text:
What neuro-motor diseases cause the lower esophageal sphincter (LES) to malfunction?
Please note: This question is neither homework nor seeking medical advice. I'm simply asking for a factual, objective, biological explanation of the various neuro-motor diseases/illnesses that can act as the underlying cause to LES malfunction.

The primary function of the lower esophageal sphincter (LES) is to prevent stomach acid from backwashing into the esophagus. This sphincter is an involuntary muscle, and so, for it to malfunction (unable to fully or properly close), it must be the result of an underlying neuro-motor (autonomic) disease or condition.
What such condition attacks this sphincter/valve, thereby causing it to malfunction and not operate properly? How exactly does this condition effect the sphincter biologically/neurologically?

Update
Looks like the Vagus Nerve (10th Cranial) innervates this sphincter, so I guess the question is: What neuro-motor diseases attack the Vagus Nerve or cause it to malfunction?

Try looking up acid reflux disorders. My aunt has this as well as Multiple Sclerosis and it causes this muscle to spasm, she has to drink water slowly in small sips to calm it down.

This is called achalasia. According to UpToDate, the mechanism for this diseases are generally unknown. What is known, however, is that the esophagus has a neural system called the myenteric plexus and if these ganglion cells in the esophagus are damaged in any way (e.g. physically, followed by Wallerian degeneration, or the primary process of degeneration after physical damaging of neurons), it can lead to lower esophageal dysfunction as these neurons regulate the inhibition of the contraction of this sphincter muscle. Dysinhibition leads to a closed sphincter.
Yes, you are right in that the vagus nerve is the primary route of the myenteric plexus to the central nervous system, so damage here might result in dysfunction as well.
Histological studies have reported fewer myenteric neurons in people with achalasia, and inflammatory cells in the region, perhaps suggesting infection or autoimmune etiology 1.
Additionally, from the UpToDate article, Chagas Disease has been associated with this disease. Chagas disease is a parasitic disease caused by the species Tropanosoma Cruzi, and these parasites multiply within cells, causing them to burst.
Check out pathophysiology of achalasia on websites such as UpToDate.
1 "Histopathologic features in esophagomyotomy specimens from patients with achalasia." Goldblum JR, Rice TW, Richter JE. Gastroenterology. 1996;111(3):648.
EDIT:
I answered the opposite, but the principles still apply. Here is a wonderful resource on this topic ("Physiology of esophageal motility," http://www.nature.com/gimo/contents/pt1/full/gimo3.html. It includes a diagram showing the vagal neural pathway and the main neurotransmitters responsible for each action (relaxation and contraction).

Thanks @Biomed_guy (+1) - however it appears that achalasia occurs when the LES closes and cannot reopen. I am interested about the opposite: what would cause the LES to remain largely open and unable to close?

Sorry about that. However, we are close. Just as there are inhibitory neurons on the LES, there are also excitatory neurons with a different set of neurotransmitters.

Thanks again @Biomed_guy (+1) - so let me see if I understand this. You're stating that anytime there is damage to the Vagus Nerve and/or the myoenteric plexus, that LES can malfunction as a result, yes? If so, then to me, it stands to reason that the root problem either lies in this plexus, anywhere along the Vagus nerve, or the place in the brain that the Vagus nerve feeds into (which, correct me if I'm wrong here, but I believe is the medulla oblongata). Can you confirm that the root of the problem has to lie in one of these areas (or any others you can think of)? Thanks again!

I believe I am qualified to guide but not necessarily completely confirm. Indeed, the medulla and vagus has been implicated for LES dysfunction (http://www.ncbi.nlm.nih.gov/m/pubmed/12061915/) Keep in mind that diseases like GERD may not always be caused by neurological dysfunction. But if you're thinking neurological, than this is a valid thought.

