-does-evolution-not-make-our-life-longer


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Is there a term for when a detrimental gene can be positively selected for because of linkage to a very fit gene?
Let's say that some piece of DNA would be subject to extreme negative selection if it were independently inherited, but it is very closely linked to an extraordinarily fit gene, and so the complex it belongs to is positively selected for.
Is there a term for this phenomenon?

related http://biology.stackexchange.com/questions/44946/infer-gene-frequency-within-a-species-over-time/45004#45004

Genetic hitchhiking / genetic draft
From wikipedia

Genetic hitchhiking, also called genetic draft or the hitchhiking effect, is when an allele changes frequency not because it itself is under natural selection, but because it is near another gene on the same chromosome that is undergoing a selective sweep.

The term "selective sweep" is used improperly in the wikipedia definition. One should replace the last sentence by [..] but because it is near another allele on the same chromosome that is undergoing positive selection or if we want to reuse the term "sweep", once could say [..] but because it is near another allele on the same chromosome that is sweeping to high frequency
Selective sweep
From wikipedia

A selective sweep is the reduction or elimination of variation among the nucleotides in neighboring DNA of a mutation as the result of recent and strong positive natural selection.

(For the direct answer to your question skip to the end!)
Genetic linkage can affect the spread of other genes. The degree of linkage, affected by the rate of recombination between the point (nucleotide, gene etc.) directly under selection and the other point. If the rate of recombination between to given points is low then linkage between them is high and occurs either because the region has low rates of recombination (rates of recombination can vary across a genome) and/or because the two points are physically very close. When two loci are associated by linkage such that they are more often associated with one another than would be expected under random conditions, they are said to be in linkage disequilibrium.
Selection on linked loci relates to a number of key terms:
Selective Sweep
When a new beneficial mutation arises (or an existing mutation becomes strongly beneficial) and its frequency in the population rises rapidly because of selection. This causes the loss of genetic variation at that locus, and at linked loci, because variants linked to the beneficial mutation also spread (see genetic hitchhiking below). The hardness of a sweep is the result of the strength of selection; hard sweeps occur when selection is very strongly in favour of the allele.
Genetic Hitchhiking / Genetic Draft
This occurs when the frequency of an allele is affected by selection in other loci. This effect is very apparent in Y chromosomes where most of the chromosome does not recombine with the X. Effectively selection then acts on this single non-recombining unit, such that if a deleterious mutation arises on a Y with many good alleles then it will fare better than a similar mutation that arises on a Y with fewer good alleles. This is one reason that the Y chromosome is low in genetic variation; good variants cannot get away from bad variants at other loci, recombination allows mutations to be reshuffled and therefore raises the likelihood of making very good combinations of alleles.

"Under the classical view, recombination allows deleterious mutations to be eliminated more efficiently, and increases the rate at which favourable alleles can be brought together, despite their association with deleterious alleles." - Barton

The effect (signature) under a selective sweep is to see a decline in genetic/molecular variation around a given point (the point being the variant that was directly under selection), with variation being negatively correlated with the linkage (molecular variation increases with genetic distance from the locus that swept). Hard sweeps then have an obvious signature, but soft sweeps are more difficult to spot; soft sweeps can occur when selection on a novel mutation is relatively weak, or when selection suddenly favoured an existing neutral mutation (which therefore had time to become associated with multiple variants by recombination).
Background Selection
Similarly, if a variant is associated with deleterious alleles then it will come under background selection. In this case, neutral alleles can be removed from a population by the action of selection on deleterious variants at other loci. Again, the strength of selection and degree of linkage disequilibrium will affect the rate at which genetic variation is lost at a given locus.

"Under background selection, neutral alleles that are linked to detrimental alleles are driven to extinction, with more drastic effects when recombination rates are low." - Cutter and Payseur

Hill-Robertson effect
The benefit of recombination should be apparent to you from the above descriptions, linkage disequilibrium will slow the rate of adaptation, and the formal name for this is the Hill-Robertson effect (or Hill-Robertson interference), named after the scientists that described it. If there is no recombination in a species with two genes, each with two alleles then the most fit combination of alleles can only occur if the beneficial mutations occur in the same genetic background; recombination allows beneficial mutations to occur in separate lineages and come together later on. Specifically, if locus 1 has two alleles A and a where A is beneficial, and locus 2 has alleles B and b where B is beneficial, the most fit individuals would have A and B, but without recombination these individuals can only come about if the mutation from b->B (or a->A) occurs in an Ab (aB) individual; recombination allows the AB type to come about even if the A and B have distinct origins.
The phenomenon you describe (deleterious mutation spreads by linkage to beneficial mutation) is a form of interference. Adaptation, which would occur by i) spreading the beneficial allele at one locus and ii) purging the deleterious allele at the other locus, is being impeded because the two are under linkage disequilibrium. The net selection effect for this "complex" is closer to neutral than one (or both) selection effect for either locus. One could describe the phenomenon with something like:

"The deleterious allele spreads, despite its very deleterious effect, by Hill-Robertson interference caused by tight linkage to a highly beneficial allele."

Note (and credit to @DermotHarnett): Haplotype is the proper word for what you called a "complex".

+1. I guess the more usual term for a 'complex' of mutations like that would be "haplotype".

Thanks @DermotHarnett - seems haplotype would be a suitable word... I used "complex" because a) haplotype didn't occur to me, b) the op used complex so I stuck to the same language

I used complex because I wanted to be more general and not specific to biology (operating on the assumption that biology is not the only Darwinian system and that linkage could take forms other than due to chromosome recombination). I of course welcome your answer.


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Is metastatic cancer always lethal if uncured?
Can matastases spread in different parts of the body of an animal suffering from cancer grow in a limited way, such as not to cause much more harm that a benignant tumor in those parts of the body would, or are metastases guaranteed to eventually cause death, if left uncured?

What you're asking is essentially to prove a negative ("Are there no ways an unchecked cancer can be non-lethal?"), which is unfortunately more of an exercise in imagination than anything else. The best way I can answer is by highlighting what about cancer actually kills, from which you can personally evaluate if a particular type of cancer fits and would be lethal.
You need to remember that it is not the metastization per se that kills something, it is the growth interfering with critical systems that causes death. Many systems in a body will prove lethal if sufficiently compromised. The brain is an obviously vulnerable point (a sample of one of its mechanisms can be found here), but even something like the lymphatic system, which is notably able to maintain its duties with some components compromised or removed, are ultimately necessary (a compromised lymphatic system will, among other things, leave one vulnerable to otherwise harmless infections). The primary checks to take away from this are "Can a body survive with this system compromised, or to what degree?".
Even in the case of a hypothetical cancer that is not particularly metastatic, but simply growing in a particular area (we'll even be generous and say the particular area is not vital to survival), tumors take resources to maintain, both chemically and mechanically (pulmonary issues are known to occur with this sort of unguided growth). Many of these effects can be highlighted in overgrowth diseases such as in Proteus syndrome (Note - My apologies, this is behind an academic paywall). Considerations for this part are "How many resources can a body afford to lose?" and "Can the heart support this extra mass?".
As an additional factor, tumors that don't allow infiltration by cells from the immune system can be prone to infections, both internally and externally. This is circumstantial, though, and not a core component of a cancer's lethality (mostly).
The mere presence of a tumor is not guarenteed to be lethal, but I would say, ultimately, any continuously-growing tumor will lead to death, simply by subverting the proper mechanisms of the body to a sufficient level.
References:

Papadopoulous et al., Neuroscience (2004);129,1009–1018
Cohen, AJMG (2005);137C,38–52

Thanks! There's a few other documents I'm looking to put in. Is the academic paywall that I'm citing through an issue?

