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Is it possible to consciously increase or decrease your own heart beat?
By doing yoga, can we manipulate our own heart beat? Is that possible for humans?

I'm voting to close this question as off-topic because it is better suited for Health SE, Fitness SE, or Hinduism SE.

@AMR please don't vote for migration because questions are "better suited" elsewhere. They should only be migrated if they are actually off-topic on the site they were posted at. Is it off-topic for Biology.SE? It's also likely not on-topic on Health.SE https://health.stackexchange.com/help/on-topic

@YviDe I tend to agree with Werner's comments on the answer to this question: http://meta.stackexchange.com/q/10249/298921 The phenomenon can occur, but I do not know that we can say from an evidence based biological perspective why or how. If the question has a better home somewhere else, which in this case it does, then it should be moved.  There are 0 questions and 2 answers for yoga on Bio, 5Q & 10A on Health, 437 results on PhysFit, and 382 results on Hinduism. Another thing is that it is also likely a duplicate question on those sites and will be addressed accordingly. Clearly not Bio.

You can change your heartbeat even by running or doing any form of exercise. You have to add more details to make this question on-topic in Biology.SE

Getting startled is a function of expectation vs.result, mentally. You can "psych yourself up" to become more likely to startle. Arousal is another case where entirely internal thoughts can trigger the state. In both cases, the body will increase heart rate. Calming yourself or angering yourself will affect rate, too. There are things that can be consciously done to affect our heart rate, even entirely mentally. If you want to ask something more specific, I recommend clarifying that point better.

Yes, you can decrease your own heart rate very simply by stimulating the vagus nerve in what are called 'vagal maneuvers'. If you stick your thumb in your mouth, wrap your lips tightly around your thumb, and blow on your thumb like you are blowing up a balloon, you will stimulate the vagus nerve and decrease HR. This technique is often used clinically, and is termed the 'valsalva maneuver'. The vagus nerve runs posterior to the oropharynx. Blowing on the thumb increases pressure in the chest cavity and stimulates a parasympathetic response. Another technique is carotid sinus massage, which works in a similar way, by modulating vagal tone. Many other techniques exist. Another is the result of the 'mammalian diving reflex', which slows heart rate in response to immersing the face in cold water.

Vagal maneuvers https://en.wikipedia.org/wiki/Vagal_maneuver
Carotid sinus https://en.wikipedia.org/wiki/Carotid_sinus
Carotid sinus massage http://www.ncbi.nlm.nih.gov/pubmed/3985038
http://medical-dictionary.thefreedictionary.com/carotid+sinus+massage
Vagus nerve https://en.wikipedia.org/wiki/Vagus_nerve
Valsalva maneuver (see section on heart, where tachycardia means high heart rate) https://en.wikipedia.org/wiki/Valsalva_maneuver
WebMD on decreasing HR http://www.webmd.com/heart-disease/atrial-fibrillation/tc/vagal-maneuvers-for-a-fast-heart-rate-topic-overview

You can do that with autogenic training too, see https://en.wikipedia.org/wiki/Autogenic_training - without blowing the thumb.

Ott, you actually should post that as an answer, since that actually is the answer to the intended question. (I'm pretty darn sure)


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How are targets formed for axon growth cones (CNS)?
Axons have growth cones which find a route to their target using multiple methods (guidepost cells, attraction to target, etc...). My question is, what is the process that actually forms the target? For some given Axon A1 of Neuron A, why does it skip Neuron B, and go straight for Neuron C? How is a target formed on neuron C for Neuron A to connect to? Are there are any articles/readings on this topic? There is also the process of following the path of a pioneering axon. Does following a path of a pioneering axon take precedence over other forms of signaling? Does distance play a factor in choosing a target (Eg: Axon growth cone prefers closer target rather than distant target?)

source: Stack Exchange

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Standard practice for generating rarefaction curves from Next Generation Sequencing data
We have a few million 18S reads from a particular environment. The reads have been clustered into Operational Taxonomic Unit (OTU), and the OTUs annotated against a reference database.
To generate a rarefaction curve, my understanding is that one randomly samples $n$ reads where $n$ ranges (with some step size) from 0 to the total number of reads, and counts the number of OTUs observed at each such sub-sampling.
Which of these two ways, as implemented by sequence analysis suites such as QIIME and mothur, is standard practice? Which would be best to use with the above situation?

Treat the original assignments of reads to OTUs as truth, and when resampling $n$ reads, just count the number of "original" OTUs observed in this sub-sample.
Re-cluster the sub-sampled reads, and then count the number of "new" OTUs in the sub-sample.

My sense from reading through the QIIME documentation is that method 1 is the standard, but I am not sure. I also do not quite understand why method 2 wouldn't be the better way to go, though it would be computationally more expensive.

perhaps related https://www.biostars.org/p/4147/ .. Colwell et al. 2012

The first one is the standard. Rarefaction curves (as they are) only make sense under invariant sets of OTUs. Since alignmnent distances are not metrics (that is they violate the triangle inequality) clusters, defined by an identity threshold, are not some geometrically stable areas in a sequence space, hence they are not invariant under reclustering given a smaller/larger set of sequences.

@ Eli, exactly, but if the point is to say "this is how many OTUs we would have identified if we had this many sequences", doesn't re-clustering make sense? Or is that not the point?

My experience is with 16S, but I can say in that context option 1 is standard. You could try running your pipeline on simulated data so that you can calculate error, and compare methods.

I actually work in the same group as Chris (QIIME author), so I hope this helps: An explanation he gave to us a while back about the basis of rarefaction curves is just to give an indication of whether your sampling is reaching saturated diversity, when comparing 2 unequal samples.
If you compare 2 samples, where sample x has less information (reads/amplicons etc) supporting it, you can't be sure you've sampled all the possible diversity.
Thus, you plot the number of OTUs you see for increasing numbers of reads. If you're saturating the diversity you should see it plateau.
To bring the 2 samples inline with the 'amount of supporting data' they have, you randomly sample the data of the larger dataset, so that it is equivalent to the smaller, and then compare the number of OTUs each is reporting.

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Why do leukemia and lymphoma cause "night sweats"?
One of the symptoms of these blood cancers is sleep hyperhidrosis (aka night sweats).  Also referred to as one of the B-symptoms, it may be used for prognosis.
What is the the mechanism behind the symptom?

Possibilities I came up with:

Body is more likely to be infected due to immune compromise and thus a bacterial or viral etiology
White cell counts may be very high causing release of cytokines which affect thermal regulation
Something else

Why is there more sweating at night and not so much in the daytime?

When the tumor cells infiltrate other tissues and then die, there's a good chance they release some pyrogenic molecules that cause sweating. But, I don't know why at night. Hence, though, it'd be considered a paraneoplastic effect.


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How to obtain virus samples?
I'm trying to observe the behavior of simple viruses in different environments. I'm just looking for simple viruses like the common cold and the flu virus nothing major. Is there a way to obtain them?

As @DonJulian stated you will not get access to human or even mammalian viruses as an individual. Even most Academic research facilities that work with viruses will be highly regulated. Viruses are DANGEROUS. They mutate easily and can go from benign to a killer easily. They can also jump species rather easily. There are, howeve,r ongoing projects to find viruses that attack bacteria, known as Bacteriophages, and these can be found by digging up soil. If you can find an academic sponsor in your school this http://www.seaphages.org/ is one of the projects you can participate in.

First of all, cold and flu viruses are not 'simple viruses', and they are not harmless. They kill tens to hundreds of thousands of people every year.
Secondly, this would depend highly on the risk group that the virus falls in. The NIH sets strict guidelines on who can handle infectious agents. Unfortunately, I can almost guarantee you that no one is going to give you even risk group 1 plant viruses, and they are certainly are not going to give you cold or flu viruses. Risk groups range from 1 to 4. To handle risk group 2 viruses, for example, you are expected to do so in a BSL-2 or higher laboratory, and anyone maintaining stocks of virus is going to do a hefty check of you and your 'facilities' before shipping you anything.
Furthermore, even if you did obtain the virus, you would need to store it or maintain stocks of the virus in tissue culture. Its not like you can just get an eppendorf tube of virus in saline and expect it to survive in your refrigerator at home, and its not like companies are shipping virus willy-nilly to anyone.
That being said, and at the expense of sounding self-righteous, there is really no reason for you to obtain virus particles. You should start by getting a book on virology and reading it. There is plenty of learning material both visual and written out there, and all I will say is if you don't already know how to culture virus or where to obtain it, you shouldnt be doing so, and no one is going to give it to you.
CDC Biosafety in Microbiological and Biomedical Laboratories: http://www.cdc.gov/biosafety/publications/bmbl5/BMBL.pdf
WHO Laboratory Biosafety Manual: http://www.who.int/csr/resources/publications/biosafety/en/Biosafety7.pdf
NIH guidelines recombinant nucleic acids: http://osp.od.nih.gov/sites/defaul/files/NIH_Guidelines.html
I think its great that you are interested, and it sounds like you are interested in histopathological changes caused by virus, so I have included some nice histo pictures below

Syncytia (Herpes Simplex Virus type 1)

Clearer example of syncytia

Characteristic owl-eye (Cytomegalovirus)

Distemper virus inclusion body

Coronavirus particles with 'crown' of surface glycoproteins

Budding HIV virus particles from the plasma membrane

Bacteriophage T4 escape by lysis

Papillomavirus

Rous-sarcoma virus

Tobacco mosaic virus


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Why does vitamin D need to be exogenous?
Vitamin D is a either a hormone or a precursor to hormones. It is very unlike any other vitamins, which are either cofactors or antioxidants, or may be other chemicals necessarily performing catalytic function, just like transitional metal.
But in all sources I found so far it says that Vitamin D doesn't really do anything chemistry-bound, but rather just works as a hormone matching some arbitrary protein receptors or something. E.g. it signals something to the body. But what? And if nothing, then why does not evolution not select out Vitamin D in favor of endogenous chemical or nothing at all?