Thanks for the update @Biomed_guy (+1) - last followup (I promise): you are correct in thinking that I am assuming a neurological cause for GERD. I am very interested in your statement that "GERD may not always be caused by neurological dysfunction." Can you elborate on this and perhaps give some examples? To me, it has to be neurological in nature, because the LES is an involuntary muscle. If you know of non-neurological root causes for LES, please fire away! By "root" causes, I don't mean "obesity", because that's just a vague blanket phrase that doesn' explain the physiology...

I'm sure "obesity" does cause GERD, but then the obvious followup is why? Again, I'm looking for root causes of GERD here, all of which I suspect are ultimately neurological. Thanks again!

Acid erosion of the sphincter. Physical rupture. Anatomical dysruption of of the junction. Just read that the diaphragm contributes to the LES pressure. A hiatal hernia can also result in the forcing open of the LES.  I don't think nyone knows for sure why obesity is associated, but there is a suggestion that these people have higher intragastric pressure which would force open the sphincter, as well as higher incidence of hiatal hernia.


text:
How do non-dimorphic birds distinguish sex of possible partners/rivals?
Some birds, such as my pet Pionus chalcopterus, are not sexually dimorphic.  People can't tell them apart, and even trained avian vets are not 100% certain with an inspection probing the vent.
I understand that when not "in season" there is no physical difference as internal sex organs are atrophied to save weight.
But how do they tell the difference?
Do they have dimorphic markings that bird eyes (but not humans eyes) can see?

Since we're not birds there's no way of knowing for sure, but I would imagine calls/songs and possibly pheromones have something to do with it. There may also be anatomical differences as well that humans haven't discovered yet.

Behavioral differences are likely a part of it, at least for some species.

As very well explained also in Wikipedia https://en.wikipedia.org/wiki/Sexual_selection_in_birds , visual signaling is only one of the way birds uses to pick a partner, olfactory and acoustic signals also play a major role.

Thanks for the link. I would still like to know about Pionus specifically though.

I can't find anything about Pionus specifically, but I don't see why it should be different.

source: Stack Exchange

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

sort: votes


text:
How do plants get carbon?
How do plants get carbon? From air or soil? How is it different for aquatic plants and algae?
According to https://en.wikipedia.org/wiki/Soil_organic_matter soil has 3.3 times the size of the atmospheric pool of carbon.

SHORT ANSWER
From the air
LONG ANSWER
Trees are autotrophs, which means that they create their own compounds from inorganic carbon. So, carbon comes from inorganic carbon. This carbon comes from $CO_2$ (carbon dioxide) that is present in the air. The process by which this carbon is transformed into organic matter is called photosynthesis. More specifically, the carbon get fixed through a chain of reaction called the Calvin cycle that are part of the photosynthetic process.
The great cycle of life
You'll note that while plants (and some other things) uses $CO_2$ to build their mass, animals (and some other things) exhale $CO_2$ when they breathe. In other words, respiration frees up carbon dioxide while photosynthesis fixes carbon dioxide into organic matter.
Then you may want to ask where does the carbon we exhale come from. From our food. If you eat a beef burger for example, you'll the carbon that was present in the cow. The beef got its carbon from the grass that she grazed on. The grass got its carbon from the air and there is carbon in the air because animals (and some other things) exhale carbon when we breathe. respiration and photosynthesis are two essential series of chemical reactions that explain the existence of this cycle.

The (very simplified) chemical equation for those two processes are

Introductory sources of information
Here is a video by Veritasium that answers your specific question
Here are a series of videos of Khan Academy to increase your knowledge about photosynthesis

Also found brief overview in https://en.wikipedia.org/wiki/Plant_nutrition

You're welcome. Yes, you are right, $C_6H_{12}O_6$ is the glucose.

Aquatic plants including algae acquire carbon from dissolved bicarbonates (HCO3-) [1,2].

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


text:
How do we call a region of low carrying capacity?
I am looking for a convenient word to define a region of the landscape where the  local carrying capacity (population size) for a given species is low but different from zero. The species is still present in this zone.
How would you call such area?

I hesitated to ask my question here or on ELL.SE. I asked my question here as I am hoping that there is a term in used in the literature.

