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In a tumor, why hypoxic regions have access to glucose?
The Warburg effect is ubiquitous in cancer. It consists of the upregulation of glucose uptake, glycolysis, and subsequent lactate secretion, sometimes by over 200 times, in cancer cells as compared to normal cells. A common explanation for this phenomenon is that tumor cells can be oxygen deprived, because they are far away from the diffusive range of oxygen in the blood supply. But if that's the case, then how are they close enough to blood supply to have access to enough glucose? How can glucose diffuse to places where oxygen cannot, even if oxygen is a much smaller molecule?

This is a very good question. I think this is in fact a major problem for the whole glycolysis/hypoxia theory. And I'm not aware of any evidence for rapid glycolysis in hypoxic tumor regions. But note that Warburg's finding was that tumor cells have high glycolysis also in the presence of oxygen; that is completely different from glycolysis in hypoxia.

This is a great systems bio question. You could also take it a step back from cancer and ask something like "what are the absolute fluxes (input - output) of O2 and glucose in healthy tissue, and how does one affect the other?"

I think this is a difficult question for which the answer is not clear --- to my knowledge there is little data on metabolism in solid tumors, and no clear consensus in the scientific community. So I'm not going to attempt to give a definitive answer, but here's at least a few thoughts / opinions.
Why transformed cells engage in aerobic glycolysis, or the "Warburg effect", is a question people have been trying to answer for nearly a hundred years now. There are dozens of hypotheses, but none of them is broadly accepted. One popular hypothesis laid out by Gilles & Gatenby says that transformed cells from solid tumors are glycolytic because they have been selected for anaerobic metabolism in a hypoxic environment, and this selection is somehow irreversible, so that the cells stay glycolytic even after being extracted from the tumor and cultured in aerobic conditions. I think this hypothesis is the origin of the idea of hypoxic and yet glycolytic tumors.
In a way the Gilles & Gatenby hypothesis is a clever idea --- it rests on the well-accepted fact that most cells become glycolytic in hypoxia, and rhymes with the concept of selection for survival in tumors. But the problem with the argument (as you have realized) is that the tumor environment would have to be low in oxygen and at the same time high in glucose. I agree with you that it is unlikely that such an environment could arise due to lack of blood supply, since oxygen diffuses more easily through tissues (and cells) than glucose does. Moreover, considering the high demand for glucose by glycolytic cells, glucose should become limiting long before oxygen runs out. So one can argue that poorly vascularized tumors should be mainly oxidative, not glycolytic!
To my knowledge, there is no data demonstrating existence of (regions of) solid tumors with low oxygen and high glucose. There is of course ample evidence that many solid tumors consume large amounts of glucose, and also many studies showing hypoxic regions in tumors. But most likely these are different types of tumors, or different regions. In an environment with neither oxygen nor glucose, cells will simply die --- which is exactly what happens in the necrotic cores of larger solid tumors.
The best source of further information is probably the tumor physiology literature. This review is a good starting point.
Finally, another issue with Gilles & Gatenby's hypothesis is that aerobic glycolysis can easily be demonstrated in cells that have never been in a tumor. For example, in vitro transformation can increase glycolysis, and normal lymphocytes induce rapid glycolysis when activated by receptor stimulation. So there is no need to assume that glycolytic tumors are hypoxic.

Personally I think aerobic glycolysis is poorly worded (though I know it is common). in my opinion ahypoxic hyperglycolysis describes the phenotype better :)

The outside of the tumor has access to the most nutrients and oxygen, sometimes even the blood supply (angiogenesis). Solid tumors have this microenvironment if you will, and the human tumor microenvironment often suffers from a lack of oxygen and nutrients, and acidosis (Milosevic et al., 2004). The distance from the outside of the tumor to the core has an established diffusion gradient of oxygen, nutrients, etc. (Cristini et al., 2005, especially since blood vessels can't always penetrate to these areas). A take home point is the larger the tumor becomes, the less nutrients available to the inward tumor cells until the cells often become necrotic or necroptotic (Huang et al., 2013). Furthermore, since tumors maintain a constant inward pressure, the dead cells are essentially eaten by the living cells and everything is pushed to the center, thereby providing the interior environment of the tumor materials to work with (Greenspan, 1972).
There are gross metabolic shifts explained below that provide the tumors different ways of obtaining nutrients. I don't think it has so much to do with glucose diffusing as deep into the tumor as oxygen as it does this metabolic reprogramming.
How does the tumor alter it's expression profile to fit it's needs under the stress of starvation? Example based approach

Hypoxia-inducible factors or HIF unfortunately modulate tumor progression. (See Bellot et al., 2009, Zhang et al., 2008 for examples of autophagy induced by HIF, Huang et al., 2014 for a non-exhaustive overview of additional ways HIF modulates cancer progression). Tumor cells suffering chronic hypoxia upregulate their GLUT transporters and glycolytic pathways via action from HIF-1α/ß because they must often begin to produce ATP without oxygen. They also, however, downregulate mitochondrial activity through transactivation of PDK1 and MXI1 Denzo et al., 2008. PDK1 ends up inhibiting PDH, and MXI1 ends up actually reducing the number of mitochondria per cell.
The incorporation, then, of glutamine into the TCA cycle where pyruvate would normally be needed supplements the now-missing carbon requirement (see figure below) where pyruvate would be involved, because referring again to the Denzo paper, in the hypoxic tumor pyruvate is converted into lactate by LDH, in part explaining the acidosis. Incorporation of glutamine however should purportedly be independent of HIF expression, so I looked at papers such as Ma et al., 2013, which showed that starving tumors of glucose ended up making them more aggressive due largely to regulation by PKCζ, and subsequent incorporation of glutamine metabolism.

Fig A. Looking here at alternative fuel pathways during starvation of the tumor, the cells can scavenge from the necrotic center of the tumor, utilize autophagy, other carbon source, etc. to fit their needs.
Source: White, E., 2013
More specifically, there is a paradigm shift in tumor cells deficient in PKCζ that involves (1) upregulation of Phosphoglycerate dehydrogenase (PHGDH) and Phosphoserine aminotransferase (PSAT1), which are normally repressed by PKCζ, (2) uninhibited mTOR activity, which is normally shut down during nutrient depletion, and (3) inhibited AMPK and autophagy pathways, which are normally active in nutrient depletion.

"Genome-wide transcriptome analysis demonstrated that PKCζ-deficient cells displayed gene alterations in pathways consistent with the use of glutamine as a glucose alternative."

In both humans and mice they conclude that with respect to intestinal cancers, PKCζ regularly acts as a tumor suppressor. But the major point here is that multiple pathologic mutations can be implicated here to try and make sense of the Warburg effect.
Leithner et al., 2015 likewise shows that tumor cells (this is specific for lung cancer) can begin to utilize lactate to form glucose building blocks by modifying the gluconeogenesis pathway, mediated largely by a mitochondrial isoform of the phosphoenolpyruvate carboxykinase (PEPCK) known as PCK2:

"Under low glucose, all three carbons from (13)C₃-lactate appeared in the PEP pool, further supporting a conversion of lactate to pyruvate, via pyruvate carboxylase to oxaloacetate, and via PCK2 to phosphoenolpyruvate."

I'd like to bring up again that in the hypoxic tumor, evidence supports that pyruvate is converted to lactate, but now I imply the lactate can potentially be converted to glucose, a positive feedback loop providing the tumor glucose. This is somewhat supported by the clinical study in Koukourakis et al., 2006 that shows tumors overexpressing LDH-5 and HIF-1α/2α that in the malignant tumors, oxygen consumption was low and glucose consumption was high. But I also want to go back to the Denzo paper because they brought up some interesting points, and I recommend reading it: The decreased mitochondrial need for oxygen might be more important than the increased glycolysis.
Some interesting points:
1) The metabolic shift induced by hypoxia lowers the tumor oxygen requirement and heightens it's glucose requirement. This doesn't necessarily mean the tumor is actually getting glucose, and sometimes, it doesn't mean the tumor cell is actually deprived of oxygen, either, rather the hypoxia is induced by simply not enough oxygen to fit the high oxygen requirement, read Takakusagi et al., 2014.
2) By reprogramming it's metabolism and cannibalizing cells that actually did die from deprivation, the tumor can viably "get" energy -though not necessarily directly in the form of glucose- through a number of pathological mutations.
3) Anaerobic glycolysis followed by LDH activity is an efficient adaptation if you look at Koppenol, Bounds & Dang, 2011, the hypoxic tumor cell can produce 26 ATP and 26 lactic acid from 13 glucose in the time it takes oxidative phosp. to produce 36 ATP from one glucose. In a time of starvation efficient energy production is a good thing, and the hypoxic mechanism is fast, especially if we consider the tumor is producing glucose from lactic acid in any capacity. They also point out that tumors become in a way addicted to the Warburg effect,

"... oncogenic deregulation of biomass accumulation for cell proliferation creates an increased, sustained bioenergetic demand that addicts cancer cells to an adequate anabolic supply."

"How can glucose diffuse to places where oxygen cannot, even if oxygen is a much smaller molecule?" I don't have such a definitive answer for this, though I would personally determine that it doesn't, not by much. Where I want to go is it's not really about glucose and oxygen getting to the same place. I suspect that they reach just about equally as deep into the tumor depending on the composition of the tumor itself and the tissue it resides in. I also want to point out that hypoxia is not the same as anoxia, where there is no oxygen and the cells are for the most part dead in those regions. If you read the length of this post, you understand that the tumor cells are experiencing hypoxia, or a deficient amount of oxygen reaching them, and likewise I would assume a deficient amount of glucose, as opposed to a lack thereof. In that sense again, and because there's not a lot of nutrients to go around, we're alluding to the efficient usage of both glucose and oxygen, and beneficial biomass accumulation, which we demonstrated the Warburg effect is key to. Because once you get to the point of anoxia, again, we're looking at anoxic cell death, but those cells get turned into what essentially amounts to recycling material.
Closing Notes

I don't see why glucose wouldn't be able to diffuse along it's gradient into the tumor considering there is a microfluid environment inside the tumor, but where we're talking about in the hypoxic region (not the anoxic regions) I suspect there is still some glucose present just as there's some oxygen. It's important, then, for the tumor cells to have more of the GLUT transporters from the action of HIF, and the efficient usage of whatever metabolites it can get. I generally lack data for how far into a tumor they can actually perfuse, but to me it would be hard to quantify since there are many confounding factors such as what tissue the tumor originated from, irregularities in the microcirculation, etc.