Please add more, great! Paywalled stuff is more than fine. To me, it testifies of someone with an academic background :)

Honorable mention for paraneoplastic syndromes which add insult to injury.

@HarrisWeinstein You can also possibly include the case of benign tumours of endocrine glands (such as thyroid/adrenal etc ) that cause problems due to hormone oversecretion.


text:
Do we know a complete list of nutrients that humans must ingest to live?
When the people who are making "nutritionally complete" foods like Soylent are developing their product, how do they know that they've covered all their bases? You need to have protein, carbohydrates, fats etc., but what about vitamins or minerals?
Has science produced a commonly accepted list of all the nutrients that humans need to live?

For babies there is certainly a formula available for a complete menu for survival: formula*
Here are the nutrition facts from Nestlé's "Good Start":

Formula nutrition facts. source: Nestlé
Comparable lists are available for people that cannot eat normally (e.g. people in a comatose state) and are fed enteral or parenteral nutrition.
*. Remember though, breast is best :)

Turning to Nestlé for advice on healthy eating is like turning to Marlboro for advice on how to stop smoking.

@FelixDombek - it's not an advise on a healthy diet, it's a reference to the composition of baby formula. The *endnote is a dietary advice for infants though!

Is the answer to this specific question (let alone this forum) really the place for "parenting wars" fodder?

@RozennKeribin - this is not a parenting wars fodder at all. FelixDombek questions the credibility of my source and that's perfectly fine. In turn they wrote a new answer, which is even better! This is not a war nor fodder, it's called a discussion.

The most complete list of essential nutrients that I have found is here, together with some scientific references and some more "conditionally essential nutrients":
http://www.nutrientsreview.com/glossary/essential-nutrients
I'll reproduce the main list here:

Water
Vitamins
Vitamin A (retinol)
Vitamin B1 (thiamin)
Vitamin B2 (riboflavin)
Vitamin B3 (niacin)
Vitamin B5 (panthotenic acid)
Vitamin B6 (pyridoxin)
Vitamin B7 (biotin)
Vitamin B9 (folic acid, folate)
Vitamin B12 (cobalamin)
Vitamin C (ascorbic acid)
Vitamin D (vitamin D2 or ergocalciferol, and vitamin D3 or
  cholecalciferol)
Vitamin E (tocopherol)
Vitamin K (naphthoquinones)
Choline (vitamin Bp)
Minerals
Calcium
Chloride
Chromium
Copper
Iodine
Iron
Magnesium
Manganese
Molybdenum
Phosphorus
Potassium
Selenium
Sodium
Zinc
Amino acids
Isoleucine
Histidine
Leucine
Lysine
Methionine
Phenylalanine
Taurine
Tryptophan
Threonine
Valine
Fatty acids
Alpha-linolenic acid (ALA)
Linoleic acid


text:
Pressure produced by blowing with mouth
I need some figures on the pressure humans are capable blowing with their mouth with zero flow. I only need very approximate figures. I'm guessing around 500mm of water? I haven't got a tube handy to try it out.
I've heard that it can also cause damage, eg playing wind instruments has been show to increase health risks due to inter-occular pressure. Any figures on what an acceptable level would be for someone repeatedly blowing for a profession?

Can you add references to "playing wind instruments has been show to increase health risks due to inter-occular pressure"?


text:
Did the Great Oxygenation Event also cause a mass extinction?
It's usually assumed that the Great Oxidation Event around 2.3 billion years ago caused a great extinction of anaerobic life on earth. However, I was reading Nick Lane's book, The Vital Question, and he writes the following:

The 'oxygen holocaust', which supposedly wiped out most anaerobic
cells, can't be traced at all; there is no evidence from either
phylogenetics or geochemistry that such an extinction ever took place.
On the contrary, anaerobes prospered.

Is there really no evidence of such a mass extinction?

The proposed mass extinction due to Great Oxidation Event is actually an elucidation by scientists.
After reading many articles online, although there are evidences of GOE, every article states the extinction of most anaerobes as something that should have happened as a fact (Because $O_2$ is considered poisonous for obligate anaerobes). To better understand this, imagine if there was a spike in Carbon Monoxide in the atmosphere, for Oxygen dependent organisms like us, inhaling $CO$ is harmful and therefore a spike in $CO$ would be toxic and lead to death.
Here are some excerpts, which state the extinction of anaerobes being factual more than anything else:
From Arizona State University, Origins Project >>

In a relatively short amount of time, Earth went from having very
  little oxygen to what may be the highest levels of atmospheric oxygen
  it has ever had. This event had wiped out most of life on the planet
  to which the oxygen was poisonous. Some of these anaerobic organisms
  were though to have survived by burrowing into the earth where oxygen
  levels were survivable.

From Slate.com - Bad Astronomy Blog >>

At some point, though, as cyanobacteria flourished, the minerals and
  other sinks became saturated. They could no longer absorb the oxygen
  being produced. It built up in the water, in the air. To the other
  bacteria living in the ocean—anaerobic bacteria, remember—oxygen was
  toxic. The cyanobacteria were literally respiring poison.
A die-off began, a mass extinction killing countless species of
  bacteria. It was the Great Oxygenation Event.

From Imperial College London >>

The permanent introduction of oxygen into the atmosphere fundamentally
  changed the ecology of the planet. The first impact was on anaerobic
  organisms, which didn’t need oxygen to survive. The rise in oxygen
  levels was poisonous to them and led to most them becoming extinct.
  Some managed to survive, but they retreated deep into the subsurface
  where there is no oxygen.  This was one of the first mass extinctions
  in the history of our planet, and it was also the catalyst for the
  evolution of oxygen-based life – us!

As a result, based on what I have read so far, we really dont have any stone cold proof that rise in oxygen lead to mass extinction of anaerobes. The mass extinction is what scientists consider should have happened as we know $O_2$ is poisonous for strict anaerobes.


text:
Can you suggest me some books/articles about how female birds indicate receptivity to copulation?
Where can I find informations about the topic? I need to find some examples.
I also really need this particular information: I know that many female mammals display lordosis behavior that indicate receptivity to copulation, but can birds do that or it is a peculiarity of mammals only?

Yes, I'm afraid the answer will depend entirely on the species. Please [edit] your question and narrow it down. It is too broad for the site at the moment. You might want to have a look at our [help] to understand what's on topic here.