Vitamin D is vitally important for the uptake of calcium, iron, magnesium, phosphate, and zinc, as well as for bone maintenance:

Vitamin D promotes calcium absorption in the gut and maintains adequate serum calcium and phosphate concentrations to enable normal mineralization of bone and to prevent hypocalcemic tetany. It is also needed for bone growth and bone remodeling by osteoblasts and osteoclasts. Without sufficient vitamin D, bones can become thin, brittle, or misshapen. Vitamin D sufficiency prevents rickets in children and osteomalacia in adults. Together with calcium, vitamin D also helps protect older adults from osteoporosis.

It also acts as a hormone, binding to the Vitamin D receptor in the nucleus of target cells which then acts as a transcription factor for genes related to multiple processes:

Vitamin D has other roles in the body, including modulation of cell growth, neuromuscular and immune function, and reduction of inflammation [1,3,4]. Many genes encoding proteins that regulate cell proliferation, differentiation, and apoptosis are modulated in part by vitamin D. Many cells have vitamin D receptors, and some convert 25(OH)D [an inactive form] to 1,25(OH)2D [an active form].

So, the truth is far from your statement that "Vitamin D doesn't really do anything chemistry-bound, but rather just works as a hormone matching some arbitrary protein receptors or something." In fact, a cursory reading of the first couple of Google results for "Vitamin D" shows that it is broadly involved across the body in many different processes ranging from inflammation and cancer to bone maintenance and mineral absorption.
Sources:

Vitamin D - Fact Sheet for Health Professionals. NIH Office of Dietary Supplements. November 2014.
Vitamin D Wikipedia
Effectiveness and safety of vitamin D in relation to bone health. A Cranney, T Horsley, S O'Donnell, et al. Evid Rep Technol Assess (Full Rep). 2007 Aug;(158):1-235.
Vitamin D WebMD

I'm going to answer your question as asked.
It doesn't need to be exogenous. In fact, it's often not exogenous at all. The truth is, vitamin D can be (and is) be synthesized de novo in adequate amounts by most mammals exposed to sufficient sunlight.[1]
Now, obviously, the presence of the correct wavelength of UVB simply allows the reaction to proceed at a reasonable rate. But the first misunderstanding is that calling "cholecalciferol" a vitamin is simply a misnomer. In reality it is not an essential dietary factor. As you allude to, it's better to consider it a hormone.
You next question is "why does not evolution not select out Vitamin D in favor of endogenous chemical or nothing at all?" Again, answering this question:
It doesn't.
Vitamin D is an endogenous chemical!
It has been in many organisms for millions of years! And very useful too. Ergosterol, previtamin D2, and its photoproducts could have acted as an ideal UVB sunscreen since they could absorb UVB radiation and dissipate its energy by the rearrangement of the double bonds.
Of course, the photochemistry of vitamin D is important and the synthesis in the body is very dependent on a variety of factors. Firstly, environment and the incidence of solar radiation with wavelengths of 290–315 nm on the skin. Other factors include the zenith angle; nitrous oxide, ozone sulphur dioxide pollution, altitude, sunscreen, skin pigment, aging, latitude, season, etc.[2]
It's vital for maintaining the skeletal calcium balance by promoting calcium absorption in the intestines, promoting bone resorption by increasing osteoclast number, maintaining calcium and phosphate levels for bone formation, and allowing proper functioning of parathyroid hormone to maintain serum calcium levels. 1,25-dihydroxyvitamin D influences a large number of biologic pathways. Hence rickets, etc.
One thing to be aware of is that vitamin D either from endogenous synthesis or the diet must be biologically activated through enzymatic hydroxylation in the liver and kidney.

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How is tolerance to an allergen developed?
My question is mainly about how allergy shots work.
I did some basic research before posting here, however I could not find an explanation of what occurs at a cellular level.
Is it the persistance of the antigen which somehow induce immune tolerance?

The allergy shot in itself is a form of therapy called allergen immunotherapy (AIT). In it's essence, we're trying to get someone to develop immunologic tolerance to a given allergen such as pollen, okay! So how does it happen at the cellular level? (Assuming the treatment protocol is known)
Understanding The Mechanism Of Allergen Immunotherapy, as an article is kind of a broad overview. Thus there are phases to AIT that include early, intermediate and late phases. The process begins with a downregulation of mast cell and basophil activity, followed by induction of allergen specific Treg cells, a decrease in Th2 cells, and then a decrease in IgE production with an increase in IgG4/IgA.
Mechanistically, it doesn't look like it's well known how basophils and mast cells get regulated by AIT, but the theory is that the mechanism may resemble H2R (a histamine receptor) receptor activity during venom immunotherapy: H2R becomes highly upregulated after therapy start, and inhibits Fcε-R1 activation of mast cells and basophils, even in the presence of IgE (2, paywall on this one).
They provide an impressive table in Akdis & Akdis 2014 as to the role of immune cells in AIT:

So in the process of encountering the allergen, the immune system produces Treg cells as a result of dendritic cell antigen presentation. An inducible type of Treg called Tr1 is capable of abrogating the response of Th2 and Th1 cells through the secretion of TGF-ß and IL-10. They have a good table for this, too:

There's an effect in there due to TGF-ß exerting its effect on B cells that ends up inhibiting class switching to most other immunoglobulins except mucosal IgA. In conjunction with IL-4, IL-10 is capable of promoting the class switch of preceding B cells to IgG4. So the classes of Ig will largely become IgG4 and IgA in response to the allergen of interest. The B cells will also begin to produce their own IL-10, and in a way become a regulatory type of B cell, or Breg, that propagates the tolerogenic response.
And so the big conclusion: (1) the mast cells/basophils aren't as prone to causing anaphylaxis, (2) the effector cells specific for the allergen have actually shifted to populations of tolerogenic DCs, Tregs and Bregs, and (3) antibody production has shifted to IgG4/IgA from IgE. The net result is due to the repeated exposure to the allergen at some optimal concentration, but the key is they performed the treatment slow enough that the immune system had time to build up tolerance without going crazy. It's also likely that we don't know how long the system stays tolerant for after successful treatment.
It's much more complicated and if you can get past the paywall on source 2 there's really good, detailed info. I didn't want to go into a novel here, but let me know if you need clarification anywhere.


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Difference/similarity between adaptive radiation and species divergence?
I've been reading various answers on different sites but I still don't know whether adaptive radiation and species divergence are different or similar.
My questions:
1) On some sites, it says that adaptive radiation is a form of species divergence, while on others it says that they are different. Which one is correct?
2) Is the main difference that adaptive radiation occurs relatively rapidly and species divergence takes longer?
3) Darwin's finches is used as an example for adaptive radiation, but is it also an example of species divergence?
4) Are the finches on the galapagos islands all difference species (one species diverged into many)? Or are they all the same species, just with different characteristics (e.g size of beak)?

Adaptive Radiation
A radiation refers to the process by which one species rapidly speciate into a number of different species. A radiation can be adaptive or non-adaptive. An adaptive radiation is a type of radiation when new species are formed through selection into new ecological niches. Such adaptive radiation typically occurs after the raise of a key mutation that allows for further specialization such as a mutation causing a change in the Pharyngeal jaw as observed in cichlids (Albertson et al. 1998).
You can learn much more on adaptive radiation in the book The Ecology of Adaptive Radiation by D. Schluter
Species divergence
Species divergence refers to the process by which two existing species diverge through time, either through the accumulation of neutral (or non-neutral but equally selected) mutations or by selection on different trait values.
Species Divergence and Adaptive Radiation
Because of the semantic difficulties behind the concept of species (see here), it is unclear from which point can we talk about species divergence and by which point the observed process of divergence is only divergence within a metapopulation.
Ignoring the eventual detail of the definition of species, and considering species divergence as referring to the divergence between any two lineage (whether or not in reproductive isolation), then it is clear that species divergence is part of the process of adaptive radiation.

To answer your multiple questions directly
1) On some sites, it says that adaptive radiation is a form of species divergence, while on others it says that they are different. Which one is correct?
Adaptive radiation is a little more than a form of species divergence as it includes also the event by which divergences starts.
2) Is the main difference that adaptive radiation occurs relatively rapidly and species divergence takes longer?
mmhhh... not exactly as the concept of radiation also refers to the event allowing the divergence to happen
3) Darwin's finches is used as an example for adaptive radiation, but is it also an example of species divergence?
Yes, indeed! No radiation, without species divergence. On the other hand species divergence will occur between any two existing species regardless of whether they speciated through a radiation
4) Are the finches on the galapagos islands all difference species (one species diverged into many)? Or are they all the same species, just with different characteristics (e.g size of beak)?
The Darwin's finches refers to about 15 (different) species. The different species of Darwin's finches do NOT refer to intra-species variation but to different species. In other words, there is some reproductive isolation between these different species. Again, you might want to make sure you understand the concept of species and you might want to read this post (same as the one linked above) on the subject.

When you talk about species divergence, you mentioned that..."two existing species diverge"...Can this also occur from a single species? (e.g variation within one species population results into species divergence?)

Yes, you can have two population within a species that diverge (yielding eventually to speciation). Then if speciation occurred, then the species will keep diverging. Does that answer your comment? Take good care to realize how poorly defined is the concept of species though.


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Do mutant alleles result from mutation of the wild type?
The allele that encodes for the most common form of a phenotype in natural population is called a wild type allele and all the rest of the alleles encoding forms other than the wild type are called mutant alleles. Do they result from mutations of the wild type allele?

Hey there, is there any particular reason you keep reverting the changes to the question's tags?

Please stop reverting edits. These are edits that experienced users in the community deem are relevant and appropriate. The question and the answers provided fit the tags that have been added. Tags are used to identify a question and make it easier for others to find when searching. It also drives how the question is indexed on Google, so there are specific reasons that they are added beyond the interest you have in the question.

Please review the Help Center on How do I ask a a good question, especially the section on Make it relevant to others and Keep an open mind.

The determination of whether an allele is wild-type or mutant has to do with the frequency that it is observed within a population.
In genetics, a wild-type allele can be defined as

an allele, or DNA variant, whose frequency is more than 1% in a population.
an allele that dictates the most frequently observed phenotype in a population.

Genetics; From Genes to Genomes, Fifth Edition, Hartwell, et. al.
A mutant allele is then defined as

an allele, or DNA variant, whose frequency is less than 1% in a population.
an allele that dictates a phenotype seen only rarely in a population.