I don’t think any of this answers the question.

Thanks for the useful information, but I agree with Roland, this does not answer my question.

I appreciate your answer. I think the most relevant aspect is that you think somehow there can be a high enough concentration of glucose in places where oxygen is not accessible, thus creating a niche for enhanced glycolysis. This is what I find tough to digest, because oxygen is so small a molecule, it should be very easy for it to diffuse, thus it should be available wherever glucose is available. But if you can find some references supporting your claim that would be great, since that is the essence of my question.

The link to the Milosevic paper is broken. I think you copy/pasted a link that goes through your university proxy or something, which I can't access. Can you fix it please?

Do you have a reference with the diffusion coefficients of glucose and oxygen?

@becko So i tried to find some relevant environments such as extracellular matrix or even tumor tissue. In this they measured for oxygen in carcinoma, and in extracellular matrix here. They took measurement for glucose in sclera here and EMT6 spheroids here. Values tend to range around 10^-5 or 10^-6 for either glucose or oxygen.

I think I finally got where I was going with this answer. There's still lots of data out there that I simply can't incorporate without producing an entire book. The TL;DR is (1) oxygen is still there, just in low amounts, like glucose, (2) the Warburg effect is about efficiently using resources that are getting scarce, and (3) there's a complex crosstalk at the end of things and this answer is far from exhaustive. I hope I was able to constructively direct your research! Please let me know if there's anything to be clarified!

Hypoxia does not mean no oxygen reaches the place, it means low oxygen tension when compared to normal well perfused tissue. In my experiments I have observed the exterior of rat glioma models well perfused but not so well inside. We have used MR based methods to study perfusion and IHC to study vasculature. In the same way, I have observed increased MCT-4 expression (indirectly, more lactic acid production) in the outer regions of the tumor but certainly sometimes there are some pockets inside with increased MCT-4. But no matter what, the whole of the tumor and surroundings is acidic. This could be due to lactic acid or maintenance of intracellular pH by proton exchangers. Though there is no clear answer, there are lots of points on which I agree with CMosychuk. Low oxygen tension increases HIF activity which has its repercussions. I also faced another curious situation. I was working with pseudohypoxic tumors. They don't have low oxygen tension but still have activated HIF because HIF is artificially stabilized thanks to some mutations (VHL, SDHB). Now, I expected more GLUT because I could see increased 18F-FDG uptake in these tumors but I saw increased hexokinase-2 expression. Remember, in this case there was no hypoxia, still activation of HIF had its effect that is increased glycolysis! So I too think that low oxygen tension might mean low nutrient supply but it certainly does not mean no nutrient supply. We see tumor parts having low oxygen tension, happily living and metabolizing and making the whole region acidic. I have not even seen a necrotic core in these tumors. When, I killed these cells giving temozolomide to the animals, the acidity was not there anymore. So, acidity was certainly from metabolism of cells. Remember, these are all in vivo studies and we do different kinds of measurements on the same tumor as the rat is alive.

Hello Jyotsna, welcome to Biology.SE and thank you for your contribution to the site. That you posted such an extensive response is great, however it would be very much appreciated if you could list some of the sources for your claims.

You're right that hypoxia (and hypoglycemia) is a matter of degrees, of course. But then you would need to argue from quantitative data. What does "well perfused" mean? What is the oxygen tension in your tumors? Respiration rate? Glucose concentration, glycolytic rate? These values are typically very difficult to determine in vivo.


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RAD sequencing: choosing the appropriate enzyme?
I’m studying Darwin’s finches genome and I say in some articles that the researchers used restriction enzymes to cut the DNA in their double digest RAD protocol. They are using EcoRI and MseI (GAATTC and TTAA), the two enzymes similar and used in Peterson, B. K., J. N. Weber, E. H. Kay, H. S. Fisher, and H. E. Hoekstra. 2012. Double digest RADseq: an inexpensive method for de novo SNP discovery and genotyping in model and non-model species. PLoS ONE 7:e37135. (they are using EcoRI and MspI (GAATTC and CCGG).
Considering the huge list of restriction enzymes how to choose the appropriate enzyme? Is it a complete guess? The size of the genome of finches is about 1.07Gb. Do I have to take this in consideration?
The reference genome is available Zhang, G., P. Parker, B. Li, H. Li, and J. Wang. 2012. The genome of Darwin’s Finch (Geospiza fortis). GigaScience.

maybe R.EcoRII or FokI/Taq52I?

Why would you choose these?

R.EcoRII because of its molecular mass (45.2 kDa), it targets CCWGG, C-terminal domain of restriction endonuclease and apologies, I meant Tsp49I rather than Taq52I and this because of its relatively high pH optimum, reaching enzyme activity peak at rather "high" temperatures, its a thermostable neoschizomer

source: Stack Exchange

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

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Why do mammals produce more carbon dioxide than insects?
I understand that mammals produce more carbon dioxide than insects on a gram per gram basis, but why is that? I'm thinking it might be because mammals are warm-blooded, which require more energy consumption. Could it also be due to the fact that insects are less active than mammals? AKA they do less work?

From where do you understand this? Could you provide a source?

Source and context, please. For example, it doesn't seem likely that a resting mammal will produce more CO2 than an insect running for its life. Could be, though

As you said, endothermic animals such as mammmals or birds consume more energy and therefore expelmore CO2 not only because of a higher betabolic rate or to keep warm, but also because they are more active. Even taking all that into account you are missing the biggest difference between them: size. The consumption of energy is not directly related to the size, in fact, the energy requirements drop exponentially with the reduction of size. The same phenomenon explains why they are far stronger, fall-resisting...

The answer seems to be okay, but please provide references to your claims so that people can check and read further.

oxygen consumption endotherms vs ectotherms http://advan.physiology.org/content/31/1/97

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


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Influence of artificial sunlight on the human body
In a hypothetical scenario, where a large, permanently manned craft is in a continual orbit, and natural sunlight cannot be used as the craft may keep moving and turning, artificial sunlight is used in the form of LED panels.
My question is this: Will the LEDs have any adverse effect on the human body? The LEDs are of the SoLED variety which have very low IR levels and almost nil UV light levels, have any adverse effects on the body? I suppose the lack of UV may cause some disturbance in Vitamin D and melanin levels. Is this valid? Would there be any other problems?

You could easily supplement Vitamin D.

But will that be the only issue?

Yes. Natural sunlight doesn't have a good substituent.
Melatonin levels and circardian rhythms are directly affected by natural sunlight.
As far as LEDs goes, a french study concluded that blue light may have photochemical risks and affect our retina.
Source
http://www.ledinside.com/knowledge/2014/4/effect_of_artificual_and_natural_light_on_the_human_body


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Polar bodies fertilization
Suppose a sperm fertilized a 2nd polar body( haploid) is there a chance of somewhat normal development?

The 2nd polar body contains almost no cytoplasm, so if only this body is fertilized it contains no maternal genes to guide the development and moreover not enough nutrients. So this wouldn't work. "Source"
Moreover, there wasn't reported even any case of "twin" resulting from the fertilization of 2nd polar body according to this article
There was reported case of twins formed by a mass of fertilized ovum and fertilized (diploid) first polar body. Source
What could happen is that if both polar body and oocyte are fertilized, these two cells merge and form tetraploid embryo. Which is sometimes able to form fetus (sometimes just ends as mola hydatinosa), but definitely not able to produce a viable child in humans.

Mpribis is 99% correct, except that the polar body does indeed contain the same amount of maternal genes as the secondary oocyte (remember, it's the product of the second division--from diploid to haploid). But like Mpbris said, since the second polar body is nutrient-poor, and lacks full complement of organelles, the odds of it remaining viable if it were fertilized are vanishingly small. Such "polar body twinning" is theoretically possible, but has yet to be documented as of the the time of my writing this.


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What other cognitive behaviors in bees, outside of navigation, are affect by neonicotinoids
It is conclusive that neonicotinoids alter navigation in bees when locating food sources. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0091364
But if so, shouldn't cognition also be affected? And if it is affected, then wouldn't the effect on the hive be even more pronounced due to inaccurate bee dances and an overall delay/inability in finding food source? Shouldn't this be conclusive in explaining neonicotinoids to be a contributor to colony collapse disorder?

It is assumed that this effect of locomotive behavior IS an effect on cognition (1-4). Navigation requires snapshot memory, learning, and attention (2-4). You asked if this effect of neonicotinoids on cognition manifests itself through other vital behaviors. The short answer, yes. Specifically neonicotinoids are shown to effect mating, queen behavior, and foraging short and long distance (5-7). It is suggestive that neonicotinoids are a contributing factor in collapsing colonies with both meta analysis and direct evidence of effects on behavior (5-8). I think you are more questioning why people have not done anything about this issue or more definitive in their action against colony collapse. That is more of a political issue. Since the pesticide does not have as many human health effects at levels that cause bee collapse, the policies to resolve this issue are not as clear. EPA has discussed making restrictions regarding use the use of neonicotinoids, but they will still be used. However, they have actually been banned in France due to these effects. Hope that answered your question!
Sources

Honey Bee Behaviors  doi:10.1016/S1364-6613(00)01601-6
Bee Navigation and Memory          doi:10.1006/anbe.1997.0574
Learning and Memory in Bees doi: 1146/annurev.ne.19.030196.002115
Behavioral Neuroscience ISBN: 978-0-87893-092-0
Bees, neonicotinoids, and Dance Behavior Effects doi: 10.1242/jeb.068718
Bees, neonicotinoids, and Foraging Behavior Effects  DOI: 10.1046/j.1365-2435.2000.00443.x
Queen and Colony Effects   DOI: 10.1126/science.1215025
Colony Collapse meta study DOI: 10.1007/s10646-010-0566-0

Can you please add DOI or Pubmed links if possible?