Thank you for the suggestion. I edited the question and I asked for reference if the topic is still too broad. Is it ok now?

Edited again because the question was put on hold


text:
Are ribosomes assembled in rough ER and Golgi body, or in the nucleolus?
I mean all the components, such as ribosomal RNA (rRNA) are synthesized in the nucleolus, but is the whole ribosome structure assembled in the nucleolus or is it also done in the rough endoplasmic reticulum and Golgi apparatus?

See https://en.wikipedia.org/wiki/Ribosome_biogenesis

Ribosome assembly starts in the nucleolus (of eukaryotes) and finishes in the cytoplasm. However, in the cytoplasm the Golgi apparatus is certainly not involved, and, as some cells have little rough endoplasmic reticulum, assembly does not require that. Thus, the abstract of a review by Fromont-Racine et al. in Gene (2003) vol 313  pp. 17–42 starts with the statement:

Ribosome synthesis is a highly complex and coordinated process that occurs not only in the nucleolus but also in the nucleoplasm and the cytoplasm of eukaryotic cells.

In the 26 pages of this review there is not a single mention of the words ‘endoplasmic reticulum’ or ‘Golgi’.
A more recent (and freely available) review by Thomson et al. in Journal of Cell Science (2013) vol 126  pp. 4815-4820 is in accord with this. It has a pretty poster insert which presents the assembly as a succession of events, starting in the nucleolus, proceeding to the nucleoplasm, and with some final polishing in the cytoplasm.


text:
Are there any (chemical) processes occuring inside a seed while it's in a dormant state?
If a seed were in a glass jar without a chance of germination, are there any (chemical) processes occurring inside the seed while it sits there?
My intuition tells me no since my understanding of seed dormancy tells me that dormancy serves as a delay mechanism to increase the chances of survival of the plant.
I deductively reason that dormancy prevents germination by pausing all reactions (processes) in a seed until a combination of conditions triggers the process that initiates germination.
I've done some research online but I can't find anything to support the "pausing all reactions” portion of my statement which would answer my question.

We can consider two processes that a seed might care about:
(1) Ordinary chemical reactions that just happen in the cytoplasm of the seed cells. It's very hard to stop chemistry! Even in the freezer, chemical reactions occur (slowly). This is why long-term storage of biological specimens is generally in an ultra-cold freezer (-80C). Chemical reactions could degrade DNA and proteins and prevent seed germination, so seeds take steps such as drying to reduce the chemistry going on. But, clearly this just slows down the reactions, as seeds of all types gradually lose their ability to germinate (some faster than others). Spore-forming bacteria are the most successful organisms in this regard: they drastically dehydrate the interior of the spore and surround it with a highly protective coat, and there is evidence that some can literally remain viable for millions of years.
(2) Seed metabolism: enzymatic reactions and the normal biochemistry of the cell. "Dormancy" means in part that seed cells shut down processes like transcription and translation and minimize their metabolism. But, research suggests that the metabolic activity of seeds is not zero - among other things, there are active enzymes that are involved in repairing damage to DNA and proteins.

This is a good answer, but your answer requires references. Please [edit] it and add support for your claims.


text:
Geographical distribution of malaria and tuberculosis
Unlike malaria, tuberculosis (TB) is found across the whole world. Why and explain? I mean why are people affected with TB more than malaria and some say that in cold and developed countries malaria is less but TB cases are more.

Malaria is no longer found around the world because it has been eradicated from developed countries.  It was common in the USA until mid-20th century.

Both diseases have totally different dynamics. Why compare them?

@WYSIWYG Please tell me why this is not a 'good' answer?

The statement in the question about the current distribution of these diseases is not strictly accurate, as shown by the graphic below.

[Malaria graphic: Wikipedia user, Percherie (2006); TB graphic: Corbett et al. (2003)]
However there is no disputing that the contemporary and historical geographical distribution of these diseases differ. Why?
The crux of the answer is that this is because of the different agents that cause these diseases. Malaria is transmitted by certain mosquitoes and is therefore restricted to places in which these mosquitoes are found. TB is a bacterial disease, the geographical range of which is determined by human contact under conditions which favour its transmission.
To expand:
Malaria is transmitted by Anopheles mosquitoes, especially in Africa by Anopheles gambia together with the Plasmodium falciparum parasite. One of the factors determining the mosquito habitat is standing water and the elimination of malaria from Southern Europe followed drainage of the marches and swamps in which it breeds.
That is not to say that this is the only factor in the elimination of the malarial mosquitos from certain parts of the world in recent historic times. For example malaria has not been eliminated from Africa partly because of the cost and logistic problems of implementing programmes of eradication using drugs etc.
Tuberculosis (TB) in humans is caused by the bacterium, Mycobacterium tuberculosis. Its airborne spread was favoured by the crowded conditions in cities following the industrial revolution, and its elimination fostered by improved living conditions and the development of antibiotics in the twentieth century.
Footnote: Some Factors affecting Malarial Outbreaks in Africa
A section from an article by Tarekegn A. Abeku, entitled Response to Malaria Epidemics in Africa, is relevant:

In highlands, transmission is unstable due to fluctuations in temperatures that are normally low. Temperature affects duration of the sporogonic cycle of the Plasmodium parasite within the Anopheles vector, survival and feeding frequency of the adult female, and duration of the aquatic stages.

and

Semi-arid areas, on the other hand, have mostly warm climates, and epidemics are associated with anomalous rainfall, which causes increases in vector breeding and survival.

This is flat wrong.  Malaria was common in the USA before the 1940s.  It was transmitted by Anopheles quadrimaculatus in the east, An. freeborni in the west, and An. pseudopunctipennis along the U.S./Mexico border. All three are still prevalent; thus there is a constant risk that malaria could be reintroduced in the United States.

@iayork I was talking about Africa and Europe, where I believe malaria originated. That is why sickle cell anaemia and the thalasaemias arose. Malaria was wiped out in Europe by draining marches. I think your comment and down vote unjustified.

@iayork I have modified my answer. Biology SE exists to provide answers to biology questions. I have therefore tried to provide an answer to the question, which was about the restricted geographical distributiion of malaria. Is my first paragraph a correct answer to that question? If you think my amplification of that can be improved, please make constructive suggestions to that end and I will consider incorporating them. The risk of the recurrence of malaria in various parts of the world may be a global health concern, but it is not the subject of the question.