Genetics; From Genes to Genomes, Fifth Edition, Hartwell, et. al.
So mutant in this respect only means that the phenotype is seen less frequently in the population.
There is a sequence difference in the alleles, which leads to a phenotypic difference, but if the mutant allele provides an evolutionary advantage that ends up being selected form then it will eventually become the most representative allele in the population and will then be the wild-type.

No, not necessarily!
The terms might be confusing I agree. The most common allele (the wild type allele) might be a mutant of one other type of allele (one mutant allele) present in the population.
The reason we call the least common alleles the mutant alleles is that beneficial mutations are rare compared to neutral or deleterious mutations. If at a given locus most mutations are deleterious, then the mutant alleles will never reach a high frequency. However, if at a given locus a beneficial mutation occurs, then this beneficial mutation will likely rise quick quickly in frequency and therefore there is only a limited time frame under which the most common allele is actually a mutant of a least common allele. In consequence, we tend to call the least common alleles "mutant alleles". This name is often a good fit to the reality but not necessarily.
Note by the way that there are other sorts of selection regime occurring at a given locus that may maintain polymorphism at relatively high heterozygosity such as any form of balancing selection.


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Is there a way to quantify in vivo cholesterol transport rates?
I have always had trouble grasping the physiology of lipoprotein cholesterol transport. The "standard" description found in the literature is that liver synthesizes cholesterol which is carried in "forward" transport to peripheral organs by VLDL (and LDL?), while "reverse" transport is mediated by HDL. Most tissues can synthesize their own cholesterol as well (which makes one wonder what cholesterol transport is needed for in the first place). The figure below sums it up (shamelessly taken from this review).

My question: what are the net rates of transport (fluxes) in this system?
Does the liver actually provide net cholesterol to pheripheral tissues, or is it the other way around? Or is the net close to zero? I can imagine this differs between peripheral tissues, some might be net producers and others may be net consumers, but reviews typically lump everything except the liver together as "the periphery". Perhaps some tissues become net cholesterol producers in certain situations, and consumers in others?
I can't find any data on this in the literature (reviews tend to focus on molecular details of lipoproteins, receptors etc.) but this is not my field and I'm sure the data is out there somewhere. I imagine people have done isotope tracing studies to quantify the rates of transport.

fantastic question! (I think) cholesterol flux is inherently difficulty to study... really depends on the state of the person - fasting or fed. Not sure if anyone has good tracer methods... in my dissertation we did some work with VLDL secretion from the liver (but that was just to look at triglyceride-VLDL secretion rates from the liver)... you give tyloxapol (detergent) which inhibits all peripheral lipoprotein lipase and then increase in VLDL/Triglyceride over time is estimate of liver VLDL secretion see http://www.ncbi.nlm.nih.gov/pubmed/20494946  for that technique

Wolf & Chinkes book - Isotope Tracers in Metabolic Research would probably have the techniques if they exist  https://books.google.com/books/about/Isotope_Tracers_in_Metabolic_Research.html?id=ZlA79DrpNQEC&printsec=frontcover&source=kp_read_button#v=onepage&q&f=false

@VanceLAlbaugh  Thanks, will check out the book!

If I'm not mistaken, shouldn't the CE exchange occur between HDL and VLDL? as opposed to HDL and LDL as shown here.. I mean the CETP thing.


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What determines whether the maternal or paternal allele is expressed?
I am taking cell biology and have this question:
During the process of gene expression, it is possible to express either the maternal allele or the paternal allele.
When and how is the determination made to express one allele over the other?

Are you talking about X chromosomes in females only?

Except in the case of X inactivation in females, and genes on the Y chromosome in males, generally speaking both alleles are expressed in cells.
A good example is the ABO blood type marker system. If the mother is type AA, she will pass on an A allele, which codes for the A antigen. If the father is type BB, he will pass on a B allele, coding for the B antigen. Therefore, any children will be type AB, as the maternal chromosome 9 will express the A form, and the paternal chromosome 9 will express B.

I see.. thank you. But, when does this happens? I assume that two different mRNA's for each pair of homological chromosomes are leaving the nucleolus? So, when does the merging happen?

@user135172 Yes, two different mRNA sequences will leave the nucleus after transcription. They don't "merge", each one is translated separately. In the case of my ABO example above, one set of mRNAs is translated to the A antigen, and the other set to the B antigen, and both are expressed on the cell surface (I'm simplifying the exact process tremendously, please read the wikipedia link if you'd like to know more).

Answer is yes. The term you are look for is parental imprinting
http://mcb.berkeley.edu/courses/mcb142/lecture%20topics/Amacher/LECTURE_13_Imprinting_F08.pdf
Take the  insulin-like growth factor 2 (Igf2) on chr7 (autosome). This gene is imprinted such that only the parental copy is active. So if a mouse inherits a defective copy from its father, it will be stunted. However if it inherited a defective copy from its mother, it will be normal.
Last I looked (about 2 years ago) there were over 1000 genes in humans that are paternally imprinted. It also should be noted that the imprinting may only be present at certain stages in development. It is even possible that one parent's allele to be active in one development stage (father in fetus) but the other at a different stage (mother, rest of life).
This is a very exciting field. How the more complicated switching between imprinted allele occurs is still understudy. However for simply imprinting... it is caused by DNA methylation and DNA silencing by heterochromatin.
Female mammals have an additional system for differential allele expression...ChrX inactivation. In a tissue, one ChrX is randomly inactivated by heterochromatisation. So most of the gene on one ChrX are off. So some cells in a tissue will express the maternal allele, while others the parental allele....


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Where does fungus store excess food?
Can anyone pin point, as to where and how, the excess food is stored in fungus (mushroom to be specific).
Like plants store as starch granules, so where does mushroom store?

From the Wikipedia article on fungi (under Characteristics -> Shared Features):

They have a characteristic range of soluble carbohydrates and storage compounds, including sugar alcohols (e.g., mannitol), disaccharides, (e.g., trehalose), and polysaccharides (e.g., glycogen, which is also found in animals).


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Is there a GPS super tiny for passerine birds?
I wonder if there is a really tiny GPS device that can be mounted on passerine birds (or circa 10 grams birds) without affecting their flight. This web site shows information for bat’s GPS. But it also only last for 24 hours. I wonder if there is some lightweight and long battery life about 2–5 grams. I found this also, but haven’t found if it contains a long battery life.
Is there a study on GPS tracking small birds?

The technology is not there (yet) for deployments on 10 gram birds. The limits for GPS technology are around the 50 g range, for birds. Also bear in mind that the smallest loggers are generally not capable of transmitting, so you would need to recapture the animals to retrieve your data.
As your question implies, there is a strong trade-off between device weight and battery life. There are GPS devices weighing as little as 1 g, but their lifespan is very limited (10 fixes for the 1 g device; 50 for a 1.1 g device).
As a side note: your question implies that small passerines can carry 20 - 50 % of their body mass in tracker without their flight being affected. The ethics boards I am familiar with generally limit trackers to ~ 5 % of the mass of the animal.

A quick search on Adafruit came up with this 8.5g GPS chip, but it's just the GPS, no battery and no transmitter. This solar panel might be their smallest, and might power the GPS, but also weighs 8g and likely couldn't power a transmitter. So after you add a battery and transmitter, is it ok to track how the birds crawl with 50g of stuff on their backs?


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How large is the variability in human bone thickness, and is "big boned" a real thing or not?
My girlfriend is arguing that there are "big boned" people, I read some articles that there is no such thing but she still didn't believe in me because she saw some articles too that big boned people exist. Am I missing something and is my girlfriend correct?
I know that some tall people or some people living in Europe or US have of course bigger bones that in some Asian countries because some Asians are really small. However, this is not how most people understand "big boned".
How large is the variability in human bone thickness in persons of the same height? Could this variation mean that a person might appear overweight, when they in reality are only having relatively thick bones (large diameter), so that the expression "big boned" might have some truth to it?
UPDATED
I'm asking about the most people perceive about the "big boned" thingy. Most people (like my girlfriend) sometimes touch chubby people and when they feel like it's not fat, they say "ohh, you're not fat, you're just 'BIG BONED'". I'm asking if there is a real health/scientific basis for that. Personally, I don't believe that 'big boned' is a real thing. However, it's hard to find information about this on the web.

Do you mean whether bone size varies across humans, or whether this has a significant effect on weight, with people of the same height having different weights because some of them have bigger bones? Those are two very different questions.

Not sure this is the correct site, as there is not a health question here.

Yeah, either way, as @JohnP said, this is not about health.

Try asking at http://skeptics.stackexchange.com/

Then migrate instead of close.

@FranckDernoncourt since this is a beta site none of us can vote to migrate to anywhere except for the Meta site. Also, in its current form Skeptics would just put it on hold. It needs links to notable sources claiming something in order to be on-topic there. It's also still unclear to me what the OP is actually asking.

updated question

Please do not answer in comments.

@JohnP This is not on-topic for Biology, and the only time I have ever heard mention of Human Frame Size is in a Doctor's office, as you will see from this article on MedLinePlus https://www.nlm.nih.gov/medlineplus/ency/imagepages/17182.htm . That being said the question is either primarily opinion based and should have been closed on Health or it is on topic on Health, at least from the perspective of the American Accreditation HealthCare Commission as they accredited A.D.A.M where the article is published.

I'm voting to close this question as off-topic because it's a Health or Sceptics question.

@Christiaan this was from Health

seems like this is best in skeptics. can someone move this?

@Ceeee I am pretty sure it needs editing before moving it over to skeptics since it will otherwise be closed there.

@Chris Thanks bud, will check to make this question suitable for skeptics

"I'm not fat, I'm big boned"

To make this question more suitable for Bio-SE I think you should frame it in terms of variability of bone diameter in persons of the same height, e.g. "How much does the thickness of human bones vary in persons of the same height, so that some people could appear overweight when only having very thick bones?"