Sure thing! I'll add the DOI at the end of each citation.


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Cesium-137 From Fukushima Meltdown
I've been reading up on the Fukushima nuclear meltdown and its effects it had on the environment. The iodine-131 initially released from the incident decayed after 8 days, but other isotopes such as cesium-137 and strontium-90 have a half-life of 28.7 and 30.2 years (about 300 years to completely decay).
Apparently, large quanties of cesium-137 were found in neighbouring countries as well as in seafood near Japan.
Now, for something like nuclear isotopes, not having the required knowledge can lead someone to fear something that might be harmless (or confirm some doubts about the issue), hence why I am here.
From my research on scientific websites and different governmental regulations, I found out that food and water in Japan have a legal limit as to how much cesium-137 a food item can contain. Especially since cesium-137 ressembles potassium and therefore being easily taken up by the body, this is worrying.
To my understanding, the way a radioactive isotope creates havoc in the body of an individual is that:

It ressembles a normal element we usually consume, like iodine, potassium for cesium-137 and calcium for strontium-90.
The body digests it and it is stored in the body.
It emits radation for a certain period of time, anywhere from 8 days for Iodine-131 to years for cesium-137.
The prolonged radioactivity from these isotopes causes cancerous cells to occur.
A tumour or other form of cancer develops.

If this is what happens for isotopes like cesium-137, how can it be possible to eat food or drink water containing ANY cesium whatsoever? Sure, the radiation isn't so bad, but what is important to take into consideration is that this is internal and highly centralized radiation. This is a completely different thing to external radiation.
For my questions about the topic, I would like to know three things (which could really put many doubts to rest).
QUESTIONS
The first is, is my understanding described above correct?
The second is, how does this affect us healthwise? We are stuck with these debris of cesium-137 and strontium-90 for the next 30 or more years, but what effect do they have on us?
If someone ingests an atom (or a small amount) of cesium-137, what affect will this have on this person's body?
Finally, for someone living in North America, how much of these debris are there, either that got here from the wind, products, food, water, etc.?
EDIT: If someone knowledgeable on the subject could answer the questions directly (highlighted by means of italics), it would be very much appreciated.

On Bio we encourage single, specifically targeted questions. Hence, I vote to close because it's too broad. I encourage you to reduce the stack of questions and generate one, or more separate questions.

@Christiaan Hi Christiaan. The specific questions are clearly listed at the end of the text. The text before that is simply to give the necassary and preliminary information for the questions. On the contrary, I think it adds precision. The questions alone could make the subsequent discussion rather imprecise. I highlighted the questions to make sure they can't be missed. Please do not close the discussion. Thank you.

If someone knowledgeable on the subject could answer the questions directly (highlighted by means of italics), it would be very much appreciated.

@samseva your last question on effects in North America is quite different and I would suggest that you remove it from this post.

@WYSIWYG Hi Wysiwyg. I should create a new topic instead?

@samseva you can but you have to add more details. Moreover, the question is more about environmental science than biology. So I am not sure if that would be considered on-topic, here. You may try posting that question in [earthscience.se] with some relevant additions.

I’m voting to close this question because the OP never corrected the problems pointed out in other comments (multiple questions, some of which are seem to be off-topic as asking for medical advice).

Most of the question has been accurately answered by @davidblomstrom, however regarding the internal exposure to of cesium-137, through ingestion or inhalation, allows the radioactive material to be distributed in the soft tissues, especially muscle tissue, exposing these tissues to the beta particles and gamma radiation and increasing cancer risk.
Also due to the consistency of Cs-137, it comes as a crystalline powder (due to its property of binding with chlorides) which makes it "easier" to be distributed after a nuclear fallout.

If the lead containers of Cs-137 are opened, the substance inside looks like a white powder and may glow. Cs-137 from nuclear accidents or atomic bomb explosions cannot be seen and will be present in dust and debris from fallout. read more

Sources

"Cesium-137." Vermont Department of Health. Vermont Department of Health. Web. 31 Jan. 2016. http://healthvermont.gov/emerg/drill/dirtybomb/facts-about-cesium137.aspx.
Albertini, Dr. R. "Cesium." University of Vermont, 2002. Web. 31 Jan. 2016. http://www.atsdr.cdc.gov/toxprofiles/tp157-c3.pdf.


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Was the frequency of mutations more during primitive earth due to radioactivity?
Primitive earth was more radioactive (or was it really?) according to radiometric analysis of C14 which suddenly appeared at 4250 million years in the Hadeon eon. Is it possible that ancient high levels of radioactivity could affect the mutation rate of early organisms? Does mutation frequency accelerate evolutionary process and/or speciation?

Can you give a reference to the "higher $^{14}{C}$ radioactivity" assertion? It sounds a priori unlikely, given that the cosmic ray processes making carbon-14 from nitrogen would surely have operated equally at that time. Moreover, since the half-life of carbon-14 is about 5700 years, I can't see how any of it can have survived from a time almost a million half-lives ago. A reference could make everything clear.


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Why are eye defects so common?
The title says it all, what makes eye defects so common in the world? Whereas defects of any other body part is quite uncommon, I searched online and one of the articles said that 6 out of 10 people wear glasses, I think that is a big percentage of people with eye defects, BTW I'm myopic and I wear glasses too. Are all body parts defective to a certain degree, but It seems more pronounced in the case of eyes?
P.S
I know nothing about biology, I appreciate if someone could explain it with preferably less technical terms, this is my first question on BSE, let me know how I can make the post better.

@Roland I think that answers my question, you can mark this as a duplicate


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Are scientist able to correct mutiple gene defect in our body by using CRISPR
Are scientist able to correct mutiple gene defect in whole body by using CRISPR recently?
AS i know, it is in a beginning stage

Certainly not yet - there is not yet any evidence that this can be used to correct specific deficiencies in an adult, though the in vivo applications are growing.
In particular, an exciting recent advance is the opportunity to better understand carcinogenesis by 'editing in' certain known mutations into a mouse, say, that should cause a cancer, and watching for when the cancer actually arises...


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How is green fluorescent protein distributed while inside an organism?
I would like to know a relatively simple thing, but something I wasn't finding the answer to.  When fluorescent protein is used in a relatively large, non-transparent animal, like a mouse, or theoretically a dog or a human, how is the protein generally incorporated into the tissue?  I suppose that it would bind to elastin and otherwise it could be transfected into different cells in and throughout tissue, both around the skin and deeper.  However, wouldn't it only be useful near to the skin, since ultraviolet light and visible light would penetrate a limited distance through tissue?  Then again, a relatively bright light source could possibly produce light from deeper in tissue.  I'm not quite sure.  It's a relatively simple question, but I appreciate it.
(Edit): I may have been a little vague with the question, a more specific version of the question I asked would be; given the brightness of a fluorescent light source that is directed at fluorescent protein filled tissue (with UV assumed to be close to the visible spectrum) and the portion of that light which is converted to visible light, approximately how could you calculate the relative brightness of the protein at a certain depth in the tissue.  Of course it probably is very difficult to get accuracy with that because that would depend on the portion of fat, muscle, collagen, etc in the tissue.  But if there's something rough and general, like the depth of the protein would reduce its relative brightness proportionally to the natural log per millimeter or something, that would be fine.

Distribution of GFP
When used as a reporter usually GFP is expressed by the cells themselves or attached to an antibody and injected. It ends up everywhere, is what I mean.
Localization of GFP
There are three solutions to the hidden-behind-tissue problem for fluorescence.

Use a functionally 2D sample (nematodes, mouse limbs, etc)
Sacrifice the organism(if it's not dead already) and use optical clearing
Cleverness

Of these cleverness is the most interesting. Types of cleverness include time-resolution imaging(Light scatters instantly but most fluorescent proteins take a few nanoseconds to relax) to separate fluorescence from backscatter. Excite a slice of the sample and look at it from a slight angle 3 ns later, and you should see a depth-map. Repeat.
You could also use optical tomography to essentially use computers and many cameras instead of time-delay imaging to solve for the 3d distribution of signal. Computed tomography is much cheaper, mostly because you don't need a nanosecond-scale laser + capture system(those are expensive).


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Evidence of species transitions
I had a debate with a person who believes in some kind of creativism, let's call it that way.
And in the middle of the "debate", an interesting question popped up.
What are evidences of "transition between species". Is there a fossil record that shows us the "transition".  I googled it and it was pretty obscure subject.
I would like to answer that question and really it "hits" my beliefs.

As it is, this reads like you are asking whether there is any fossil record at all for evolution between species, which I am pretty sure is not what you want to know. Can you clarify what you mean some more? What evidence would you accept? What transition are you looking for?

Speciation is a gradual and continuous process. A new species does not pop up in just one generation. It takes many. This, combined with the highly incomplete fossil record makes that transitions between two species are likely to be difficult to document. As YviDe asks - what are you after?

Also, what search term did you use to conclude that it is an "obscure" subject? The search for "transition fossil" or "transition species" gets a lot of good hits on the subject.

Welcome to Biology.SE. There are millions of evidence in evolutionary biology. You can find a long list of evidences on this post. However, the question is a little unclear for the moment and I don't really know which evidence would answer your question. I am voting to close as unclear.

You might eventually have a look at this post too.