@iayork I have further modified my entry by adding some maps. This means that the one-line answer is no longer the first paragraph, as stated in my last comment, but the italicized sentence starting "The crux of the answer..."


text:
T cell sensitivity and persistence to specific bacterial proteins
Currently, the standard tests for Lyme Disease measure antibody production after exposure to a bacteria, Borrelia burgdorferi. Often, the tests are performed too soon after infection, before antibodies can be produced.  Also, infected patients experiencing immune suppression may not have detectable levels of the antibodies to the antigen. In both cases, test results are often false negative.
A new test for Lyme Disease has been developed, ISPOT Lyme by Pharma Labs, which focuses on T-cell activity instead of antibody production. Modeled after the ELISPOT test for TB, it measures interferon gamma (IFN-γ) secreted by T cells in response to stimulation by the B. burgdorferi antigen proteins -- DbpA, OspC, p100, and VlsE-1. After isolating and culturing lymphocytes from a patient's blood sample, they expose the cultured lymphocytes to the B. burgdorferi antigens. If the lymphocytes 'recognize' the antigen, due to previous exposure, they secrete IFN-y which reacts with a blue-colored dye visible in the culture.
Question: Can T-Cell exhaustion affect the usefulness of a serological assay which measures T-cell sensitivity to specific antigens?

It is called ISPOT for Lyme Disease, Pharmasan Labs.  Unfortunately, the only acess I have to information about the test is promotional literature.  However, it is fast being touted among patients in the Lyme community as THE answer to diagnostic testing because it focuses on T cell sensitivity instead of antibody production.

If at all still interested:  The iSpot Lyme test uses the ELISPOT technique to count B. burgdorferi-sensitized T cells by capturing IFN-γ secreted by these T cells. More specifically, when IFN-γ is released a spot of insoluble precipitate is formed at the site of the reaction. Evaluating the number of spot forming units (SFUs) provides a measurement of B. burgdorferi sensitive effector/memory T cells in the peripheral blood. The SFU count correlates to a patients T cell reaction to B. burgdorferi.  That's all I've got.


text:
Exponential growth equation and bacteria
I'm a microbiologist, but I'm teaching some ecology in my intro-level course, so when we got to population growth, I thought I'd use the example of a microbial population. But, I hit a strange problem that I thought maybe an ecologist could help me understand:
Imagine a population of bacteria that can divide every 30 minutes. In one hour, every cell produces four cells. Since no one really dies, the intrinsic growth rate (r) is 4. The exponential growth equation, dN/dt = rN works fine to show the growth of the population: starting with one cell, in one hour it's 4, then in two hours rN = 4*4 = 16, in three hours rN = 16*4 = 64 and so on. At 16 hours, we get to about 4 billion bacteria, which is exactly what the microbiologist expects.
But, we then tell the students that to make it easy to predict future numbers, we can do some math and get N(t) = N(0) e^rt. If N(0) = 1, t = 16 hours and r = 4 bacteria/hour/cell, this gives e^64 which is about 6x10^27. Yikes! Kinda far from 4 billion.
So...why doesn't this work? I feel like either I'm not understanding r correctly (it would have to be down around 0.6 for this to work out, I think) or maybe there's a limit on the equation and it just doesn't work for the absurdly high r of bacteria?
Thanks for the help...

Considering your assumption:

I'm just looking at the exponential part, where the simple exponential
  equation works. If we assume there's sufficient nutrients for bacteria
  to grow unchecked for a number of hours (more-or-less true in a real
  culture)

In your original model you are using discrete states and fixed time steps. So, if 30 min is one time step then after n-steps you have $2^n$ or $4^{(n/2)}$ cells. You are basically counting double steps, which is fine. For a continuous approximation you should estimate the rate like this.
You have the first-order growth equation:
$$\frac{dN}{dt}=rN$$
When you integrate this equation (definite integral) you'll get:
$$ln\left(\frac{N_f}{N_i}\right)=r\tau$$
Where $N_f$ is final number of cells, $N_i$ is initial number of cells and $\tau$ is the time interval.

When the cell number doubles then $\dfrac{N_f}{N_i}=2$ and $\tau=30\ \text{min}$ (doubling time).
 Then your rate constant would be: $\dfrac{ln(2)}{30}\approx0.023\text{ min}^{-1}$
After 16 hours (16×30min) your number of cells would be: $e^{0.023\times16\times60}\approx 4.27\times10^9$ (approx 4 billion).
So what is basically wrong? You haven't rescaled your rate. Since the exponent is $e$ and you know that $a^x=e^{x.ln(a)}$, all you need to do is scale the rate constant with $ln(a)$ (a=2). Moroever, in a continuous model, you don't have fixed time steps. So you scale the constant with the doubling time as well.

@Jon If this answer addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered.

Real bacteria population will likely reach some carrying capacity that will prevent them to grow exponentially. As a consequence, the exponential model will be a good fit for early growth only but after a while, one will need to use some other model (typically a logistic model).
Logistic model
Here, I quickly present one standard model of logistic growth for countinuous (and not discrete) time.
$$\frac{dN}{dt} = r N(t) \left(1-\frac{N(t)}{K}\right)$$
, where $K$ is the carrying capacity. From the above model, you can see that when $N(t)$ is low compared to $K$, then the differential equation is well approximated by the exponential model you described $\frac{dN}{dt} \approx r N(t)$. Setting $\frac{dN}{dt}=0$ shows that an equilibrium is reached when $N(t)=0$ (unstable equilibrium) or $N(t)=K$ (stable equilibrium).
The equivalent model in discrete generation can yield to all kind of behaviour when $r$ reaches high enough values including cyclic variation and chaos.
More advanced models
There are other more realistic models. For example, real bacteria populations could as well consume their resource at a rate that is higher than the rate at which resources are produced and population size would then decay to eventually reach extinction.
You will here the description of a model of population growth that includes predation populations.
Build your own model of population growth
These models are not so hard to build up t fit your needs. The first chapters of A Biologist's Guide to Mathematical Modeling in Ecology and Evolution (by Otto and Day) will help you to build and analyze your own models of population biology if you are interested.

This is helpful in terms of understanding the bigger picture, and I appreciate the reference to what looks like a really helpful book. But for this example, I'm just looking at the exponential part, where the simple exponential equation works. If we assume there's sufficient nutrients for bacteria to grow unchecked for a number of hours (more-or-less true in a real culture), then I think the dN/dt equation and the e^rt equation should give the SAME approximation of population size at a given time. Why do they give such different results?

Either your $r$ is too big (but I think it is not too a bad approximation) or the assumptions that there is no competition for access to resource is violated.

The quantity $r$ must be a frequence, measured in hours $^{-1}$. So it cannot be measured in bacteria/hour/cell. If the number of bacteria is multiplied by 4 each hour, this means that $\exp r= 4, $ or $r= \ln 4 $ , or 1, 39 per hours.


text:
Why is chronic lymphocytic leukemia (CLL) most common leukemia in the West but so rare in Asia?
In "Advances in Chronic Lymphocytic Leukemia" (2013, Edited by Sami Malek), several times it is stated that CLL is very common in Western countries.
However, it is quite rare in Asia. (I do not have data regarding other regions in the world.)
Why would this be? I am familiar with cancers being related to lifestyle, which varies by country. (The obvious example would be how countries with high rates of smoking have higher rates of lung cancer.)
Do we have any reasons why this is? Thanks for any help.