Since the argument with my girlfriend was finished days after this was posted(sadly we were waiting for this but it took so long, we posted this question to have an answer right away) I'll just post here what I conclude about the "big-boned theory" based on searching through internet.
Let me site this link; that says,
"However, the initial findings of this study show that having big bones does not make you fat, being fat gives you big bones". What the link says, having more fats forced our body to increase the size of our bones for it to endure the stress brought by having heavier weight. Which means big-boned really do exists. (Damn lost the argument with my girlfriend because of this link)
Another site that says, "If your scale weight indicates that you’re overweight, it’s most likely because you’re carrying too much body fat.   Not because you’ve got 'big bones'". This site says that we cannot use the "big-bone theory" to reason out being fat. In the article, The heavier weight was caused mostly by fats and not by bones. Also the article says that tall person having 6'2 height will have of course bigger bones that a person with height of 4'2. Also the article says that "Still others definitely seem to have a larger “frame” as evidenced by a larger circumference of the wrist and ankles.  [NOTE:  The wrist and ankle joints typically do not have much fat or muscle, it’s mostly skin and bone.  So a person with a larger wrist would most likely have a larger bone circumference.]" (My girlfriend's face would be so happy to read this)
The last site that I would like to post here have chart to know if you're big-boned or not. The site also agrees that there is big boned

TL;DR
I lost, "Big-boned theory" is real but having heavier weight not mean your big-boned.
P.S. : Also instead of saying "ohh, you're not fat, you're just 'BIG BONED'" to someone just to make their feelings well, you're not doing it right! Just tell them the truth and tell them to do more exercise and have healthy lifestyle. :)


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Is there an evolutionary reason why so many white matter tracts decussate in the brainstem and spinal chord?
From a developmental perspective, I would tend to assume that it would be much simpler for the fibers descending from (for instance) the pyramidal tracts, superior cerebellar peduncles, or ascending from the dorsal columns to remain ipsilateral. Can anybody think of a reason why some white matter tracts developed contralaterally?


text:
How does lactic acidosis lead to pain?
I come from Physics, not biology. My understanding is that without sufficient oxygen present, the Krebs cycle terminates in lactic acid formation for the body to later continue the reaction when oxygen becomes more available for oxidation.
If I understand correctly, for a period of time there will be an excess of Lactic acid in the body which will change the pH of the cell. How does that translate into the perception of pain?
I was taught in a Cognitive Science class that pain is cause my a neurotransmitter (Substance P) which is released due to bodily damage. This might not be entirely true, please correct this if wrong.
So my thinking is:
Lack of Oxygen => Lactic Acid production => ... (?) => Substance P => Pain
Thus possibilities for the "..." would be, bodily damage => Substance P, or Lactic Acid signals Substance P release without a need for bodily damage.
My question is then, how do I get from Lactic Acid to Pain?

I am assuming that lactic acidosis does cause muscle soreness (at least some of it!). The following supports my assumption, http://www.medicinenet.com/script/main/art.asp?articlekey=78966 , but http://www.ncbi.nlm.nih.gov/pubmed/6392811 seems to reject lactic acidosis as a cause of DOMS. NOW, this DOESN'T imply that lactate acid does not cause pain. This would be an extension to my original question.

First, acidosis during hypoxia is not due to production of lactic acid, as commonly believed; it is due to loss of respiration, which normally acts as a proton sink. See https://en.wikipedia.org/wiki/Lactic_acidosis, section "Pathophysiology". Second, if you're considering exercise-related acidosis, I think you must separate acidosis itself from muscle fatigue / damage, which is painful for other reasons. I don't think acidosis itself is particularly painful, although headaches are reported. See https://www.ncbi.nlm.nih.gov/pubmed/19932372 . So I'm not sure your premise is correct.

Thank you. My premise is based upon questionable sources. Wikipedia, "This is incorrect, as cells do not produce lactic acid; pyruvate is converted directly into lactate, the anionic form of lactic acid." If so, then what happens to the proton? It seems that there would be a charge imbalance. Is there any local change in pH if there is a lack of oxygen in the system? Is this pH change significant?

Never mind. I found it, Wikipedia for Lactic Acid - "The production of H+ during exercise,[13] has been claimed to be a "construct" or myth, pointing out that part of the H+ comes from ATP hydrolysis (ATP−4 + H2O → ADP−3 + HPO4−2 + H+), and that reducing pyruvate to lactate (pyruvate− + NADH + H+ → lactate− + NAD+) actually consumes H+."

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


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The effects of auto-brewery syndrome
Why are some people affected so differently by auto-brewery syndrome differently if the syndrome seems to be caused by the single organism saccharomyces cerevisiae? It is known that the syndrome has been used to waive DUI charges — like most recently for this New Yorker whose blood alcohol level was 0.4 but she had none of the usual symptoms of intoxication, even though she had ingested alcohol earlier that day. She also carried out most of her daily activities normally, even with high levels of alcohol in her system.
On the other hand, there was another case where the carrier experience the effects of auto-brewery syndrome differently:

Cases involving the yeast Candida albicans and Candida krusei have
  popped up in Japan, and in 2013 Panola College Dean of Nursing Barbara
  Cordell documented the case of a 61-year-old man who had frequent
  bouts of unexplained drunkenness for years before being diagnosed with
  an overabundance of Saccharomyces cerevisiae, or brewer's yeast, the
  same yeast used to make beer.

The quote can also be found at the link of the CNN article.
Could the difference in symptoms and effects due to variations in how the carrier bodies could deal with the overabundance (maybe depending on age, gender, or ethnicity) or are they attributed to variations in the nature of the yeast?

Did any of the people in those cases have diabetes? They likely have high levels of blood glucose. Women with diabetes are prone to recurrent complicated fungal vaginosis as they have higher than average amounts of blood glucose creating an environment where yeasts have abundant nutrients. The metabolic byproduct of yeast is ethanol.

People could also have a disruption in their bacterial microbiome, as is the case when we take antibiotics that allow the fungi more room to grow. The more space they take up, the more access to resources they have, the larger their numbers get and the more metabolic waste they produce. Yeast produce ethanol. So more yeast equals more ethanol. Also if the person has a defective alcohol dehydrogenase gene, then they are not going to be able to process the alcohol that the yeast are excreting.

The gut microbiome is extremely complicated, and almost anything related to it is only partially known, therefore prone to oversimplification. Trying to explain the phenomenon of gut fermentation syndrome in such a limited fashion (age, gender, ethnicity, quantity of one particular yeast, etc.) will not help us understand it.

Common yeasts (C. albicans, C. tropicalis and Torulopsis glabrata) and Saccharomyces cerevisiae are able to ferment sugars through the homolactic, heterolactic or mixed acid fermentation pathways, with ethanol as the major end product.

Candida is a very common yeast found in the environment and in and on our bodies wherever it's warm and moist (therefore the GI tract.) Candida species are the most common cause of invasive fungal infections in humans (followed by Cryptococcus and Aspergillus) and can involve any organ. Yet it's omnipresence does not result in clinically recognized cases of ethanol intoxication in even a minute fraction of people who carry it in their gut.
Case reports started appearing in the literature starting in 1972, yet it is still a rare event to see one. In 2001, the case of a 13 year old girl was published. She had short gut syndrome and became intoxicated after ingesting carbohydrates. She had been placed in a rehabilitation facility with no access to alcohol, but still had positive blood alcohols. Aspirates from her small intestines grew Candida glabrata and Saccharomyces cerevisiae. Short-gut syndrome is complicated.
We have no idea how common fermentation into alcohol is in the gut, or what the results are, but it is probably far more common than recognized, can probably result in effects other than intoxication (for example fatty liver disease in non-drinkers), and probably has a role in other illnesses.
It's complicated:

Carbohydrate metabolism by gut microorganisms is a central process allowing supply of nutrients and energy to the host. This fermentative process is complex and involves several functional groups of bacteria with complementary metabolic activities that interact to ensure the biotransformation of polymers (resistant starch, nonstarch polysaccharides, proteins, mucins…) into end-products (mainly short chain fatty acids and gases). Hydrolytic communities transform complex substrates into smaller fragments that can also be used by other bacterial groups unable to hydrolyse polymers. Other microbial cross-feeding interactions are related to the utilisation of fermentative products such as succinate, lactate or hydrogen and involve specific groups of microorganisms.

All we know is that it happens in some people, and that it can respond to antifungal treatment and some probiotic supplementation. "Why" is still a mystery, and speculation only.
Gut fermentation syndrome
Invasive Fungal Pathogens: Current Epidemiological Trends
IwataK., “A Review of the Literature on Drunken Syndromes Due to Yeasts in the Gastrointestinal Tract,” University of Tokyo Press, Tokyo, 1972, 260-268. Not available online
Functional dysbiosis within the gut microbiota of patients with constipated-irritable bowel syndrome
Obesity and female gender increase breath ethanol concentration: potential implications for the pathogenesis of nonalcoholic steatohepatitis

Interesting. Also how often do we routinely test for blood alcohol levels? Plus as one of the science writers in those articles put it, if we think about alcoholism and how the body grows accustomed to increased blood alcohol levels, then that could mean that it is very prevalent, it is just that we never look and we don't feel the effects because we are acclimated to it. Though I also wonder how much diabetes and elevated blood sugar levels might play in the syndrome.

@AMR - It is. In one study after a 50 g glucose challenge of people suspected of gut fermentation into ethanol, 61% (311/510) had positive blood alcohol levels, whereas "almost none" of the controls did. What a summary! It makes one wonder.


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How do cellular waste products enter arterial blood?
I recently learned that blood in renal arteries contains waste materials, which is filtered via nephrons in the kidneys.
My question is, how are these waste materials getting into the arterial blood? I believe arterial blood is pure and devoid of waste (since all the waste from cells and tissues must enter veins).

there's numerous "waste" products that are continuously produced via metabolism - like urea and ammonium - these are continuously excreted in the urine or eliminated in the feces - they are present in the entire circulation

Arterial blood isn't "pure". It is simply in one part of a complex circuit which carries varying degrees of oxygen, nutrients, and waste products, etc., to varyious parts of the circuit.

...how are these waste materials getting into the arterial blood?