Could you clarify what you mean by transition between species

People who think in creationism or think about species rigidly might have a bit problem with that, so let me describe an example:
When are humans "adult"?
Legally, at 18 (or your national equivalent). However, everyone understand that people are becoming adult gradually. Sometimes, they "age" very quickly after some harsh experience (16 years old student who parties all days because parents pay for it vs 16 years someone whom father died and he has work to help feed his small sisters as family did depend on father's wage).
Now imagine that you don't have all this information, but very incomplete "images" or "screenshots" of this kind of development. There would be quite a mess from it. You have image of one kid at 13 who is still young, another kid at 19 who is partying, single image of this 16 year old adult who has to feed his family and image of 48 year old gentleman.
If you go with this mindset that most of species that ever lived you can't get and you are just guessing something from a few snapshots that are themselves incomplete as well (e.g. we often don't have whole skeleton but just single bone from a lot of species), your idea on what to expect will change. This is a first step. Then you need to realize that most of fossils that shows some transition do not form lineage, but instead branches that are related. Finally, when you understand this (and modify your expectations and "what to look at", you can take any relatively complete and well-studied set of fossils like human ones. On human lineage (with great apes), we can see gradual increase of brain and in the case of human, gradual decrease in size of jaw. Development of hip bone is nice as well as it shows gradual process of adaptation to upright walking.
Another line of examples, but again, you need to redefine your expectations, is to point on dogs. If we had dogs in our fossil records, there would be large amount of species, instead of one "dog" species.
Or you can just point out at plants and say that "species" does not really mean anything.

I appreciate the analogy with adult age to explain why the question makes little sense.

@Remi.b: I don't think it's nonsensical question per se. Rather, you really need to know what you are looking for unless you will miss the elephant in the room. Furthermore, these "transitional states" show nicely how some systems have developed. Currently, I am working on some anthropological/sociological stuff and if you find these "transitional states", you might understand how particular cultural motive or practice did develop and reconstruct the actual process.


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Do the antibodies in a patient suffering from Hashimoto's, attack the thyroid hormones or the thyroid gland (or both?)?
If oral thyroid hormone supplement is administered, is the attack stopped or does it just create an excess of thyroid hormones so that even after a lot of it is destroyed by the antibodies, there is still enough for normal bodily functions?

Welcome to Bio. Where did you hear that thyroid hormones are targets for antibodies? Could you add that source in the question?

Thank you. It was based on a misunderstanding.My endocrinologist just said that the antibodies attack the "thyroid". While he might have thought it's obvious that "thyroid" means the the "thyroid gland" ,for someone with very basic knowledge in biology like me, it either meant the "thyroid hormones" or the "thyroid gland".I had previously asked a question here on stack which was based on this misunderstanding and the responses that I got made me realize that something wasn't right.This question was intended to get things completely straight and to clarify a few things( as you can see ).

Hashimoto's Thyroiditis is an autoimmune disorder where autoreactive attack on the actual thyroid tissue results in hypothyroidism. Pyzik et al., 2015, provides a good review of what we know about HT. The prevailing theory is that nonspecific infection can induce HLA expression on thyroid cells through the action of interferon gamma.
HLA is an antigen-presenting complex in humans that in our case is the major histocompatibility complex II or MHC-II you will see in texts (to avoid confusing names). Processed segments of protein are loaded onto the MHC-II, and displayed to the extracellular space where T cells positive for CD4 can recognize them. CD4+ T cells, upon recognition of MHC-II, are stimulated into T-helper or Th cells that are specific for the protein antigen they found on the MHC-II. The problem with MHC-II expressed by thyrocytes and the like is they can load either foreign or self peptides, so if it loads a part of thyroglobulin (Tg) on there and that's what the T cell recognizes, it's going to produce an immune response specific for Tg in a complex series of downstream events.
Being said, supplementation of thyroid hormone is a good treatment for hypothyroidism but it won't stop the attack on the actual gland. Thyroid hormones aren't often attacked by autoimmunity because they aren't protein antigens, and different subsets of cells respond to non-peptide antigens.

Thank you so much! So,ultimately would the entire thyroid gland be destroyed bit by bit and will the patient have to completely rely on supplements ?

It can boil down to that. Cases/treatments vary and one of the things you have to watch out for during the course of HT are malignant B cell clones in the actual thyroid, in which case excision of the entire gland might be necessary. A medical doctor will know the best route of treatment for a given patient.

I've an appointment with an endocrinologist but it's not in another couple of weeks.I decided to get a head start here and I am glad I did. Just one last question though. Is there anything that can actually suppress the antigen attack like maybe a drug or leading a very healthy lifestyle ?


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Diffusion coefficient of cells in blood?
What's the diffusion coefficient of white cells in blood?
Is it well defined, or are cells too large and few as to be treated as particles in this context?
P.S. I have tried to look this up, but what I find inevitably is about diffusion coefficients of molecules inside cells, which is not what I want.

Cells in blood flow will in the first approximation follow the flow. Of course blood flow is very complex and includes many interactions, so there'll be some kind of 'effective diffusion' arising from this, which will depend on many parameters (such as the flow velocity, pulsatility, hematocrit...)

Cells absolutely can be considered as diffusing objects.  However, the origin of the "diffusion" can be very different than for, say, a bead in water.  The reason is that the thermal motion that creates the diffusion of a micron-sized bead can be much less important for a (large) cell.  For instance, the diffusion coefficient due to thermal forces of a sphere in a fluid with viscosity $\eta$ is
$$D_{therm} = \frac{k_B T}{6 \pi \eta R}$$
where $R$ is the cell radius (this is the "Stokes-Einstein" result).  For a white blood cell (say 10 microns in radius), this would - assuming blood is at least as viscous as water - lead to thermal diffusion coefficients around 1 microns$^2$/hour- i.e. we would need many many hours for a cell to travel its own diameter.  This result neglects a bunch of complexities - blood is not perfectly viscous, there is a really high density of red blood cells in blood, etc... but the basic result is that the thermal buffeting that drives the diffusion of a colloidal bead is not enough to drive a cell.
However, cells are not passive beads!  They crawl, both randomly, and (as cancerconnector notes), in response to signals like chemical gradients.  If a cell crawls with a speed $v$ and maintains its orientation over a time $\tau$, it's reasonable to describe its motion (over times much longer than $\tau$ as being diffusive with an effective diffusion coefficient
$$D_{motility} = \frac{1}{2} v^2 \tau$$
which you can get mostly from dimensional analysis, or more rigorous models.  For white blood cells, $v$ is on the order of microns/minute - at least when measured on slides - it might be different in the body.  $\tau$ is a few minutes, so $D_{motility}$ is on the order of many microns$^2$/minute - orders of magnitude faster than mere thermal diffusion.
A good introduction to modeling of this question is probably chapters 9-11 of Leah Edelstein Keshet's "Mathematical Models in Biology" and she cites some classic Lauffenberger papers on macrophage response, etc.  You may have access to this online: http://dx.doi.org/10.1137/1.9780898719147
Also, note that everything I've said so far neglects blood flow - if this is important in your problem (which will depend on the context), things can get more complex (have to include flow in your diffusion equation).  But using diffusion equations to model the spread of randomly motile cells is a very common approach, and there is a lot of literature on it!

This is a difficult question because white blood cells do exhibit chemo and haptotactic responses, and also because of their large size - though cells are often modeled as moving by diffusion (cancer cells in particular, see: "Modelling biological invasions: Individual to population scales at interfaces" as one of MANY examples). One could model their movement in a dish, and come up with a diffusion coefficient, but I'm not sure what the utility of this would be. Why do you want to know?  Is there another underlying question?

No underlying question. I am developing a mathematical model of cells in plasma. Just need some order of magnitude estimate.


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Lack of yolk in mammalian oocytes as compared to other vertebrates?
Why do mammalian oocytes have little to no yolk? How does it compare to other vertebrates such as frogs, fish, and birds?

In oviparous animals (those that lay eggs which hatch outside the body), the eggs need to be provided nutrition for embryonic growth, which is the main function of yolk.
In placental mammals, the embryo is provided nutrition directly from the mother via the placenta.
Therefore, most mammalian oocytes do not need to develop large quantities of yolk to support the embryo in the way the eggs of most birds, reptiles, amphibians and fish do.


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What tools are used in animal cloning?
So I was reading up on articles to do a project about cloning but there were no places in the article where It states the tool used to take the gene out of the nucleus and insert it into plasmids ? can anyone accurately tell me what the tool is. I don't mean the process but the actual names of the tools like CRISPR etc.
As a reference The article was the wiki https://en.wikipedia.org/wiki/Molecular_cloning

biolistic particle delivery system, TALEN (Transcription activator-like effector nuclease), Homing endonuclease

What kind of cloning are you interested in. Gene cloning can be done in plasmids using restriction endonucleases also. You have to add specifics.

About cloning a whole new animal

@hoodlamic1 Cloning a new animal is done using a technique called Somatic Cell Nuclear Transfer. Is that what you are interested in? Can you add more details? Molecular cloning is different and your question and your comment are conflicting each other.


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Why do heterozygous individuals have increased resistance to malaria?
I am aware that there is such a thing called heterozygous advantage, which is due to the presence of a certain single allele, and that an example of this could be with "sickle-cell anemia".  I am quite curious as to how exactly this heterozygous advantage is created.
Could the increased resistance against malaria be due to natural resistance or natural selection?