This paper should help get you started. The exact reason is not yet known, but is most likely related to germline genetic differences between the two ethnic groups, as Asian immigrants to the US continue to have a low incidence of CLL.
References:

KAWAMATA N, MOREILHON C, SAITOH T, et al. Genetic differences between Asian and Caucasian chronic lymphocytic leukemia. International Journal of Oncology. 2013;43(2):561-565. DOI:10.3892/ijo.2013.1966.
American Cancer Society: What are the risk factors for chronic lymphocytic leukemia?


text:
Serological assays measuring antibody response
Given that an appropriate immune response to a bacteria may be thwarted in an individual, including not producing all of the antibodies which are known to occur in people who have been infected, or producing insufficient amounts of antibodies specific to a bacteria --- Are all serological tests using antibodies as a basis for detection of a systemic infection inherently flawed? In this instance, I'm assuming appropriate application of a test and competent laboratory methodology. But, equally important, what criteria can routinely be used to consider the efficacy of a particular antibody test, across the board.

Can you give some example conditions under which the immune response may be "thwarted"? Are you talking about immunocompromised individuals, or something else?

Infections, such as flu, mono, and CMV can temporaCrily, suppress immune function so we don't produce antibodies to new antigens.  If these infections are known -- fine. Would be considered when evaluating results from subsequent antibody tests.  But, the primary infections I mentioned may be subclinical for symptoms and still effect overall immune function.  So, I'm wondering if or how results of antibody tests "adjust" for this factor.  Is it a consideration when evaluating antibody tests?  This is the flaw I wondered about and still may not be clear enough.

Antibodies used for serological tests are performed in vitro, and are not required to be effective for eliminating the pathogen. For an infected individual, antibodies may play a role in neutralization, opsonization, or activating the complement system (checkout Janeway's Immunobiology for more details). There are a number of reasons why antibodies may be present and not trigger an effective response down these pathways.
For example, E. Coli O157:H7 produces Shiga toxin and there are immunoassays to test for the presence of the toxin in feces (1). Only low amounts of the toxin is needed to cause disease. Antibodies against the toxin have been seen in individuals with the disease, suggesting the toxin is not a strong enough challenge for an immune response Discussion of (2).
You could go case-by-case for each of the immunoassays and see why their targets are difficult to turn into therapeutics.

Can you add sources to the first part of your answer?

Are all serological tests using antibodies as a basis for detection of a systemic infection inherently flawed?

No
Every diagnostic test must be interpreted in the context of the clinical features of an individual and according to the data about that particular test. Tests of serum for antibodies are no different. See Cecil Medicine Chapters 8 and 9 for a discussion of this. A key passage:

Most tests do not provide a definitive answer about diagnosis or prognosis, but instead reduce uncertainty

Except in cases of passive immunization (e.g., transfused IVIG), the presence of a specific antibody in a serum sample indicates both exposure to an antigen and an immune response. What exactly this means depends on the individual and the test. Though not generally the test of choice for diagnosing active or chronic infection, some antibody tests are excellent indicators of infection in many individuals. A good example would be antibody to HIV.
As with any diagnostic test (again, see Cecil), antibody to HIV was evaluated relative to a standard, giving us a sensitivity (how good the test is at finding disease when it is present) and specificity (how good the test is at excluding disease when it is not present). It's not perfect (I've seen one false positive in my career), and it is not useful in the first few weeks after exposure, but, in general, it is an excellent diagnostic test.
Antibody tests are used for many other things, and again, as with any diagnostic test, they are evaluated for that purpose. Sticking with the use of these tests in infectious diseases, Hepatitis B antibody tests are an interesting example, since antibody to different antigens mean different things. Surface antibody, for example, indicates immunity either from exposure and clearance or from immunization. Core antibody indicates exposure to the virus itself, since core antigen is not present in the vaccine. As with most antibody tests, the antibody class can also give you useful information. IgM antibodies typically represent the initial immune response, where IgG antibodies represent a later response, and either clearance or chronic infection.

Are all serological tests using antibodies as a basis for detection of a systemic infection inherently flawed?

You're thinking theoretically. Serological assays aren't theoretical, they're empirical.
When any assay is being characterized, it will be correlated with a particular outcome. Serological assays are no different. So long as there's a strong correlation with the targeted phenomenon, it doesn't matter if they're theoretically "flawed" (whatever that means); if they tell you what you need to know, then they're functional.
If every time a serological assay reads 40 or higher, an individual can be shown to be infected and every time it's less than 40 the individual isn't protected, then it doesn't matter what theoretical problems there might be with the assay, it can be used to predict infection. For that matter, if every time a ceramic saint wept salt tears it correlated with infection, then the saint test would be perfectly valid in the clinic, no matter how flawed the theory is.
How do you correlate your assay to the presence of infection, or whatever? Typically there are gold-standard tests that are perhaps too time-consuming, or difficult, or expensive to routinely run, and the serological assay will be cross-referenced to that for validation, and then hopefully approved by whatever regulatory body is in charge (in the US, often the FDA).
Don't confuse theoretical reasons with practical considerations.

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


text:
Moth with silver marking on wings
This is a moth that we found on a curtain inside the house a couple of days ago. Unfortunately, these pictures did not come out as well as I thought before I realized it outside. But I was struck my the silver-white eyeglass-shaped spots on the wings. It also had an interestingly shaped head, but that didn't come out well. The closest I have come to identifying it is that it looks similar to a Dot Moth, but those don't seem to be native to Southern California (Los Angeles).
It was about an inch long, maybe less. It vibrated its wings after I disturbed it.

Whatever its identity, it is so wonderful

Based on the overall apparence and the distinctive metallic patches on the wings it looks like a moth from the subfamily Plusiinae (Looper moths). I'm not familiar with North American moths, but after a quick check at species found there Megalographa biloba (Bilobed looper moth) seems likely, and this species is also found in California.

(picture from wikipedia)
Also see the pictures at Bugguide.net.

Excellent! I agree with your determination - I think you have it right. The front legs are similar, as are the markings (I hadn't even noticed the smaller silvery one). And the Wikipedia page shows the distinctive shape of the head that I wasn't able to capture in the photo.I would have had a lot of trouble determining that species on my own. Much appreciated!


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Does the edge effect promote biodiversity?
I define the edge effect as:
A term used to describe what occurs at habitat boundaries where two bordering communities influence one another.
My question is whether it generally leads to an increase or decrease in biodiversity (both evenness and richness) and why.
Also, what are the biogeographic factors that impact biodiversity relating to this edge effect?
I believe that species diversity would increase, as at such habitat boundaries species that inhabit the bordering habitats and those that can also be found in habitat boundaries would be present.
I do remember reading that light intensity increases due to the edge effect and thus also allows for shade-intolerant species to thrive, but I do not understand why.

The question is interesting. The question might be considered as too broad but to even start thinking about the question we'll need a definition of biodiversity. Biodiversity can mean many different things. Did you mean number of species per square meter or something like that? There might have issues with what you would call "different communities" too. Also, if you can include thoughts (if any) and what you've found so far (if any), it may help.