The most simple and direct (but teleological) answer to this is that toxins need to get into arterial blood to ever get to the kidneys to be filtered. The arteries carry blood to every part of the body, detoxifying organs included. Veins carry blood away. If there were no waste products in arterial blood, the kidney would be superfluous.
Waste is produced in all tissue. Blood carries oxygen and nutrients to the tissue (where some of it is used), and via the venous side (all over the body) blood carries the waste products (as well as unused oxygen and nutrients) away toward the heart. The blood carrying waste products collects in increasingly larger veins until it is dumped into the right side of the heart and pumped into the lungs, where a major waste product (CO2) is partially removed. Things that need to be removed by the kidney are all still there. Blood carrying these toxic products is dumped into the left side of the heart, and thus enter the arterial blood supply. The kidney then can remove waste products partially or completely when it reaches them.

Good grief. Now that I have 10K, I can see how unnecessary my answer was. :-(

That was helpful.


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What is the relationship between the light and dark reactions of photosynthesis?
My main concern is why are the dark reactions (those that produce hexose) needed? As far as I understand, the sole purpose of photosynthesis is to synthesize carbohydrates, which are only used for energy storage. So, why don’t plants store energy directly as ATP (by photophosphorylation) and not as carbohydrates? (Of course, that would be too bad for other creatures.)
Elaborating my question:

Plants use chlorophyll to convert light energy into chemical energy of ATP and NADPH by photophosphorylation and chemiosmosis.
Then plants use the ATP and NADPH to synthesize glucose by the Calvin cycle.

So, what is the need of step 2? Why don‘t plants just use that ATP and NADPH for their metabolism?

PS: although @David has provided a nice answer to the current form of the question, the selected answer by @christian still remains selected since it answered my original query i.e. why excess ATP is not feasible for plants instead of why synthesis of carbohydrates is important. Any further answers/comments shall address the latter one, although none of them can be selected as correct since the latter query is not the original one.

No, photosynthesis is used to assimilate inorganic carbon in order to use it in biosynthesis (that's what "synthesis" stands for). It has little to do with energy. There are quasiphotosyntetic bacteria that only use light to harvest energy, hence they depend on first-level producers for organic carbon (organisms with functioning Calvin cycle, Arnon cycle etc).  You need organic carbon to make proteins, nucleic acids and lipids.

thanks, i was actually misled to the fact that carbohydrates are only synthesized for energy storage, and totally forgot that all our body is carbon-based, which we basically get from carbohydrates & their derivatives ;-)

Plants are Eukaryotes and have Mitochondria, so they perform glycolysis and oxidative phosphorylation as well. Animals don't store energy in ATP any more than plants do. We store it in glycogen and fats.

Yes sir @AMR I've understood it now and thats why I've selected the answer below as correct and said thanks to Eli for the comment ;-)

Carbohydrate doesn't easily release the energy, so they can be used for storage and long-distance transport. Like a piece of paper (though cellulose), fires-up only if it gets a touch of flame, though the reaction is exothermic.

Why many biological processes are unnecessarily complicated. Anything (structure/function) found in nature, is result of accident. Nothing happened 'purposefully'. In random events of mutations etc, which one become beneficial for a certain small context; is selected.

In response to your PS. If what you say was really your intent, why pick on plants? Animals don‘t store energy as ATP either. And your original title "Why is photosynthesis so complicated?" had a focus on photosynthesis, as if you had just been introduced to the subject and could see the importance of the light reaction (perhaps considered in one chapter of a book such as Berg et al., and were puzzled about the added complexity of a separate chapter on the dark reaction, which you assumed was for storage — as you admitted in your response to @EliKorvigo.

@david you're assuming just too much. I picked plants because animals dont synthesize glucose (well, from scratch). And my question title had a focus on photosynthesis because light and dark reactions are in (quite) direct relation, but no such relation is present elsewhere (especially in animals). Again, why this question was asked is a long story that I dont wish to touch upon.

@another'Homosapien' Regarding: "animals dont synthesize glucose" –  we actually do, that's called gluconeogenesis.

@eli ah, my friend! Thats why I said "from scratch". Comments, having size limit, really aren't places for writing with proper semantics, you just have to understand some things. All right, lemme tell you the story: this account belonged to my son, he asked this (and a few more) questions. I, reluctant to make a new ID, started using his account and answering questions. He barely uses this site anymore. So, please dont think I'm a newbie ;)

Possible duplicate of Why is ATP produced in photosynthesis used to synthesize glucose? or the other way round.

@WYSIWYG this one was actually asked earlier than the other one, so... :D

@another'Homosapien' I realized after tagging. I asked the mods to merge the other question to this one, if possible.

ATP is a bad medium for storing energy as detailed here.

ATP has a molecular weight of 507 Da
Glucose has a molecular weight
  of 180 Da, and contains the same amount of energy as 31 ATP molecules

This answer addresses one aspect of the question "Why store energy as carbohydrates rather than ATP?" It could have also considered the actual storage forms (polymerized hexoses) and factors like their neutrality and osmotic properties. However, it does not dispute the assertion in the question  that the sole purpose of the synthesis of carbohydrate in the dark reaction is for storage. It is not, nor is it even the main purpose, as explained in my own answer.

Apology
This question has a very simple answer which was provided in a comment by @EliKorvigo (and acknowledged by the poster) two years before writing this answer. However the commenter did not post an answer so the poster, instead of withdrawing his question accepted an answer that, although not factually incorrect, is not a full answer to the question. I feel that photosynthesis is an important enough topic that a more comprehensive answer should be provided.
The Fallacy
The poster writes in his question:

“the sole purpose of photosynthesis is to synthesize carbohydrates,
  which is only used for energy storage”

In fact, as is emphasized in simpler accounts than bloated biochemistry text books,

“the essential purpose of photosynthesis is to synthesize the
  carbohydrates — and from them the other organic compounds — that
  constitute living organisms themselves (plants and photosynthetic
  bacteria)”

The Purpose of the two reactions of photosynthesis

Dark Reaction: Converts CO2 to carbohydrate compounds
Light Reaction: Converts light energy to chemical energy to enable the
  synthesis of the carbon–carbon and other bonds of the carbohydrates,
  and the NADPH needed to reduce the CO2.

(For details see e.g. Ch. 20 and Ch 19, respectively of Berg et al.)
Distribution of carbohydrate in plants and other functions
Photosynthesis occurs in those (green) tissues of plants that contain chloroplasts. The carbohydrate product must be distributed to those other tissues that do not contain chloroplasts. This transport is done through the phloem, with the glucose 6-P and fructose 6-P first converted to the neutral transport form, sucrose. (see SparkNotes for a simple summary, or Liu et al. (2012) for a more advanced treatment.)
Although much of the sucrose will be metabolized to provide the structural components that constitute the tissues (especially cellulose), some of it will be used to generate the ATP and NADPH needed for metabolism.
Storage of carbohydrates in plants
The accepted answer can be taken as accepting the fallacy in the question that the purpose of  hexose production in photosynthesis is for storage, and further of implying that glucose is the storage form of carbohydrate in plants. Of course, polymeric hexoses, starch and sucrose are the main storage forms of carbohydrate in plants, together with some fats and oils, especially in seeds.

It is a good answer, but I selected the earlier answer because it was to the point. I do not have any problem with the modified form of the question (which, indeed, takes it to another direction) since it is also a good question for the site, but I cannot accept your answer now because it does not answer the original query (how I came to ask this question is a long story). Anyways, +1 for the effort :)

@another'Homosapien' — No problem about which answer is accepted. Just came across this question by chance and felt that an answer addressing the purpose of the dark reaction was required in addition to one dealing only with energy storage.


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why is cellulase not found in animals?
As it is really beneficial for all organisms, why are animals, especially mammals (I don't know about other vertebrates) unable to synthesize cellulase enzyme in their body? Is it linked to some DNA defects or have we not evolved from cellulase producing bacteria?

Doesn't the bacteria flora in some higher vertebrates (ie: cows) allow for the celluase, and therefore the digestion of cellulose? We lack the bacteria and therefore the enzyme. I am not sure I understand the last part of your question, " or have we not evolved from celluase producing bacteria".

i actually meant 'why cant mammals synthesize their own cellulase?' or 'why are cows dependent on bacteria for cellulose digestion?' and, by the last part i just meant that if we lack cellulase producing gene, then we must not have received it from our ancestors, which could thus not be cellulase producing bacteria ;-)

I think its a symbiotic relationship, so the bacteria bet something benifital, as do we(the calories).  Bacteria flora are often passed down from mother to child anyway, so why would we even need to have it in our genome? Couldn't we extend your logic to why we don't have any gene "x" that provides benifit "y"; for evolution tinkers and not engineers right?

thanks, and maybe its because of those bacteria only that mammals never needed to develop that gene (if i got you right)

Or they lost the gene. That is usually the better assumption. Think about gene duplications. Once a gene is duplicated, only one copy need be under selection, so the other one can be mutate, either becoming a nonfunctional gene or a newly functional gene. Also remember that there is a cost to maintaining and expressing a gene in the genome. If a symbiont is producing something for you, then it costs you less to maintain your own genome if you lose the gene you don't need to use.

Duplication of If a trait would be advantageous to an organism why hasn't it evolved.

@AMR your last line "If a symbiont is producing something for you, then it costs you less to maintain your own genome if you lose the gene you don't need to use." is confusing me now. How can a gene be expelled or lost just because a symbiont is already providing the resulting protein to you. Its just like you cut off your legs just because a horse is there to carry you. So I doubt "Or they lost the gene.". Maybe that gene gradually became non-functional with time or is still present, but works on feedback mechanism.

You cannot call it duplicate as that question says "This is a general question that would be applicable for any kind of trait."

These are molecules, not body parts. If you do not have a symbiont that produces the product, then you have to maintain the gene or a mutation that causes the gene to be non-functional would be deleterious and could lead to the organisms extinction. A mutation that makes the gene non-functional can occur if there is a symbiont producing the gene product and so you remove selection for that gene and it can mutate to non-function without hurting the host organism.

Substitute cellulase for any trait and that is your question which is why it is a duplicate of that question.

Why substitute? (don't mind) This question is specifically about a single trait which, according to me, has probably evolved but never showed up. Anyways, this discussion is now going off-topic, so thanks everyone for your help.

Histidine is one of the most important amino acids for proteins, but humans cannot produce it. So if I asked, Why did humans not evolve (or retain) the gene to produce histidine? then it is a duplicate of that question. That is why we have it as a community wiki.