The heterozygous advantage generally lowers natural selection against the carriers of mutated alele, because it helps them to survive some specific conditions (which have to have some major impact on the survival rate). This means these individuals have bigger chances of reproducing, which means spread of the alele.
Sickle cell anaemia is one good example in countries with big incidence of malaria (caused by a protista plasmodium falciparum). This parasite reproduces itself in human Red Blood Cells (RBCs), destroys the cells and releases its sporozoits (which can infect other RBCs and the cycle continues). This massive destruction of RBCs is called haemolytic anaemia. Without enough RBCs and haemoglobin, the organism isn't able to function properly (falls ill in malaria).
Individuals which are heterozygous for HbS alele (which in homozygous state causes sickle-cell anaemia) can catch the parasite, but the chances are bigger, that the infected cells will be phagocytized by macrophages and the parasite will be unable to reproduce in them. Illustration Therefore the chances are bigger that they will survive the infection by plasmodium, therefore they can pass their genes (containing HbS gene to the next generation. (The whole process is a bit more complicated by presence of other genes, some details can be found here, but this mechanism seems to be the most important one.)
In general, many homozygots for "normal" Hb alele die as a result of malaria infection, most homozygots for HbS alele die for sickle-cell anaemia. So the winner is heterozygous conformation, which is saved from both. This influences the frequency of HbS alele (it makes it higher until this effect gets balanced with the effect of selection against HbS alele because of too many homozygous individuals with sickle-cell anaemia)
Another good examples in European population are heterozygozity for CFTR mutated alele, which helps during epidemics of cholera. Vibrio cholerae which causes this disease modifies the effects of G protein pathway for release of some ions (and water) into the lumen of intestine, which causes massive diarrhea. Specific mutations in CFTR gene deplete its function (the transport of Cl-) which in heterozygous conformation lowers the loss of water, which is the main cause of death in cholera, therefore helps the individuals to survive. Homozygous conformation however results in cystic fibrosis.
Hope this helps. :)

The heterozygous advantage generally lowers natural selection against the carriers of mutated alele,  sounds a little weird. "Heterozygote advantage" refers to the situation where  the heterozygote has a higher fitness than any homozygote. "Natural selection" refers to a differential in fitness between genotypes. Btw, allele takes two "l".

yes, I think that could be more understandable, thanks. But I hope the principle is clear from my comment.

Very interesting explanation has been proposed by Ferreira A. et al. 2011. Briefly, red blood cells of individuals carrying homozygous point mutation in haemoglobin beta-chain tend to be more prone to disruption.
Red blood cells are full of haemoglobin, so once their membrane is damaged, they release free haemoglobin and heme to the plasma. This is called intravascular haemolysis. Too high level of free heme is toxic and you can read about its consequences, for example here.
In the plasma of individuals with heterozygous mutation also there is an increased concentration of free heme, but definitely below harmful level.
However, it is enough to trigger mechanism that protects us from toxic effects of free heme. Heme oxygenase-1 (HO-1)catalyses heme to biliverdin, iron and carbon monoxide (CO). CO makes the vascular environment very unfavourable for Plasmodium.sp and probably protects from infection.
The study was performed in the mouse model.

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


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How fast can a panda run?
Pandas are going extinct, mostly due to habitat destruction. This leads me to the question:  How fast can an average adult panda run? (more specifically Giant Panda)

How does panda's habitat destruction lead you to wonder about their top speed?

@Remi.b habitat destruction -> pandas dying  -> animals dying -> being prey -> escaping predators -> running -> running speed

Adult pandas don't have predators. But anyway. The question is valid without needing justification for your interest :)

I think that in comparison to a North American bear species, giant pandas would not give chase for very long as they prefer to move slowly.  Recent research into giant panda biology indicates that the foraging speed of a giant panda is 50 feet an hour.  Their metabolism is very slow, lower than a three toed sloth.  Their entire way of life is slow movement so considering all that, I would say that you might be able to outlast them in a run.
http://www.livescience.com/51505-giant-panda-metabolism.html


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How is "fine mapping of pelvic regulatory region" done in the stickleback PitX1 paper?
I'm working through this paper for a class. I'm a bit confused by the methods they used in one experiment.
So the researchers are studying spine development in stickleback fish. They noticed some fish have spines and some do not. They have a good hunch that spine development is under control of PitX1. They work out through cross breeding spined/non-spined fish that spine development is regulated in cis.
They then attempt to find what piece of intergenic DNA regulates PitX1 expression. And this is their explanation of how it was done:
"To further localize the position of the cis-acting changes, we looked for the smallest chromosome region co-segregating with bilateral absence of pelvic structures in a cross between pelvic-complete (Japanese marine (JAMA) and pelvic-reduced (PAXB) fish, 13). High resolution mapping identified a 124kb minimal interval, containing only the Pitx1 and Histone 2A (H2AFY), genes, which showed perfect concordance between PAXB alleles and absence of the pelvis"
The attached picture is the accompanying figure, where part A refers to this experiment and part B refers to a promoter bashing experiment later.
I have no idea what it means to "look for the smallest chromosome region co-segregating with bilateral absence of pelvic structures in a cross between pelvic complete and pelvic reduced fish". I assumed they did at QTL mapping, but spines appear to be a mendelian trait. Since QTL mapping is done on polygenic traits, it wouldn't work.
Could anyone shed some light on this experiment?

It's captioned: "(A) VISTA/mLAGAN alignment of Pitx1 candidate region from pelvic-complete stickleback (SALR), medaka and zebrafish. Red peaks, >40% sequence identity in 20bp sliding windows; grey bars at top, repetitive sequence; An external file that holds a picture, illustration, etc.
Object name is nihms-215525-ig0003.jpg symbols, microsatellite markers ..."

Providing a link to the full text of the paper would be extraordinarily helpful...


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Can stem cells from male convert to cells of female-only organs, and vice versa?
As we know, stem cells can convert to different cells of other organs, can male use their own stem cells to convert it into cells of female-only organs(and vice versa)?

Well a stem cell is what every cell comes from, they go through differentiation to become any cell in the body. So theoretically, yeah that kind of differentiation could occur, you'd just need the correct stimulation.

@user19270 no, you are completely incorrect. There is no "stimulation" to change an X chromosome into a Y, or vice versa.

I am assuming you are talking about embryological stem cells and embryological development of genitalia.
The answer is no.
Male stem cells have XY chromosomes. Y chromosome is the sex determining chromosome with SRY gene that determines testes development. Absence of the Y chromosome leads to female development by default. That is why XX forms women and there are people with only one X chromosome which are women. (Turner's syndrome)
It might be possible that SRY gene undergoes a mutation and the gene isn't expressed. There are Y chromosome linked diseases.
You should read up about Y chromosome and development of genitalia.
https://en.wikipedia.org/wiki/Y_chromosome
https://en.wikipedia.org/wiki/Development_of_the_reproductive_system


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Why is ATP produced in photosynthesis used to synthesize glucose?
In photosynthesis ATP is produced in light-dependent reactions only to go to the Calvin cycle to be turned into glucose to make ATP during respiration:

Why isn't this ATP just directly released into the cell? Is there a benefit to using the ATP to make glucose? Also, ATP can be made in the chloroplasts with cellular respiration? What happens to this ATP?

Okay so i did edit some of the text too, in it's initial form it didnt make sense to most of us, as in the ATP isnt converted to glucose, it's used to catalyze reactions that fix CO₂ into 3-carbon sugars that can result in glucose, bear in mind lipid/nucleic acid metabolism also need these sugars so glucose isnt the only output!

As far as I can understand your question, you wish to know why a plant cell consumes ATP to produce glucose when it can directly use the ATP as an energy molecule.
ATP is an energy currency and is required in different biochemical pathways. However, it is not a good energy storage molecule. Following are the reasons why production of an energy molecule such as glucose is essential:

Not all parts of the plant are photosynthetic. These non-photosynthetic parts need an alternate source of energy. Since ATP is unstable, it cannot be transported to different parts of the plant without degradation.
Since photosynthesis cannot happen in the dark, the plants would require some energy molecule that can be utilized later on, in the dark conditions.
Chloroplasts themselves require ATP in the dark conditions. They express an ATP-ADP translocase that actually imports ATP from the cytosol while pumping out ADP+Pi (See this review).
Plants also need energy storage for seeds. This storage is usually in the form of starch (a polymer of glucose).
Glucose is required for synthesis of cellulose which makes the cell wall of plants.
The glycolytic pathway (including pentose phosphate pathway) produces important metabolites such as ribose (in the form of PRPP, which is important for nucleotide synthesis), pyruvate (which is used to synthesize alanine) etc.
Glucose and some glycolytic metabolites (such as glycerol) also serve as osmolytes i.e. they maintain osmotic pressure in the cell.

Basically, points 4-7 convey that Calvin-Benson cycle not only produces sugar but what it actually does is fix inorganic carbon (as CO2) to organic form (in the form of sugar). So, most (practically all) of the carbon that a photosynthetic plant has, comes from this carbon fixation process and that's how plants are photoautotrophic.

Also NADPH produced should be oxidized to keep constant supply NADP+ for light reaction


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Did the Zika virus mutate?
The Zika virus was already present and known to the world (mostly in Southeast Asia) before the current outbreak.
Why has the virus caused such an extreme outbreak?
Has it mutated from its ancestral form such as that found in Southeast Asia?

There is one main answer to this question: The Zika virus spreads so fast because it never emerged in this part of the world. Hence there is no natural immunity available in the population and a lot of infections occur. Once this "first wave" of infections is over, the level within the population will fall drastically. Some more information on this topic can be found here.
It is of course possible that the Zika virus has acquired a new mutation which adapts it better to humans and allows spreading much easier, but this is not yet known, since the situation in South America is still changing very fast with a lot of cases occurring and analysis going on. It still can be enough that the virus never emerged in Southern America and that there is no natural immunity available.
According to the paper in reference 1 (which is only a brief communication) the sequences of the envelope proteins of the virus are similar to the strains circulating in Asia and do not carry novel mutations:

The Surinam strains are the ones published in the paper mentioned above and are from South America. I haven't (yet) found any other analysis, but this will only be a matter of time. At the moment we cannot make a final statement on this although there is some speculation around.
Edit 23/02/2016: There is still no final conclusion available, but there is an interesting paper available on the Biorxiv-Preprintserver, which analyses the mutation rate in the genomes of the publically available strains. It can be found in reference 2.
Based on the available genomes, the author calculates the mutation rate of the Zika virus to about 10 Mutations/year. The virus is a RNA virus which have generally higher mutation rates than DNA viruses.
In the analysis he finds a number of non-synonymous mutations (mutations which lead to a basepair exchange), as seen in table 2:

Especially named is the M2634V mutation, but since this is in one of the envelope proteins, the author finds it relatively unlikely (although not completely), that this causes a much higher mutation rate.
In the Diskussion of the paper he writes:

The sudden spread of Zika to South and Central America does not appear
  to have been due any particular change in the mosquito vector or
  anything to make the Zika virus itself more virulent. But rather from
  the fact that infected people are now able to fly rapidly from country
  to country, thereby spreading the disease extremely easily. This means
  there is little to stop the epidemic continuing to spread to further
  areas of population which have little, if any, herd immunity against
  the virus.