EDGE EFFECT PROMOTES BIODIVERSITY.
EDGE EFFECT OCCURS IN ECOTYPE.
ECOTYPE IS THE TRANSISSION ZONE WHERE TWO COMMUNITIES MERGE.
HENCE SPECIES RICHNESS IS FAIRLY HIGHER THAN THAT OF THE SURROUNDING ECOSYSTEMS.
IF ANY OF THE SPECIES TENDS TO EXPLOIT THE RESOURCES OF THE ECOTYPE IT WHOULD HAVE TO MODIFY ITS CHARACTERISTICS BY THE PROCESS OF  ADAPTIVE RADIATION AND EVOLUTION .
HENCE NEW SPECIES EMERGES PROMOTING BIODIVERSITY.

You have something that needs fixing.

Can you please edit your answer and fix the typing? All caps is hard to read.


text:
How many rounds of TCA Cycle would a complete oxidation of a triacyl(15-Carbon fatty acid)-glycerol, give?
This was a trickier question on a previous test, and I'm still not sure why, but the answer was "at least four". I answered "more than 22" and got it marked wrong. I assume that each fatty acid chain would break down into 1 propionyl CoA and 6 Acetyl CoA, but I'm not completely sure how many rounds this would give us. Can anyone help me out here? Thanks!

I am not too sure but this is my logic:
There would be in total of 18 molecules of Acetyl-CoA which means 18 TCA cycles. Propionyl-CoA gets converted to Succinyl-CoA which is a TCA intermediate (at about half of the cycle). If you do consider this, the 3 molecules of propionyl-CoA would only give you 3 partial rounds (or lets assume 1.5 rounds) of TCA cycle. Still 19.5; less than 22. Even if you consider the metabolism of glycerol, then 1 molecule of glycerol will give you 1 molecule of pyruvate i.e. 1 TCA cycle. So, the total is still 20.5 rounds i.e. less than 22.
I don't know what the other options are but "more than 22" is certainly not correct.


text:
Cell division - meiosis
Really confused. How many chromosomes pairs do humans have in their sex cells? How many single chromosomes do humans have in their sex cells?

Human sex cells, or gametes, have 23 chromosomes - they are haploid. Somatic cells are diploid - they have 23 pairs of chromosomes, for a total of 46.

To add on @MattDMo's comment, each chromosome can be made of a single or two chromatids depending on the phase of the cell cycle you are in.

Terminology is what is holding you back.
What chromosome implies depends on context, i.e. is it replicated or not.
In Meiosis. Gametes arise from Germline cells that have 23 PAIRS of chromosomes. That means, that while there are 23 different chromosomes they come in doubles/pairs. This is the typical X like shape we think about when we hear chromosomes.
Another way, chromosome can means either 1X or 2 single chromatid
MEIOSIS I -- 23X chromosome pairs are duplicate and end up as 46X chromosome pairs (46 pairs of X OR, 92 separate chromatid)
These 46X are divided equally among two daughter cells just like in mitosis. Where now each daughter cell receives 23X = 23 pairs.
MEIOSIS II. The daughter cells in end of Meiosis I divide without DNA replication and the 23 pairs are split among 2 new cells. So now each new daughter cell (in total 4) has 23 individual chromatid (individual chromosomes)
and these are the gametes.
When the gametes fertilize to form a zygote, the zugote product ends up 24X each.
Each X contains, 1 chromatid (|) from the father and 1 chromatid {|} from the mother.
Haploid means once copy of each chromosome.
23
Diploid means two copies chromosomes or 23X
Ref
- Allison Q.N,.(2015), Freeman Biological Science.

Gametes have 23 PAIRS of chromosomes. No. Gametes have 23 chromosomes - they are haploid. Somatic cells are diploid - they have 23 pairs.

Cheers MattDMo cleared it up.


text:
Why human hair is losing its color over time?
Human hair is losing its color over time, that's a known fact.
I would like to know why, meaning what biological processes are involved in this?
Also, is it part of the DNA somehow, i.e. the exact rate of losing the color is known when one is born?

Human hair is losing its color over time, that's a known fact. Is it? I know plenty of elderly people who still have dark hair.

@Matt none that I know of, and even they can't retain the original color, just might lose less color. Unless you have a link to some official post about it?

@rg255 thanks, I searched for "hair" and "color" key words, that one doesn't contain any mention of "color".


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Extinction of non-mammal Synapsida
I am following M.J. Benton's Vertebrate Palaeontology, which explains how many groups of Synapsida were already extinct in the Mesozoic Era, with one obvious exception being the group of Cynodontia, which includes modern day Mammalia.
Nevertheless, I cannot find when the last non-mammal synapsids got extinct and I would be very grateful to anybody giving more information about the topic.

OK, I don't know how I did it but I misread your question as being why all the non-mammalian Synapsids went extinct. I answered your question at the end, but I'm leaving the rest as-is until I figure out how to rewrite it (it was rather too much work to delete).
According to The Wikipedia page for Synapsids, the answer really depends on the Synapsis since there are quite a gap between the start of the Synapsid clade and the appearance of Cynodonts.
The first big "culling" of Synapsids (i.e. the extinction of all groups except one clade that led to mammals - Therapsids in this case) seems to occurred over the Permian era. Some groups went extinct in the early Permian but most groups went extinct at various points during the Middle Permian. No clear reason is given for these various extinctions (though the page for Dinocephalia suggests "disease, sudden climatic change, or other factors of environmental stress may have brought about their end"... which basically covers all possible extinction reasons so that's helpful); it's probably various reasons specific to each. Most species do go extinct after all.
Among Therapsids, the only clade that survived the Middle Permian, most seem to have been wiped out in the Permian-Triassic extinction, the largest extinction event in Earth's history, of which only three Therapsid clades survived: Therocephalians, which went extinct soon after, Dicynodonts, which were extinct by the Early Cretaceous, and Cynodonts. Aside from the usual environmental factors, a reason for the extinction of those two clades could have been competition from the then-ascendant Dinosaurs, and Cynodonts themselves.
As for when the last non-mammal Synapsid when extinct, it appears to have been a member of the Tritylodonts, which survived into the Cretaceous (and arguably having a representative after the K/Pg extinction, emphasis on "arguably"). Mind you these are very close cousins to Mammals indeed:

Tritylodontids ("three knob teeth", named after the shape of animal's teeth) were small to medium-sized, highly specialized and extremely mammal-like cynodonts, bearing several mammalian hallmarks like erect limbs, endothermy and lactation. They were the last known family of the non-mammalian synapsids.

Very interesting and exhaustive answer. Thank you so much!


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What is the most appropriate way to normalize gene expression data?
This question comes because reading a paper about normalization of gene-expression data, is not clear if the method for normalize the data is just for RNA-Seq data or could be applied also for microarrays.
For RNA-Seq data, there are methods of normalization which adjust for GC-content effect or other gene-level effects. It make sense consider these effects in the normalization of microarray gene-expression data?