But thats different. Humans can eat proteins and breakdown them to get histidine, but humans cannot eat cellulase and become able to digest grass.

AMR is absoltely right. The question is opinion based and we can go on debating for hours upon hours on this topic

The answer to questions like this is just a guess (Primarily Opinion Based), and I've voted to close. But some food for thought too long for a comment:

As it is really beneficial for all organisms...

Why do you think that cellulase is so very beneficial to mammals? Animals did have cellulase (some ancient invertebrates still do, like sea squirts, abalone; crayfish have it); we may well have faulty copies of the gene (as @AMR suggested in comments.) But you presume to know we'd be better off with it. That's a belief without any objective evidence.
What might happen if we could convert cellulose into sugar? This is also important to think about. If some of that surfeit glucose in out guts were fermented into alcohol (this condition does rarely occur in humans, and the living people afflicted with this are truly afflicted), because we have a gut microbiome, we would walk around drunk much of the time (ok, maybe even only some of the time), which would make escaping predators less drunk than we were difficult. Maybe the body would be incapable of handling that level of glucose ingestion, and we'd all be T2 diabetics by the time we were just out of toddlerhood.
Humans need fiber in our GI tracts. I don't know all the reasons why we developed that way, but we do. Cellulase would do away with that. Do you know for sure that this would be good for us?
The thing is, you've made an assumption (we'd all be better off with cellulase) that has no evidence to support it at all (or, at least you have not provided any.)
It's always tricky to assume that you know what's more beneficial for a mammal in the presence of billions of mammals that seem to be doing OK. There are millions of reasons that they are doing OK. We don't know all of them, but the absence of the very thing you presume would be a benefit may be what allowed vertebrates to develop at all.
Ancient Origin of Glycosyl Hydrolase Family 9 Cellulase Genes
Structure and function of a cellulase gene in redclaw crayfish, Cherax quadricarinatus

"I don't know all the reasons why we developed that way, but we do" lack of cellulase might be the reason for it. As you've said, answers to such questions are, and will be, opinion based and also, as you said "It's always tricky to assume that you know what's more beneficial for a mammal in the presence of billions of mammals that seem to be doing OK" one can never estimate how would something have affected our evolution. My point was that maybe having cellulase would have enabled us to live more easily in food scarcity. But, again I cannot assume this to be perfect solution.

@aayushsrivastav - gosh, you missed my entire point, entirely.

I know, I was just justifying my point.


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What is this sand covered insect?
I have found in a wooden house, in the mountains of central Spain this very curious insect:

I was wondering if that was its skin or whether it's decomposition or sand or saw-dust.  That particular region of Spain does have stink-bugs ... but this one doesn't look like anything I've seen before.  A google image search returns mostly arachnids ... but it seems to have only 6 legs.

Possible duplicate of Identifying an insect looking like a crumle

@fileunderwater - Wow, good catch!

The insect in the related question looks quite different. Is it maybe a different species of Masked Hunter? Or at a different age? (When compared side by side, http://imgur.com/a/ovpRW, and given they were in different countries, I'm not sure if I would have recognized it)

@fileunderwater I see what you mean, but the format of anongoodnurse's answer is better than the accepted and upvoted answer on the prior question. If the questions can be moderator merged so that this answer appears on the other, then I would agree with the close, otherwise I think it should stay open. Also it is a bit difficult to identify by search if you don't know where to start.

It's a kind of assassin bug, specifically a Masked Hunter:

The surface of an immature Masked Hunter is sticky and it attracts lint and dust which helps to camouflage this predator.

and

The name refers to the fact that its nymph camouflages itself with dust.

Though they feed on small insects, they will bite defensively, and when they do, it's fairly painful.

I recognize it as a species of "wheel-bug" or, as others have noted, a species of assassin-bug. (I don't know the specific species, though; sorry.)
These predators have a vicious "bite" using hypodermic mouth-parts, and some routinely inject a type of enzyme in the "venom/saliva" that causes great burning or pain; the compound is intended to help the creature suck the internal organs out of "prey" creatures. Depending on the species' size, these may even kill and consume young frogs and toads.
As noted by others, the younger ones stick soil, plant-matter and other material to their exoskeleton as camouflage. This is because, in part, they are cannibalistic; parents and elders have no compunctions about eating their smaller offspring. Of course; if the youngsters get a chance, they will dine on their parents or elders, too.
Aside from some wasps that lay eggs on the paralyzed bodies of spiders, these insects are one of a very limited number of species that will often actively hunt down and prey on spiders.


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Is there is difference between "homozygosity" and "homozygosis"?
Are these just two terms for the same phenomenon, i.e., the state of being homozygous? Merriam-Webster says so, but I know dictionaries sometimes miss the nuance of scientific terms. If they are indeed synonyms, it seems homozygosity has won out, according to Ngrams

The question is currently receiving close votes because it looks like a homework question. You should try to show your attempt at answering your question if you want to avoid having your question closed.

Ha, fair enough. I am not student. I am a hamster breeder with a keen interest in genetics. I had this question because I only saw the term "homozygosis" in publications from several decades ago. I edited the question as suggested.

I edited my question to show my attempt at an answer. Can it be returned to open status?

I made the changes that were requested. Why was this question closed?

Homozygosis and homozygosity are NOT synonymous. The two terms refer to the same concept though.
Homozygote
An indivdidual or a cell is said to be homozygote for a particular gene (or any DNA sequence) when identical alleles of the gene are present on both homologous chromosomes. (Wikipedia > Zygosity).
Homozygosis
Homozygosis is the state of being homozygote (Wright 1933) for a particular gene (or any DNA sequence). According to freedictionary.com, homozygosis may also refer to the process of formation of a homozygote. I have never encountered this sense in the literature though. As you found out by yourself, Homozygosis is a term that is rarely used in the literature (in comparison to homozygote and homozygosity)

Expected Homozygosity
Expected Homozygosity is the probability of two randomly sampled alleles (in a population and at a given locus) to be identical by descent.
Expected homozygosity and Expected heterozygosity
As shown in Nei 1973, the mathematical expression of expected homozygosity $Ho$ is
$$Ho = \sum_{a=1}^{n} x_a^2$$
where $n$ is the number of alleles and $x_a$ is the frequency of the allele $a$.
It is more common to use the concept of expected heterozygosity $He$ (a.k.a. gene diversity) rather than the one of expected homozygosity $Ho$. By definition, $He=1-Ho$, that is
$$He =1- \sum_{a=1}^{n} x_a^2$$
In the special case of a bi-allelic locus, and replacing the two allele frequencies $x=1$ and $x=2$ by $p$ and $q=1-p$, the above formulations becomes
$$Ho = p^2 + q^2$$
$$He = 1 - (p^2 + q^2) = 2pq$$
Hardy-Weinberg equilibrium
Under the Hardy-Weinberg assumptions, the observed frequency of heterozygote (a.k.a. observed heterozygosity) is equal to the expected heterozygosity and observed frequency of homozygotes (a.k.a. observed homozygosity) is equal to the expected homozygosity.


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Can skin be removed and replaced so that it maintains its original cellular structure?
The cells in our body that form tissue, such as our skin, are interconnected. I would think that cutting out tissue or trying to repair/replace it, as is done in surgery, or after an injury, could not be accomplished without damaging this network and creating irreparable damage.
Am I mistaken and is it possible to remove and replace skin, close a wound without damaging the underlying cellular structure and having scar tissue form?
When it is healing, is the tissue that is healing in some way weaker than the tissue that remained intact, say just beyond the margin of the wound?
If someone has surgery, can their skin be repaired completely with the proper amount of healing time?

As pertains to skin, no. As pertains to your other fears, that's a different question.
Every cut that extends into the dermis significantly (and to remove skin, it must include the dermis) will leave a scar behind.

Cuts that extend only very superficially into the dermis may hit some capillaries and bleed, but these will usually not bleed much, and can heal "seamlessly". But anything that extends deeper will bleed more. Those are the cuts that often get stitches if they are long enough, won't stop bleeding, etc.
Lifting and replacing a piece of skin would necessitate the damage of many cells and the destruction of a lot of fine blood vessels, but even with the best microsurgical techniques, a scar will form. The best techniques combined with the best pre- and post-surgical care will only minimize scar formation; it can't be eliminated.

In skin, the process of wound repair can be generalized into three cascading phases each with characteristic cellular events: 1) inflammation; 2) fibroplasia or proliferative phase; and 3) scar formation.

Wound Healing in Development

I have the honor :-) congrats on 10k :-D


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When was the last common ancestor of pig and human?
Some religions regard pigs as unclean on the grounds that pig flesh is closest in composition to human flesh. I don't believe this for one instant, but it got me thinking, just how close is pig and human on the evolutionary tree?

Can you please stop editorializing your questions. The story, or your opinion are not relevant to the question and do not change the answer.

Also, if you're talking about kosher or halal dietary restrictions, it is more than likely the elders saw people eat pork and get very sick or die from trichinosis before anyone knew that was a thing, and either they believed that cause of illness was an affront to God or in order to dissuade the masses from risking it and eating pork, especially if other food was scarce, they, quite literally, instilled the fear of God in them by declaring swine as unclean and consuming it as an offense to God. Oddly enough, we now know the cause, but pork is banded but cigarettes are perfectly kosher... .

A bit of context to a question does no harm at all. AMRs objection is tosh.

That's where you're wrong. This question was closed by the community, even though there was a valid question there; because of all of the superfluous detritus in the question: http://biology.stackexchange.com/posts/41836/revisions. I distilled the question out of it, edited it, and got it reopened. Your question is simply When is the last common ancestor of pig and human? and Is it a fact that pig tissues are highly similar to human tissue? The rest just makes you come across as a bit of a whacker... Leave it out, ask the question, get your answer and then fight it out at the boozer.

Last common ancestor is about 97.5 Million Years Ago.
TimeTree.org Pig vs. Human
That being said, they are close enough to us that they are a vector for influenza viruses that are able to make the jump to human pretty easily.
Also we use their tissue as a homologue for human in forensic research. We also use valves from pig hearts to replace defective human valves.
This Nature News Article reviews some of the work being done with Pig to Human Tissue Transplantation. Though granted the methods they are looking at rely heavily on targeted gene editing.