Edit (23.10.2016): There is now an interesting website which builds a realtime phylogenetic tree from the data published (it can be found here). The data also shows where in the virus the mutations occur:

References:

Zika virus genome from the Americas
ZIKA - How Fast Does This Virus Mutate ?

A mutation isn't necessary to explain the outbreak in the Americas, given the low immunity of the population, but there is tentative evidence that this strain of the Asian lineage of the virus may have developed some novel characteristics, which appear likely to have first emerged in the South Pacific.
The virus in Brazil is very similar to the form that drove a 2013 outbreak in French Polynesia:

Phylogenetic studies showed that the closest strain to the one that emerged in Brazil was isolated from samples from case-patients in French Polynesia and spread among the Pacific Islands

Two of the novel features of the Brazil outbreak were also seen in French Polynesia in 2013:

WHO note that, like in Brazil, it was concurrent with a rise in the auto-immune condition Guillain-Barré syndrome, which can cause paralysis:

During the first outbreak of Zika from 2013 - 2014 in French Polynesia, which also coincided with an ongoing outbreak of dengue, national health authorities reported an unusual increase in Guillain-Barré syndrome

While they didn't notice it at the time, a retrospective analysis in French Polynesia prompted by the Brazil outbreak noted that their outbreak had also been concurrent with an increase in cases of microcephaly. I can't find a primary source but here's a quote from  Dr. Lyle Petersen, director of CDC's  vector borne diseases division, taken from an official CDC briefing transcript:

...in French Polynesia where an outbreak occurred which involved more than 30,000 persons retrospectively after the Brazilian data became available - they went back and looked and saw an increase in microcephaly cases in their area

It has been theorised that it may have mutated significantly, for example by Flaminia Catteruccia, associate professor of immunology and infectious diseases at Harvard T.H. Chan School of Public Health, who concludes:

What is worrying is that we don’t know what may have changed, and why. There need to be genetic studies to understand the origin of this virus.

It's been a profound backdrop to the American anti-vaccine movement I've witnessed, when you see what happens in a population with no intrinsic immunity. WHO advertently just declared Zika an emergency.

There is no need to speculate, the complete genome sequence of an isolate from the Americas has been published and can be compared to earlier isolates. These data show that the genome is very close to the sequence of the virus isolated from French Polynesia.

"Very close to the sequence" still allows potential for mutation causing the spread, so this is still speculative and therefore misleadingly assertive - a single nucleotide point mutation could explain it

For those viewing this in the LQP queue - just because an answer may be incorrect or lacking details does not necessarily make it low quality or a target for deletion. It is an attempt to answer the question. If you don't like it, simply down-vote.


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What is a catalytic domain?
I have to answer a few questions from an article I'm reading, and I am just really confused on defining "catalytic domain." I have to relate it to the antibiotic Teixobactin. Is catalytic domain the same as the enzyme's active site?

The catalytic domain is roughly referring to the same part of the protein as an active site and may be used interchangeably in some circumstances:
See here, where "catalytic domain" redirects to "active site."
There is, however, a difference:
From a free online medical dictionary:

active site:
  the place on the surface of an enzyme where its catalytic action occurs.

From Wikipedia:

catalytic domain: structurally conserved (tertiary) structure containing the catalytic function of the protein.

To further clarify: the catalytic domain is the 3D structural independent folding unit of the protein that contains an active site, while the active site (aka "catalytic site) is the area located within the catalytic domain where substrate molecules bind and undergo a chemical reaction.

More precisely, the 'catalytic domain' is the domain of the protein that contains the active site. Of course, there are different definitions of the word 'domain', but a simple one might be an independent folding unit of the protein.

@gilleain very true. I will update my answer.


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How does symbiogenesis explain reproduction of organelles along with the cell?
Symbiogenesis is an evolutionary theory that says that prokaryotes eventually evolved into eukaryotes (having multiple organelles and better structure) by forming symbiotic relationships with other bacteria that have been absorbed, or have entered the cell in an initially parasitic way.
My question is that when the individual bacteria have become organelles, what happens when the cell reproduces? The bacteria were individual entities with their own reproduction mechanisms before they became organelles. Do they still divide in their own way inside a cell (and are subsequently present in both halves of the cell when it is dividing itself), or does their division somehow get incorporated into the cell's own DNA?

I'm not sure about all organelles but mitochondria and chloroplasts are commonly used examples of independent devision in eukaryotic cells. They have independent DNA that forms separate mitotic spindles during division. Similar mechanisms likely existed for other organelles originally but the genetic material may have eventually been combined with the nuclear DNA for simplicity. This is a very simplified explanation but I think addresses the basic question.

Welcome to Bio and thanks for your answer. Could you cite references or other sources to allow users for background reading?

My impression is that other organelles like golgi and ER that are essentially contiguous lipid membranes split by fission in association with cytoskeletal components, independent of DNA. I'm looking and it appears that it mayalso occur by different mechanisms in different organisms.


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How does a test like the Natera Panorama distinguish the child's genome from the mother?
Blood tests on an expectant mother, like the Natera Panorama, are now being used regularly to screen fetuses for chromosome abnormalities. At my wife's recent prenatal visit, she wasn't really even asked if she wanted the test; apparently it's standard in that office. I understand some of the science of how such a test could be performed. When the placenta implants, some of the fetal cells get into the mother's bloodstream, and even though the chromosomes from those cells are breaking down, these pieces can be scanned for the markers for genetic disorders and gender. But I don't understand how the fetus's maternal chromosomes can be identified against the background of the mother's genome.
For example, one of the things that they can rule out with pretty high certainty is Monosomy X: only one X chromosome and no Y. I can see that after determining the mother's genome, it could be determined if there was no evidence of an X or Y from the father. But how would they know if an X was not contributed by the mother. If they are looking through decomposing pieces of DNA in the mother's bloodstream, are they not guaranteed to find each of her X chromosomes, whether or not the fetus has a copy of either one? How can they determine that any piece of a maternal fetal chromosome really came from the fetus rather than from the mother?

Disclaimer: I do not endorse Natera over any of their competitors. I mention them by name only because they are the only ones I am familiar with.

As you correctly discerned, distinguishing the fetal cell free DNA from the mothers cell free DNA in the blood stream is one of the major challenges in this type of diagnostics.
Consequently, the results that can be directly linked to the paternal DNA are the most reliable.
In the case of the example you give, the high accuracy stems from the fact that in case of Monosomy X, there is no indication of neither a paternal Y nor a paternal X chromosome. While the Y chromosome is the most easily discerned, a paternal X chromosome could also be detected because in that case the cell free DNA would contain fragments of three distinct X chromosomes.
This publication summarizes the issue nicely:

Once the cell-free DNA fragments have been purified, small differences
  between the fetal and maternal DNA sequences are exploited in order to
  make a specific fetal diagnosis. To date, the majority of studies have
  focused on the detection of paternally inherited sequences that are
  entirely absent from the maternal genotype, such as those on the Y
  chromosome of male fetuses. This target is particularly attractive as it
  comprises a large portion of DNA which is not otherwise present in
  women.
Variable regions of repeated DNA (short tandem repeats or
  STRs) can be used to identify paternally inherited sequences, by comparing
  the number of repeats present with the paternal and maternal sequences.
  Paternal alleles on the autosomal chromosomes can also be detected, if
  they are known to be absent in the maternal genome, but this requires
  detailed sequence knowledge of the paternal genotype of interest, as
  well as detection methods that can distinguish DNA sequences that
  might only differ by a single nucleotide. Importantly, all these methods
  rely upon the fetus inheriting a uniquely paternal sequence that is conveniently
  located for a particular diagnosis.

The reliability of these tests can apparently be improved by enriching the fetal cell free DNA:

Selective enrichment of fetal DNA, based on a difference in the
  average physical length of fetal and maternal DNA fragments, which
  can be exploited to increase the relative amount of cffDNA. Fetally
  derived DNA fragments are generally smaller than those that are
  maternally derived, being predominantly ,313 base-pairs in length
  (Chan et al., 2004). Therefore, by using standard size fractionation
  to select only DNA fragments ,300 base-pairs, circulating cffDNA
  can be enriched such that it comprises around 70% of the total cellfree
  DNA (Li et al., 2004b), prior to detection and identification by
  either PCR (Li et al., 2005) or mass spectrometry (Li et al., 2006).

Tell me if I have this right: If we see no sign of a paternal X, then obviously we have monosomy X. But if we do see it, then in the enriched cellfree DNA, because an inherited maternal X chromosome would be represented throughout the entire sample of enriched cellfree DNA while a non-inherited maternal X would only be represented in about 30% of it, we should  find approximately 3.3 times as much of one maternal X than the other to rule out maternal monosomy X. Or we would expect to see about the same amount of each maternal X if we have a problem. Is this about right? It's based on quantity?