These methods correct for the biases during the sequencing experiment. Since microarray is a different technique, the biases it suffers from would be different. There are bias correction techniques for microarrays as well, but they are different from the ones used for RNAseq. They cannot be used interchangeably.

Normalization of expression data is a big topic with new methods being published regularly. When approaching something like this you generally want look at people who have done similar things to what you've done, and then once you understand why they did what they did, you can ask what you need to do to answer your questions. Always keep your biological question in mind. For instance if you're measuring QTLs, you'll need to be a lot more careful than if you're just looking for genes effected by a knockout mutation.
In general you want to use quite different methods for RNAseq and Microarray data. The two data types follow completely different distributions (RNAseq gives you count data, microarray data gives you continous signals) and have different types of technical noise effecting them (GC content will effect both, but in a different way). Some methods can be used on both, but usually involve coercing the data into a different form (e.g. mapping counts to a normal distribution). The limma package for R can handle both, using different distributions, and is a good start. Newer, purportedly better methods exist for RNAseq, which I haven't personally used.

Generally speaking for RNA-seq data, you don't want to correct for GC content or other gene level effects (e.g. length) because you compare expression values between conditions WITHIN a gene. For this reason, it is recommended to use raw counts and not normalized values such as FPKM. See Section 2.7 of the edgeR user manual.
This recent benchmark comparing RNA-seq quantification methods may be worth a look.


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Do different emotions produce different tears?
Do tears of joy, laugh, grieve, and others contain different things or are they all the same?

Basal tears

are always in our eyes to serve the purpose of lubricating, nourishing, and protecting the eyes.

Reflex tears

protect the eyes from irritants, including wind, smoke, or onions.

Tears produced by emotion

Although these tears contain higher levels of stress, such as ACTH and enkephalin, and endorphin and natural pain killer, they can also work by directly calming the iris down while signaling the emotional state to others.

Secretion of tears

The lacrimal gland, located in the outer part of the upper eye, is constantly secreting a protein-rich, antibacterial liquid. This fluid goes from the outer edge of the eyeball toward the cornea and lubricates the entire eye surface every time we blink.

Sources:

http://archopht.jamanetwork.com/article.aspx?articleid=625096
http://www.sciencedirect.com/science/article/pii/0002939481906516

Could please post the references to all these claims. Without the references, these are just sentences.

Please cite references that are either peer-reviewed publications, books, educational/informational websites hosted by reputed agencies (universities/research institutes/educational foundations) or even a well curated wikipedia (other encyclopaedia) article. I personally do not consider science blogs as valid references, especially if they are written by non-experts, for non-experts. They are often exaggerated and lack cross references.

@WYSIWYG I agree, I'll add a "good" reference later when I get home


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How does the brain know what to remember and what not?
People remember some information for example when learning for an exam, or remember to go to a shop after work etc., but we don't remember usually much other stuff like people passing us, what was the weather some days ago etc. How does the brain know what to remember and what not, how does it filter important information from not important?

Look at https://en.m.wikipedia.org/wiki/Engram_(neuropsychology).              Totaly anecdotally i would imagine that there is a thershold level/s of excitation of certain neuron to network (check out Jennifer Aniston neuron study) which leads to an imprinting of a memory trace. How you recide to recall would be interesting001

The body of work on this topic huge, so I'll just try to mention a few things.
On the cognitive level, one possible answer is salience (also see here for an article specific to the visual system). You can think of this (in a somewhat circular answer) as the thing that makes certain stimuli stand out from others. Salient stimuli capture bottom-up attention. Another possible answer is top-down attention. This is where you actively/deliberately pay attention to something.
In terms of mechanism, we have to think about different types of memory. For example, there are separate long-term and short-term memory systems (among many other distinctions). In general, there are hypothesized gating mechanisms that determine the information that can enter memory. The gating systems are controlled by some signal that says 'store this information' or 'ignore this information'. Different memory networks can have different gating systems.
There's a lot of work looking at neuromodulators as gating signals. Dopamine and acetylcholine are some prominent examples. For example, people have found that dopamine can modulate synaptic plasticity (the strengthening and weakening of connections between neurons, which is thought to be a primary mechanism of long term memory storage). It can also cause cortical remodeling. For just a couple examples, see:

Zhang et al. (2009) Gain in sensitivity and loss in temporal contrast
  of STDP by dopaminergic modulation at hippocampal synapses.
Bao et al. (2001) Cortical remodelling induced by activity of ventral
  tegmental dopamine neurons.
Froemke et al. (2007). A synaptic memory trace for cortical receptive field plasticity.

On the behavioral level, stimulating the dopamine system can induce particular forms of learning (which you can think of as a form of memory). For example, if you stimulate the dopamine system, an animal may tend to repeat the behavior that led to the stimulation. A pathological version of this is thought to be what happens during addiction with certain classes of drugs that stimulate the dopamine system (e.g. cocaine, but not lsd).
Interestingly, many of the same mechanisms appear to work across species, from sea slugs to humans). Although,sea slugs can't remember going to a shop after work.

Well I have a theory; I think that when we see at something or some event, our brain processes this information in two separate parts. One of them is composed of the objects on which we are focusing. That part is saved in our memory and we know about it. all other objects from that scene on which we are not focusing our attention, are handled by sub conscious part of our brain. And these are also stored in our memory but we dont know about them.
So memory in brain can be considered as a book with events as its contents. Those events on which we focus are placed in the index of this book. Other events are also stored in the book but are not in the index. When we try to remember something our brain checks the index to fetch the relevant information. So even though majority of stimuli received by brain from our senses are stored in brain, we only perceive to remember those events of which we have created an index ( focused stimuli )


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Do bacteria grow on pure dry glucose?
I've accidentally touched pure glucose with my bare hands (fingers to be specific), which was intended for cell-culture.
I'm worried that bacteria from my skin may start to grow on the glucose and contaminate my animal-cell cultures.
Should I be worried about this really and get another glucose packet for it or just proceed to feed cells with that one?

Bacteria or other microorganisms cannot really grow on anhydrous (totally dry) glucose because they need water.
However, they can remain there and cause contamination. Even if you haven't actually touched the glucose sample, there are many bacteria suspended in the air and they may settle down in your glucose packet. When you take the glucose out for weighing, then also bacteria that are in the air, on your gloves, on the paper that you use for weighing, can settle on the glucose sample. In fact any substance, for that matter (salts in PBS, water etc).
That's why before using solutions in cell culture, you have to sterilize them by autoclaving or filtering. Glucose solutions should not be autoclaved because the heat chars glucose. You should filter them using a 0.2 micron filter. All the materials that are to be used for cell culture purposes should be opened only inside the laminar hood.

I wasn't aware of it ! Thank you very much !!!


text:
Does CoA always bind to organic molecules through a thiol bond?
Does CoA always bind to organic molecules through a thiol bond? Sometimes I see it written as SCoA in textbooks but sometimes it's just written as CoA, are those actually chemically different, or just laziness on the part of the author?

This is coenzyme A (CoA). As you can see, it has an -SH group at its end. So when it interacts with other reagents, it forms thiolesters. CoA is just shorter.