Good one man. Nice, crisp answer.

Another thing I forgot to mention. Until we engineered E. coli to mass produce it, we used to use pig insulin for the treatment of diabetes....

Are you serious! That is insane!


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Genotype of children conceived after stem cell transplant?
If you have sickle cell disease and have a succesful stem cell or bone marrow transplant, your blood type changes to AA. But what about your future children? Do your sperm or egg cells continue to express the SS genotype or do they become AA as well?

Bone Marrow Transplants should not make any changes to the germline. I say should not, because killing the bone marrow prior to transplant usually involves full body irradiation and or chemotherapy, and there is the possibility that you could accumulate mutations in the germ cells, however that genome will still be that person's and not the donor's genome.

Infertility is common after chemotherapy or irradiation done for transplants, so the question in that case would be moot.

Spermatozoa are produced in a process called spermatogenesis. They come from germ cells, which in the human males are located in the testes. These are not affected by stem cell transplants.
In females, the equivalent oocytes are already present at birth. They undergo meiosis later, but since their genetic composition is already set at birth, they, too, are not affected by stem cell transplants.
This might make the process clearer: Primordial Germ Cells and Sex Determination in Mammals

In all vertebrate embryos, certain cells are singled out early in development as progenitors of the gametes. These primordial germ cells migrate to the developing gonads, which will form the ovaries in females and the testes in males. After a period of mitotic proliferation, the primordial germ cells undergo meiosis and differentiate into mature gametes—either eggs or sperm

A stem cell / bone marrow transplant only affects the bone marrow, where the blood cells are produced.


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Of people who develop Alzheimer disease, are those people genetically predisposed to it?
I have read a lot lately about microbiological pathogens that are found in blood vessels in the brain of patient's with Alzheimer disease (positive association).
So, I am confused whether there are genetic markers and testing of susceptibility to this disease, or whether there is some other type of disease process occurring here (given the microbiological pathogens association). Is that widely discussed in the popular press?

In part, there are in fact numerous polymorphic markers that detail genetic predisposition to AD. Markers can differ between the type of AD they predispose, however: familial versus sporadic, for example. To give a good example, of four isoforms the apolipoprotein ε4 isoform is known to greatly increase the chance one will develop AD.


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What are the effects of removing CD4 receptors?
If the gene for the CD4 receptor was removed, would the person's immune system work normally?  Could a new artificial receptor be substituted in place of CD4?
Could HIV infection be prevented in this way?

The CD4 receptor is vital for the proper functioning of the immune system. It is found not only on T-Lymphocytes, but also on macrophages and dendritic cells. Its function on T-cells is to stabilize the interaction between the T-Cell receptor and the MHC Class 2 (often known as HLA II in humans) antigen complex on antigen presenting cells and improves the affinity dramatically.
CD4 is also vital for the activation of Helper T-Cells (2). It is needed in the signaling which occurs in the thymus that selects for CD4+ T-Cells. If you were to delete CD4, you are, in effect destroying the adaptive immune system in humans, as there would be no CD4+ produced. In this situation, you would not get activation of B-Cells or Cytotoxic T-Cells, and the immune system would only be left with its innate defenses to protect it. This is found in diseases such as Severe Combined Immunodeficiency and can only be cured with early bone-marrow transplantation.
A better target would be the CCR5 receptor. This receptor acts as a coreceptor for the interaction between GP120, the receptor on the surface of the HIV capsid and the CD4 receptor. People who have a mutation in the CCR5 receptor are resistant to the most prevalent isoform of HIV, as the interaction is necessary for the capsid to fuse with the plasma membrane of the CD4+ cell.
See this article about the CCR5-∆32 mutation. HIV Resistant Mutation

I think it's deathly important to note how critical CD4 is for the activation of T-helper cells, and thus a myriad of downstream immune cells such as B cells:
When an APC presents an antigen through its MHC-II molecules, the TCR-II complex must interact with the Ag-MHC complex to transduce an activating signal. Note that the T-helper TCR is composed of α/ß molecules associated with the CD3 complex and CD4. CD4 is associated with an intracellular tyrosine kinase called Lck. Upon recognition of MHC-II by CD4, Lck phosphorylates the CD3 complex intracellular tails and the ITAMs of the CD3 zeta chains in concert with Fyn. Zap70 binds these phosphorylated sites to transduce the signal further (CD4 function, TCR signal transduction, and ignoring co-stimulation). To that, end there's some risk in knocking down CD4, or inadvertently modifying the receptor into loss-of-function.
Knocking out CD4 in a human would probably result in something similar to SCID (severe-combined immunodeficiency syndrome). If you're unable to develop T helper cells (Thymic selection), you're cutting off much of the ability for your immune system to modulate its defenses. B cells can still activate in a T-independent manner, but the types of antigens and responses are largely different (T-independent activation).
Being said, HIV primarily binds to CD4 through its gp120 membrane protein, and then facilitates membrane fusion through association with a chemokine coreceptor. Because of the above, you can't just delete CD4, it's quite dangerous from an organismal standpoint. Engineering a different receptor is a difficult way to go about it, as we don't know how that'll affect normal functioning, either. You can modify the chemokine, but it's also not guaranteed that the HIV wont shift to a different coreceptor (HIV tropism). Thus the best preventions so far have been to block adsorption, block HIV normal functioning through antiretrovirals, etc.
The take-home message is that modifications to our own cells have a capacity to do a lot of harm, but through good experimental design we can also do a lot of good, see chimeric antigen receptor T cells. We're also at an arms race with the pathogen as well, however, so it's a multi-dimensional problem that goes beyond the viral receptor!

Kudos on a very detailed answer, but you've introduced a lot of jargon and abbreviations in your second paragraph that won't be accessible to people without a decent grounding in immunology—which almost certainly includes anyone looking for an answer to this question. A simplified explanation of how CD4 has a crucial role in cell-mediated immunity would be helpful to people with less immunology training.

Firstly, I would like to talk about the CD4 receptor. This receptor is present on the T-helper cells. These receptors help stimulate immune cells. HIV cells target these T-helper cells and reduce them in number. This reduces the hosts immunity overall. We could build an artificial cell with just the CD4 cells or make a substitute like you said. The HIV virus would bind to these artificial cells and then those cells would destroy the HIV cells.

(source: davidson.edu)

Reasons as to why it's not possible
  This would still not be a cure as it would do nothing to address the cells that are already infected with HIV and are either latent or actively producing more virus. You would also probably have to continuously give infusions of these to the patients and thus would be to save only a few lives.

Sources:
source1
source2


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Would some dinosaur egg be the most massive cell that ever existed? Are dinosaur egg relatively small compared to eggs of modern birds?
The egg of a large modern bird is a very large cell, not the largest possible biological cell since there are very long nerves in squid, but it's likely the most massive modern cell.
But, what about the cells of prehistory? Many dinosaurs were far larger than modern birds, but I had trouble finding information on just how large their eggs could be. I was also surprised that the eggs were not bigger than those of modern birds. It seems the ratio of egg size to dinosaur size was much smaller... or has that even been studied?
Maybe the large eggs were all destroyed?

I was also surprised that the eggs were not bigger than those of modern birds. It seems the ratio of egg size to dinosaur size was much smaller. - where have you read this?

I suppose that you define "large" in terms of volume. Note that there will have some issue of definition about what a cell is when you consider cases where cells of an entire tissue vanished to end up with more or less a big single cell with many nucleus.

I didn't read it. It's an observation I'm having a hard time confirming or invalidating.
Let's just use mass for largest. Volume is confusing.

The largest known dinosaur eggs were the size of a basketball. The egg of an ostrich is also very large, comparable in size to dinosaur eggs.
The reason why even the very large dinosaur laid relatively small eggs is diffusive ventilation of oxygen and "breathing" through the eggshell.
The rate of ventilation is proportional to the eggshell surface area while the required amount of fresh oxygen is proportional to the volume of the egg. The surface area is proportional to the square of its radius while the volume to the cube of the radius. As the size (=radius) of the egg increases the ratio between the incoming oxygen through the shell to the amount of oxygen needed is decreasing, making too large eggs unsustainable.
Another consideration, also related to oxygen diffusing through the eggshell is that a very large egg requires a thick shell, and too thick shell prevent oxygen diffuse through it to the embryo.
References:

USRA.edu: how big can eggs be?


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What is the surface area to volume (SA:V) ratio of a red blood cell?
According to this author, red blood cells (RBCs) are biconcave to allow easier bending. The standard explanation in biology for higher surface area to volume ratios is that it improves reaction rates. When a RBC squeezes through narrow veins I imagine that it gets deformed. Considering that a RBC's function is to exchange oxygen in narrow capillaries, I was wondering whether it is appropriate to reason that the biconcave shape promotes gas exchange. So what is the SA:V of a biconcave RBC and by how much does the SA:V change depending on where in the body the RBC is traveling?

I googled "surface area of a red blood cell" and this paper was the first result.  It should answer your first question. Though it was unclear to me what the surface area unit of measure was, which may require a bit further reading.  There's also this article, which goes a lot more into the math of calculating these two things.
As for your second question about how much it changes, intuitively I would guess very little and it probably does not significantly change exchange rates.  I couldn't find any research on the topic.  The hard part is defining all the shapes they may get squeezed into, then either calculating or measuring SA:V. Possible?  Surely, a well written computer model could do it at some point.  But worth the time/money?  Probably not.

The first article is interesting. SA:V ratio is mentioned a few times but without specific numbers. Table 1 in the article shows RBC volumes and Table 2 shows RBC surface areas. However, there is no approximation of the ratio. Dividing the entries in the tables with each other gives lower than expected results. The SA:V of a sphere, for example, is 4.836 One would expect the SA:V ratio of a RBC to be higher than that. Googling "surface area to volume ratio of a red blood cell" doesn't return the results I'm looking for either. Plenty of references to the SA:V being high, but no approximations.

Can you run me through the calculation you're using to get 4.836?  When I run it for a sphere of 6um diameter I get 1,000,000.

See this link.

I see the number, but I'm still unclear on how it's derived.

I don't know either.