I think in case of paternal chromosomes, the test is not only based on quantity but also on marker gene sequences (DNA fingerprints). From the blood sample, the DNA fingerprint of the maternal chromosomes are known from DNA contained in white blood cells. Now if the enriched cell free DNA contains DNA fingerprints of a X chromosome that does not belong to the mother, then its a girl, if we see DNA fingerprints of a Y chromosome, it's a boy and if we see neither, its a monosomy X.

However, excluding trisomy 21 has to rely to 50% on quantity of maternal chromosome 21 material because the trisomy could be caused by the child inheriting two chromosomes 21 from the mother which would only show up as an increase in chromosome 21 material in the cell free dna.

Oh. You're saying that monosomy X only happens paternally. It doesn't ever come from a missing X chromosome in the egg?

Honestly, I hadn't thought of that possibility. Of course, that could also happen...


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Explain allelic complementation at molecular level
I know that Allelic complementation is a phenomenon where two recessive loss-of-function allele generate a functional gene product by compensating each others' defect. But I don't get how do they compensate each others' defect.

I don't know much about molecular genetics but you should probably specify that an example of the mechanism by which such "allelic compensation" occurs would be welcome to answer your question.

Allelic complementation meaning that the offspring could have functional gene product

As Matej said, mutations in two different genes (or even a gene and a non-coding regulatory element) can lead to complementation and as they pointed out, the complementation test is designed to check if mutations are on separate genes or not.
Molecular mechanisms that may lead to complementation (apart from Matej's example):

The double mutation in two enzymes in a pathway basically that does not alter the metabolic flux. Lets assume the pathway is linear i.e. no branches. The net flux would be limited by the slowest enzyme in the pathway. If a mutation increases activity of the rate limiting enzyme-1 while another mutation reduces the activity of enzyme-2 then the net flux may not change.
If a regulatory gene acts on another gene by some kind of molecular recognition (protein-DNA, protein-RNA, RNA-DNA, RNA-RNA, protein-protein), then the effect of a mutation in the recognition domain in the regulator can be complemented by another mutation in the target such that the binding affinity is preserved. For e.g. a miRNA regulating a mRNA. If a mutation in miRNA, A→G, is compensated by a mutation, U→C, in the target, then there may be no change in the molecular phenotype. This logic also applies for two gene products that function as a heterodimer.

However, different mutations in the same gene may also lead to complementation like effect. I cannot cite an example but there is a theoretical possibility. Therefore this answer is speculative. There can be two cases here:

Two different mutations in the same allele
Two different mutations in two different alleles

For case-1 you can imagine a situation in which the activity of the gene product depends on intramolecular interactions (secondary and tertiary structures). Two mutations can preserve the intramolecular interaction in a manner similar to the case of intermolecular interactions discussed above.
For case-2 you can imagine a gene-product that functions as a homodimer. If the two mutations preserve the intermolecular interactions in the dimer then you would see complementation. Case-2 can also be observed in a situation when the mutations occur in two different functional domains of two different alleles such that finally the dimer is still capable of carrying out its activity.

The main principle is that the loss-of-function mutations have to be on different genes and recessive. Source
I wouldn't say they compensate each other. If either of them was in homozygous conformation, their effect would be full-shown.
The thing on the molecular level is that often less than 50 % of the gene product is necessary for the gene to "work", to fulfill its function. (in other words, the loss-of-function mutation is recessive and one functional allele is sufficient to show its effect). If the individual is recessive homozygot for the mutation in the gene, there isn't enough functional product to fulfill the function.
However, sometimes, mutations in two different genes can result in the same phenotypic outcome (e.g. one gene making colorless precursor of stain, the other one making protein which turns it into the actual coloring molecule). If there is a homozygous conformation for mutation in either of these two genes, the molecule of stain won't be produced and the flower will be colorless.
However, if two individuals aaBB and AAbb (both colorless) pair, the offsprings will all have colorful phenotype (AaBb) because there will be some of the stain precursor and some of the enzyme that makes stain molecule from the precursor, hence there will be some stain. This event is called complementation.
This was actually used in the past to determine, whether some recessive-trait-carrying individuals had mutation on one gene or on two.


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Animals in predicting disasters..!
I have been working on a project related to how different animals help in predicting natural disasters. But google searches and news only give evidence where animals showed some signs before disasters. But I am really interested to know what special sense they have due to which they can predict disasters early like earthquakes and tsunamis.
Particularly about the following animals -

Flamingos
Dogs
Elephants
Cats
Weasels
Bees
Bats
Snakes
Horses
Cows
Sharks

If anyone can suggest a book related to this or any website please mention .

Animals do not have any special sense which allows them to predict earthquakes or similar disasters, but humans do have an ability believe most anything they hear, or, especially, see written down.

I googled it and read it in a book . This site is for clearing misconception isn't it . Thanks for help

ReReading your question, I realize I probably misunderstood it. Your question is definitely opinion based. You should first find a claim that a given animal has some kind of supersensory power and then ask whether it is true on skeptics.SE

@Pi5 then please cite your sources in your question so we can evaluate them. Just because you read something on the internet or in a book doesn't mean it's true, unfortunately. Google "chemtrails" for an example.

The question is currently too broad and your list of species is rather unexpected!
Important Concepts
You probably want to learn about the concept of bioindicators

Bioindicators are a species that can be used to monitor the health of an environment or ecosystem. They are any biological species or group of species whose function, population, or status can reveal the qualitative status of the environment. One example of a group of bio-indicators are the copepods and other small water crustaceans that are present in many water bodies. Such organisms can be monitored for changes (biochemical, physiological, or behavioural) that may indicate a problem within their ecosystem. Bio indicators can tell us about the cumulative effects of different pollutants in the ecosystem and about how long a problem may have been present, which physical and chemical testing cannot.1

You also probably want to hear about ecotoxicology

Ecotoxicology is the study of the effects of toxic chemicals on biological organisms, especially at the population, community, ecosystem level. Ecotoxicology is a multidisciplinary field, which integrates toxicology and ecology.

I would advice that you read more on bioindicators and ecotoxicology.
Why is the question too broad?
If you are interested freshwater toxicity you will probably be interested copepods (as stated above). If you are interested in soil toxicity you will probably be interested in Collembola (see here). The question is currently too broad.
You should first address these questions to narrow down your question

What disaster are you interested in?
What kind of ecosystem are you interested in?

Why is the list of species unexpected
Typically, cats and horses are probably the worst bioindicators one could think of as their survival depend mostly on humans care and not so much on the environment.
It is unclear too why you are only interest in animal species.


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Is there a special reason why ferns are so early in evolution?
Reading about plants in history it seems that ferns where already in the Devonian period (400 million years ago) growing. Probably the climate in that time was very different from now, but what made them so good surviving in that time?

Could be due to them "having" Neochrome, a protein which enables them to respond simultaneously to red and blue light in both the way that they grow and the way the photosynthetic elements in their cells, the chloroplasts, organise themselves. I'd recommend reading into http://www.economist.com/news/science-and-technology/21600856-survival-ferns-present-depended-ancient-accident-time-and (mostly about why fern survived for so long) and http://www.britannica.com/plant/fern (general information about fern) and https://u.osu.edu/eeob3320/category/ferns/ (properties of fern)


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Why is AIDS not a congenital disease?
AIDS can easily pass from mother to the newborn, then why do we not consider it to be a congenital disease (or syndrome)

Technically speaking, a 'congenital disease' is a term used to describe some (or any) disease that you had at birth. From that point of view, AIDS could be considered congenital too. But, usually, or most often, the words 'congenital disease' are used to explain those diseases which the mother does not have but the child has. Typically, those would not be diseases caused by some sort of germ.

@JordiZambrino - I'm not sure that's correct; e.g.congenital syphllis.

Why do you think it is not considered to be acquired congenitally?

@anongoodnurse do you mean congenital syphilis because it is caused by Treponema pallidum? Or because it is transmitted to the foetus pre-birth via the placenta? Are there further exceptions to the "known" congenital diseases?

@JordiZambrino - yes, there are. That was just an example. Maybe the whole thing could be better expressed by the use of "congenitally acquired" instead of simply "congenital," e.g. congenitally acquired HIV?

@anongoodnurse thank you for clearing that up for me

A congenital disorder or disease is a disorder that is present at birth.  This term can be applied to many conditions, including some that are infections.  More typically, the term is used for developmental birth defects such as spina bifida and cleft palate.
Although HIV/AIDS can be congenital (since a mother has about a 25% chance of passing it to her newborn), most cases of HIV/AIDS are not transmitted by pregnancy and birth, but rather by sexual contact between adults.  Hence it is inappropriate to call AIDS congenital since most cases do not occur in newborns.  This can be contrasted with, for instance, spina bifida and cleft palate, which essentially only occur in newborns and so can reasonably be called congenital disorders or diseases.
A specific case of HIV/AIDS, one which has occurred in a newborn, can be called congenital HIV/AIDS, but HIV/AIDS cannot, in general, be called congenital.

Congenital HIV and Childhood AIDS. You should probably add more detail. Of course HIV can be congenital, and should be called so when the criteria are met.

That was my initial thought that we can not generalize that its congenital.Although it could be in case of a pregnant mother suffering from AIDS though a very less chance of occuring is there


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How does food preservatives effect salivary digestion?
What effects do common food preservatives have specifically on saliva?

First you'll have to provide evidence that preservatives do have an effect on saliva.


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Amplified Fragment Length Polymorphism (AFLP) primers
I am trying to blast AFLP primer sequences to the genome to find the locations of the AFLP markers. However, I can't seem to find full alignments for the primers on the genome.
For example, in the paper "AFLP fingerprinting of the human genome", Human Genetics,  108(1):59-65, Table 1 reports 100's of location of each primer pair:

Now the MseI primer is GATGAGTCCTGAGTAA. So the M-CAA primer should be GATGAGTCCTGAGTAACAA. When I blast this on the reference human genome at NCBI, the results show the best alignment only covers 6-21 of the query:
Homo sapiens chromosome 7, GRCh38.p2 Primary Assembly
Query  6          TGAGTCCTGAGTAACA  21
                  ||||||||||||||||
Sbjct  148723256  TGAGTCCTGAGTAACA  148723241

However, there should be close to a thousand matches for MseI-CAA across the genome according to the table. Does AFLP not require the whole primer to be matched?
According to the original AFLP paper, "AFLP: a new technique for DNA fingerprinting", NAR 1995, the figure 1, the whole primer is being aligned.