Your answer is correct. However, I would mention a third alternative that the questioner may encounter — the one I prefer myself. This is not to use SCoA, but HSCoA in equations. That way e.g. acetylCoA can be written as CH3CO-SCoA and the chemistry of the reaction is apparent.

@David CoA-S-Ac is a term  for acetyl CoA, that I have commonly encountered.

@WYSIWYG Fashions change. I distinctly remember writing CoASH, in fact, but that was many years ago. There may well be a rationale for the change/variation. Anyway readers may encounter different abbreviations for the same thing.

Okay, thanks for these hints. This may will diminish understanding issues.


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Which ingested allergens can be transferred to a partner via bodily fluids?
Can some allergens, such as peanut traces, appear in bodily fluids (saliva, sweat, semen, vaginal secretion) after ingestion?
I would like to know in particular intake of which allergens should be avoided to prevent allergic reaction of a partner due to contact with bodily fluids.

It depends on several factors: what's the biochemical nature of the allergen? Is it a protein? What's its size?
In short, the answer seems to be yes, to some particular cases. For instance, this paper deals with allergens from Brazil nuts transmited by the semen:
http://www.jiaci.org/issues/vol17issue03/10.pdf
According to the paper:

We report the case of a 20-year-old woman with
  documented Brazil nut allergy who developed widespread urticaria and mild dyspnea after intercourse with her boyfriend who had earlier
  consumed Brazil nuts.

Of course, there is no general rule, and each case has to be individually analysed. This makes very hard, if not impossible, to answer your second question ("I would like to know in particular intake of which allergens should be avoided to prevent allergic reaction of a partner due to contact with bodily fluids"), because it depends on the case in question: the allergy, the allergen, the people involved etc.
This Scientific American blog post makes a good overview of the matter:
http://blogs.scientificamerican.com/food-matters/sexually-transmitted-food-allergens/


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Are there specific non-protein substances that pathogens release into their host?
Reading research articles, I have found out that proteins called effectors get released into the host cell when a pathogen attacks a host. My question is, whether pathogens also release non-protein substances?
Have these substances been extensively studied and classified? Is there a list of such compounds? Are these compounds unique to pathogens?

Sticking my neck out (and expecting it to be bitten by a black swan) it appears that all the examples of toxins secreted by bacterial pathogens when they infect an animal host (exotoxins) are proteins.
However fungi secrete a variety of exotic (and often very nasty) small non-protein molecules (mycotoxins). It’s not clear from the question whether you would be interested in these systems as they differ somewhat from those involving bacteria. One difference from bacterial toxins is that fungal toxins not secreted inside an infected cell, but just into their environment. Thus, cercosporin is secreted onto the surface of plants on which Cercospora reside and may be taken up through lesions in the plant. However it is not clear whether the plant is the main target of such toxins, rather than bacterial ‘foes’. So the host/pathogen concept is less clear in this context.
A similarly ambiguous host/pathogen situation would appear to exists with toxins such as saxitoxin, the paralytic shellfish toxin secreted by certain marine algae and cyanobacteria.

I am not sure if mycotoxins actually are secreted by the fungi to aid its parasitic lifestyle.

@WYSIWYG No, neither am I. After reading a bit more I've edited my answer to clarify the situation a bit so the questioner can decide it the mycotoxins are relevant to her research.


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Can all elements be found in our body?
There are many Natural occurring atomic elements.
Can they all be found in the human body?
Is our system capable of letting them all in?
Are they all contained in our food?
Three in one.

On http://www.lenntech.com/periodic-chart-elements/human-body.htmlanguage, you find 118 elements sorted by the percent of appearance in the human body, starting with oxygen (65%) down to "very low traces of lead". There are a lot of elements which can't be found, including Osmium.
You can sort the table by other orders like name, symbol, mass, and others.

Perhaps this is more of a chemistry question than a biology question? Our body doesn't make use of all elements, as far as we know, (somewhere between 20 and 29 elements have been suggested to have some use by mammals) but it probably contains every naturally occurring element in some tiny concentration, if you measure with sufficient sensitivity. Barring obviously those which are extremely rare or unstable.
Proving a negative is very difficult - I don't know how you could say with confidence - "there are zero atoms of osmium in this body".

This question is about biology. It concerns living beings. Bio. -1

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


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Plasmolysis vs Flaccidity in cells
When is a cell said to be flaccid and when is it called plasmolysed?
So far I found that there is a specific relation to osmosis.

Is it a homework question? Please use the homework tag and show you effort at answering the question.

Its not a homework question. ....my doubt !!

Everything isnt homework. .... tge stack community should understand this !@

Flaccidity in plant cells

The failure to display turgidity especially as seen with plant cells.
  The suspension of cells from plants in isotonic solutions results in the state termed flaccidity. On a cellular level it represents a lack of pressure of the plasma membrane against the plant cell wall. A more extreme state, termed plasmolysis, is seen given suspension of cells in a hypertonic solution, i.e., as occurs with bacteria suspended in solutions containing high salt or sugar concentrations.

A flaccid cell is one which is in an isotonic solution, this means that the solution and the cell have an equal water conc.. Although there are always water molecules flowing into and out of the cell, they balance each other out. So a cell is referred to as flaccid when it is between being turgid and plasmolysed.

Plasmolysis in plant cells

If a plant cell is placed in a hypertonic solution, the plant cell loses water and hence turgor pressure by plasmolysis: pressure decreases to the point where the protoplasm of the cell peels away from the cell wall, leaving gaps between the cell wall and the membrane and making the plant cell flaccid.

Sources:

http://www.biologyaspoetry.com/terms/flaccidity_cell_biology.html
http://study.com/academy/lesson/what-are-plasmolysis-deplasmolysis.html
https://en.wikipedia.org/wiki/Plasmolysis

If only some water is removed from the plant cell... then is it flaccid or plasmolysed

Are you sure because my teacher said flaccid.  Flaccid is when little watr is removed and plasmolysed is when full water is removed

Even the definition of flaccid agrees

@Abcd a flaccid cell is one which is in an isotonic solution, this means that the solution and the cell have an equal water conc.. Although there are always water molecules flowing into and out of the cell, they balance each other out.
So a cell is called flaccid when it's between being turgid and plasmolysed.

Ohk ... i agree to you but this book of mine says  : FLACCIDITY IS THE CONDITION IN WHICH THRE CELL CONTENT IS SHRUNKEN AND THE CELL IS NO MORE TIGHT

I m a tenth grade student using icse concise biology


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Opening and Closing of stomata
Which is the more accepted theory for the opening and Closing of stomata : the sugar concentration theory or the k+ ion theory ?

I am unaware of these two hypotheses (not theory). For my curiosity (and the curiosity of other readers), can you please link to descriptions of these hypotheses?

You may want to refer to this link.

Wikipedia states K+ transport as main factor for stomatal opening & closing, which shows that K+ ion pump hypothesis is more widely accepted.