I wouldn't use a number you don't understand as a start.  I believe it's supposed to be the SA:V of a unit sphere but the numbers don't come back right to me.  The important thing is you can ignore that entirely as it doesn't really matter.  The SA and V you're looking at can be calculated easily, at least for a sphere.  From the first paper you can just compare SA:V ratios.  A sphere comes up at 0.833 and the biconcave at 1.49.  So it's almost twice as high.  I imagine when units are factored in properly its 833,000 and 1,490,000 for the true ratio.

https://arxiv.org/ftp/arxiv/papers/1403/1403.7660.pdf
human erythrocyte avg dia: 7.2, vol 91.31 cubic microns, surface area 136.55 square microns

The biconcave shape or desk of the RBC enables gas exchange because the biconcave desk enables it to bend in other words travel through narrow blood vessels or capillaries for exchange of gases e.g oxygen, remember one of the functions of RBC is to exchange gases, now gases like oxygen for example is found in the blood vessels because it is transported in the blood. Now for exchange of gases to happen in the blood vessels by the RBC the biconcave desk enables it to be able to squeeze or bend into the blood vessels for exchange to take place. This means that if RBC didn't have a biconcave desk there'd be problem with exchange of gases because RBC won't be able to enter the blood vessels for exchange of gases. Hope this helps

You seem to have stated the same thing three times, and none of the times is it an answer to the question. You would also be expected to support an answer with references and citations. Please take our [tour] and refer to the [help] for guidance to our ways. Enjoy the site.

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


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Engineered CD8 T-cell therapy for HIV infection
CD8 T-cells are effective in controlling HIV during the early phase of the infection. However by the time, the virus mutates and develops an evasion mechanism against CD8 T-cells.
Since cancer cells also develop immune evasion mechanisms, and scientists are using several technics to block those mechanism, i think it would also be possible to control "viral escape".
I made some research regarding HIV immunotherapy, however the only thing i found was antibody based immunotherapy.
My question is, would it be technically possible to engnieer custom CD8 T-cells which will targed HIV infected cells ?

And drive the patient into AIDS even sooner?! The problem is that CD8 cells do their job and wipe out all of the infected CD4 positive cells. Once someone is infected, our current course of action is keep viremia low and don't allow for escape mutants, you do this by attacking multiple pathways using HAART.

If you have access to Janeway's Immunobiology 8th edition, read the Acquired Immune Deficiency Syndrome section in Chapter 13. It will give you a good feel for why you don't need better killers (CD8+), you need ways of blocking the virus from propagating, keeping as large a population of uninfected CD4+ cells as possible. There will always be a reservoir of the virus that has been integrated into the genome of cells that lays dormant, that's how lentiviruses behave; well except for the Berlin Patient.

@AMR , Since you are expert in immunology, my questions may sound too elementary. Sorry for this, but i have one more question if possible. Once patient is at a early stage of infection, Are all of the CD4+ T Cells infected ?  As far as i know, we can't complately eradicate HIV from body because HIV drugs don't affect HIV hiding in resting CD4+ T cells. My Question is,   assuming,  the patient still have uninfected CD4+ T cells at the early stage of infection, May killing all infected CD4+ T by CD8+ T cells, and killing the virus itself with drugs may be an effective treatment method ?

There are protocols that allow people like healthcare workers that have been accidentally infected,  to go on HAART very soon after exposure. This will usually prevent the infection from taking hold. The way HAART does this is through 1)Entry inhibitors 2)Nucleoside Reverse Transcriptase inhibitors 3) Non Nucleoside Reverse Transcriptase inhibitors 4)Integrase inhibitors, and 5)Protease inhibitors. If you can keep the viral genome from integrating into the host genome, the virus will clear. Once the infection has integrated, you will never get rid of it; only happened once with Berlin Patient.

T-Cells aren't the only cells that have CD4. Macrophages, Dendritic Cells, Monocytes, Precursor T-cells, Natural Killer Cells. Let's say you have any of these infected cells encounter a cytotoxic T-Cell with specificity for the HIV amino acids, but the provirus is dormant and is not expressing its genes, then the CD8 cell will not identify any problems and will not kill the cell. Months, years, even decades after, the provirus can activate and start producing virons. The strategy currently is don't get it, block it ASAP if you are exposed, or suppress it with a multi drug regimen.

but the provirus is dormant and is not expressing its genes  -  I think even this sentence alone is  enough to explain why CD8+ T cell therapy would not be  useful.  Thanks

HIV is a difficult problem, but this might be a step in the right direction and hold promise for the future of HIV treatment. http://www.nature.com/articles/srep02510

People in the comments suggest that this would "Drive the patient into AIDS sooner", or that this will be ineffective because of dormant virus.  Neither is correct.
The question is asking about engineering CD8 with engineered T cell receptors specific for HIV.  This is a logical approach, and multiple groups have tried it:

In Vivo Suppression of HIV by Antigen Specific T Cells Derived from Engineered Hematopoietic Stem Cells
Reconstitution of anti-HIV effector functions of primary human CD8 T lymphocytes by transfer of HIV-specific alphabeta TCR genes
Development of CD8+ T cells expressing two distinct receptors specific for MTB and HIV-1 peptides
T-cell engineering by a chimeric T-cell receptor with antibody-type specificity for the HIV-1 gp120

A brief search on Pubmed will turn up many other articles. Some of these approaches have entered clinical trials; for example:

Redirected High Affinity Gag‐Specific Autologous T Cells for HIV Gene Therapy

The problem with this approach is not that it will "drive the patient into AIDS sooner".  A strong CD8 T cell response controls HIV well, and although it might be one contributor to CD4 T cell loss it's no longer believed that it's a major cause, especially in the early stages of HIV infection.
The general problem with CD8 control of HIV is that the virus is capable of mutation to avoid control by CD8s. Essentially, every case of HIV is effectively controlled by the CD8 T cell response in the early stage of infection, but the virus then mutates and escapes control, then the CD8 response adapts and controls the virus once again, and the virus mutates and escapes ... This can and has been tracked in many patients, showing repeated rebounds of the virus in the blood correlated with CD8 changes.
Better CD8 control of HIV is linked to a broader CD8 response -- that is, attacking many viral proteins, so that viral escape requires multiple simultaneous mutations (exponentially more difficult for the virus).  (Alternatively, the CD8 response can attack a small number of proteins that are very constrained, so that the virus can't successfully mutate them.  However, for reasons related to MHC restriction, that seems to only work in a small minority of people.)
An engineered CD8 T cell response will inevitably be to one or a small number of viral proteins.  That's conceptually similar to the natural situation following HIV infection, meaning that the outcome could be the same -- viral mutation and immune escape.
Because engineering the TcR means you can pick your targets rationally, you might be able to do better than the natural situation, but it's not obvious.  Overall, the fact that groups have been working on this approach for decades, without a breakthrough cure yet, suggests that it might be useful but isn't going to be a slam-dunk.

You have three ways that HIV leads to AIDS: 1) Apoptosis: The cells recognizes it is infected or integrase messes up the cDNA insertion and the cell undergoes programmed cell death. 2) Lysis: Budding of HIV destroys the cell 3) CD8 targets and kills infected CD4 cells. Escape mutants are much more of a problem for Immunoglobulin neutralization than CD8 cells because CD8 is only "looking" at the primary amino acid sequence of the viral proteins that the infected cells are presenting. and if viral reservoirs weren't a problem then we could cure people with HAART and time or BMT. We can't.

Escape mutants are much more of a problem for Immunoglobulin neutralization than CD8 cells because CD8 is only "looking" at the primary amino acid sequence - this makes no sense, and is immediately proven wrong by the frequency of HIV CD8 escape mutants (rapid and repeated) vs immunoglobulin escape mutants.  Very basic HIV biology here.

Love the downvotes.  Want to explain?


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Why are plant buds called 'eyes'?
I was reading the etymology of the Latinate English verb 'inoculate' which contains the following part that generated the question entitled above:

[...] inoculare "graft in, implant a bud or eye of one plant into another," from in- "in" (see in- (2)) + oculus "bud," originally "eye" (see eye (n.)).

The OED confirms 'eye' as a synonym of 'bud,' but I doubt that 'potato buds' generated this meaning because it already existed in Classical Latin that (I am assuming) South Americans did not speak in the 1500s when they introduced potatoes to the Spaniards.

Maybe its cause the buds can "open" into a larger structure, like an eye lid can "open" in general. That's just a random guess though

Also, my answer is just one perspective. There can be many more reasons :D

You might get a better answer on linguistic.SE.

if he's looking from a linguistic perspective, then you might get a better answer like Remi said in linguistic stack exchange

I think this question was wrongfully closed. True, this term likely has some esoteric beginnings, but if the etymology of the word-form can be traced, than perhaps so could the origin of that usage.

@theforestecologist - can you?

@AliceD who knows? But I think because none of us immediately know doesn't mean that the answer is not known or that any potential answer is necessarily opinion based.

I'm voting to close this question as off-topic because it is a question about etymology not biology.

Early usage of "eye" in a bud context can be found here in Volume 1 (1733) of Practical Husbandman and Planter ,or, Observations on the Ancient and Modern Husbandry, Planting, Gardening, &c. Page 117 of Number II regarding licorice and p80 in Number III regarding potatoes.

etymonline suggests usage for potatoes originated 60 years earlier. "Of potatoes from 1670s"

Merriam-Webster suggests that a secondary definition for "eye" is something having an appearance suggestive of an eye: such as... an undeveloped bud (as on a potato) providing some support for the appearance theory

etymonline provides the following for the word inoculate: inoculate (v.) mid-15c., "implant a bud into a plant," from Latin inoculatus, past participle of inoculare "graft in, implant a bud or eye of one plant into another," from in- "in" (from PIE root *en "in") + oculus "bud," originally "eye" (from PIE root *okw- "to see").

Just take a look at a potato and observe each of its eyes. You will see that each of them has two parts:
1) An "eyebrow" : this is a vestigial leaf
2) A small bud in the axil of that leaf
Thus, the two of them together form an eye + eyebrow
The eyes are not evenly distributed in a potato plant. One side may have just one or two but the other side will have lots of them. This is because that is the growing spot!
Examples:

Please provide some support/reference for this answer if possible. Right now it comes across as your own opinion.