Cross-posted to Biostars.
Update: One needs to use the digestion enzyme recognition site to map the AFLP markers. Example: http://insilico.ehu.es/AFLP/info.html

@TalhaIrfan please see these guidelines on tags - you've been adding a lot of very narrow and new tags

@rg255 Thanks RG! I would dare to disagree a bit and I still believe Biology SE needs more tags (I haven't added any of tag blindly). Like BCI wasn't even a tag week ago. Similarly ncRNA and lncRNA must be tags as many researchers want to work with them. GRCh37 and GRCh38 maybe narrow to biologists, but they are important for a bioinformatician.

@rg255 Having said that, I have still revised the guidelines in order to ensure I am serving the community. Thanks again!

Just that things like ncrna and lncrna are likely to be better served under a more broad tag like rna or noncoding-rna - people don't follow hundreds of tags but may subscribe to a handful of favorites (e.g. I follow evolution but wouldn't follow the tag evolution-in-the-jurassic-period if it existed)


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ADCs: by what mechanism are antibodies internalised
I read that ADCs (Antibody-Drug Conjugates) act by a -mab for a particular target being bonded to a cytotoxic compound. From my high-school-with-crayons knowledge of antibodies, however, one part of the mechanism stands out as being strange: the internalisaiton of the complex into the cell.
In my head, antibodies are either free in plasma or expressed bound to the surface of cells. How and why (mechanistically/evolutionarily/functionally) does this antibody internalisation take place? Is it a natural process in most organisms, or a backdoor which must be engineered into the ADC?
The usual sources for neophytes are quiet in this area, and the advanced material is bewildering.

It's a natural process, endocytosis, but endocytosis is also very complex. If you can gain access, really good article, but some general conclusions: "There are many distinct endocytic pathways that coexist in mammalian cells. Although some cargoes enter exclusively by one pathway, most cargoes can enter by several pathways. Any endocytic mechanism requires the coordinated action of proteins and lipids. The best-understood mechanism is clathrin-mediated endocytosis"

This is actually an extremely broad question, which is why I have voted to close. As @Kendall indicates, the primary (but not only) method of antibody internalization is endocytosis, but there are multiple different forms, and the exact mechanism will depend on the structure of the Ab, its target, where it binds, and the physiological context (normal vs. cancerous cells, etc.). The Annual Reviews article linked might be a little above your head (if you can get access to it), so I'd start with the wiki article I linked, as well as google searches.

Actually, knowledge that the process is called endocytosis helped me greatly in searching, and I've learnt a lot about the process today. I'll take a look at the review article tomorrow. I think it likely that this question with an answer along the lines of the comments above would help a fair few people, but vote as you will to make the place as it should be.

@Kendall perhaps you can add a bit on Fc receptors and convert your comment to an answer.

What we're basically looking at with ADC internalization

Courtesy of Bayer
So the way an ADC works: The antibody-drug conugate binds to a target antigen like a transmembrane receptor, the cell in response engulfs the entire complex and send it to an endosome. What the cell can do with the endosome depends on the cargo. Digressing, the ADC internalization mechanism is often attributed to receptor-mediated endocytosis, where the most prominent mechanism of receptor internalization is the clathrin-mediated pathway. We're going to be referring here most of the time.

Clathrin-mediated endocytosis commences with the recruitment of adaptor proteins, accessory proteins and a clathrin polymeric lattice to phosphatidylinositol-4,5-bisphosphate-enriched plasma membrane regions

A common adaptor protein here is AP2 that's capable of binding to motifs present on the cytoplasmic tails of membrane receptors. What it's doing is selecting which receptors are the cargo. Then the clathrin mobilizes to the now-enriched membrane regions, and the polymerization of clathrin causes the membrane to displace and curve. Dynamins, large helical GTPase proteins capable of stretching the invagination in the membrane to a vesicle, bind the phosphatidylinositol-4,5-bisphosphates in the membrane, and may work in concert with BAR domain-containing proteins and actin tension to stretch the membrane into a vesicle and cut it away (Doherty & McMahon, 2009).
Obviously there's some missing information, as we don't fully understand it. I think reading the first reference, published in mAbs in 2013, is a really good place to start however!


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Glucose to Glucose-6-phosphate
What does actually occur- ATP is hydrolysed and esterification between glucose and HPO4^2- (formed as a result of hydrolysis) take place to form Glucose-6-phosphate or nucleophilic attack of O- of glucose on ATP leads to formation of ADP and Glucose-6-phosphate?

I think since this is about chemical reaction mechanisms, it will be better suited at chemistry.stackexchange.

Duplicate of http://biology.stackexchange.com/q/10938/3340


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Are the cells (structures) of deep sea fish different? And can they survive in shallow water?
In the deep oceans the pressure is enormous. But still there are fish living. But are the cells of them different from fish who just live at the surface of waters?
For example, are the cells smaller because of the pressure? And if so, does that influence the inner metabolism? If not, how do they succeed in maintaining their size?

Yes there can be differences in biochemical composition if that is what you are asking for. Please clarify your question.

Pressure equilibrates: it will be the same inside the cell as outside in the ocean. As said by Thawn in his response, the water inside the cell will not vayr much its volume even with enormous pressure, so the volume will not vary. This would of course be different if there was some air or other gas somewhere in the organism, which would both reduce dramatically in volume and dissolve much more into water.

Cells consist mainly of water and the compressibility of water is very low. Wikipedia states:

The low compressibility of water means that even in the deep oceans at 4 km depth, where pressures are 40 MPa, there is only a 1.8% decrease in volume.

This means that the pressure alone does not affect the size of the cells much. However, the pressure affects the cells and the metabolism of organism living in extreme depths in other ways:

Under pressure, the folding and unfolding kinetics of proteins can change drastically. Which means, that the protein structures may need adaptation to great pressures.
Under pressure the fluidity of the cell membrane lipids changes, requiring adaptations in membrane lipid composition.

In conclusion, I would say that the pressure in the deep sea does not directly affect the size of cells but rather their metabolism.
Edit: I just saw the second part in the heading of your question ("and can they survive in shallow water?"). Again, I'll quote Wikipedia:

The extreme difference in pressure between the sea floor and the surface makes the creature's survival on the surface near impossible;

The reason for this is that pressure works thermodynamically in many ways similar to temperature: As explained above, changing the pressure significantly alters reaction kinetics and phase transitions. Thus, the whole metabolism has to adapt to increased pressure (similarly to the adaptation to increased temperature).
However, at least some deep sea creatures seem to be able to adapt to surface pressure if the transition is not too abrupt (from the same wikipedia article as above):

A marine biologist, Jeffery Drazen, has explored a solution, a pressurized fish trap. This captures a deep-water creature, and adjusts its internal pressure slowly to surface level as the creature is brought to the surface, in the hope that the creature can adjust.


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Is it known how human sweat glands evolved?
If human descends from apes than probably we lost our hair. Perhaps in the age of homo erectus we lost our hairs and began transpiring through our skin with sweat glands. But how did these glands evolve? Is it from another kind of cell which is similar?

Welcome to Biology.SE. You probably wan to replace created/evolved by just evolved and replace if humans descends from apes then ... by knowing that humans descend from apes ... or even better, Knowing that humans are apes ....

As a side note: Understanding Evolution (UC Berkeley) is a very introductory online (and free) course to evolutionary biology and you might want to have a look at it.

I am not sure exactly what you are after when asking "how did these glands came?". It seems that you wrongly believe that similar glands do not exist in other primates. Here is a short answer that will help you to search for more information about the evolution of these glands.
Chimpanzees and Gorilla also have sweat glands. The use of sweat gland in thermoregulation is however quite unique to humans and is thought to have evolved in parallel of hair loss and bipedism. See The evolution of sweat glands (Fold and Semken 1991) for more information.


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Etymology of the term monilophyte
I would like to know the origin of the term Monilophyta. I know it's from Kenrick and Crane, but where did they get monilo-? It's not in my enormous Liddell and Scott Greek dictionary, nor is there any word starting with ilo- or hilo- that seems at all likely. Is it from the Latin word "monile" meaning necklace?
This is driving me crazy.

The Division has its name from a cross section of the stem, are lobes of protoxilema which remember the look of a necklace

Phylogeny and evolution of ferns (monilophytes) with a focus on the early leptosporangiate divergences:

The monilophytes (= Infradivision Moniliformopses, sensu Kenrick and Crane, 1997⇓) share a distinctive vasculature, having protoxylem confined to lobes of the xylem strand (Stein, 1993⇓), therefore the Latin moniliformis appellation for “necklace-like.”

Monilophytes = Leptosporangiate ferns, horsetails, whisk ferns, marattioid ferns, & ophioglossoid ferns.
According to A Dictionary of Entomology:

Latin, monil = necklace

As for "phyte," I'll quote this Source:

Greek, -phyte = denoting a plant or plantlike organism

So it literally means "necklace plants. "
From Rai & Graham (2010) :

The extant monilophytes (a name based on a “moniliform” or necklace-like stele thought to be ancestral in the group; Kenrick and Crane, 1997; Pryer et al., 2004)

Note : stele = the central core of the stem and root of a vascular plant, consisting of the vascular tissue (xylem and phloem) and associated supporting tissue.
In other words, the vasculature of all of these plants are arranged like a beaded necklace. This is further alluded to in Pryer et al. (2004) as quoted in @Kendall's answer.

Note: not to be confused with Molino- = "mill" [Source]