If you ask about quantity/numbers only, I would suggest using "the zone of low population density" or "intermittent zone" which in turn borders the "buffer zone" and "the zone of intermediate/high population density".
The "buffer zone" is the zone between two different populations where the number of the animals in question is zero.
J.Potts, M.Lewis "How do animal territories form and change? Lessons from 20 years of mechanistic modelling"
There are other classifications based on the "main usage" of the territories.

Thank you for your answer. Reading your answer I reazized my question was unclear. I meant a zone of low carrying capacity surrounded by zones of high carrying capacity. I edited my post. Your answer seemed very correct as one possible interpretation of my previously answered question. Sorry, my mistake.

@Remi.b IMHO, you should roll back to your original formulation and use ADD word (or UPD) before a new part of the question. I answered the original question, now you ask another question (which is obscure as well), so the answer looks not relevant...

I rolled back to my previously unclear question. I'll open a new post (or just ask my colleagues) for the question I really wanted to ask. Thank you. +1 Btw, what does "ADD" and "UPD" mean?


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Size of the glycan chain in a glycosylated protein
I would like to know where I can find the (experimental/estimated) distribution of glycan sizes attached to proteins.

Uniprot includes glycosylation info if known...

@MattDMo I was expecting something more "digested". Anyway, thank you I will check uniprot.


text:
genes map to eQTL/pQTL

Of the 192 target genes, 79 map to a significant eQTL or pQTL in at
  least one dietary condition.

is the line for a paper "Multilayered Genetic and Omics Dissection of Mitochondrial Activity in a Mouse Reference Population"
As far as I know an eQTL is a SNP (particular genotype) affects gene expression. How can I map then a gene to an eQTL? A gene is a sequence on a reference genome. Genotypes of one specific gene are just variations of the sequence of this specific gene. So, a gene itself cannot be an eQTL, a specific genotype (with a variation) can be, right?
So, how can it be possible that one gene (let say GENE22, location: 10-100) is mapped to eQTL(SNP within GENE22, location: 12) in one dietary condition but is not mapped to eQTL in another dietary condition if we are still speaking about the same gene and the same location of an eQTL? So, I am not quite sure what they mean or what they mapped there.

The QTL is a locus in which the genes/markers have been correlated with some phenotype. It may include markers such as SNPs but they are not SNPs in themselves. A gene can be part of a QTL, but the QTL itself is made up of  a number of markers!

"but they are not SNPs in themselves." There are studies that have lists of eQTLs as SNPs. "A gene can be part of a QTL but the QTL itself is made up of a number of makers". So, you want to say, that they had a list of eQTLs and pQTLs and they just looked in which genes they are located, right? It does not make sense for me because they are referring to dietary conditions and if the looked only at the location then there should not be differences in the conditions because location is always the same.

You take a list of SNPs and a list of gene expression values and you plug it into something like this: http://www.bios.unc.edu/research/genomic_software/Matrix_eQTL/

So, how can it be possible that one gene (let say GENE22, location: 10-100) is mapped to eQTL(SNP within GENE22, location: 12) in one dietary condition but is not mapped to eQTL in another dietary condition if we are still speaking about the same gene and the same location of an eQTL? So, I am not quite sure what they mean or what they mapped there.

The SNP is associated with expression level changes in that gene for one dietary condition but that same SNP is not associated with expression level changes in another dietary condition. Its possible that the SNP never appears in samples from the other dietary condition.

I edited my question.

so, the right way would be to say: "markers within 79 genes map to a significant ...." , right?

I'm not sure the phrasing for which is significant, my guess would be something like: "we find X significant eQTLs when testing Y genes and Z snps"


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Can sexual selection operate in temperature dependent sex determining organisms?
Or more broadly, are distinct forms of genetic inheritance (ie. sex chromosomes) needed for sexual selection?
My thinking was that since there are no sex determining loci, there could not be linkage to mutations that are subject to sexual selection.
Given the large sexual dimorphism in crocodiles (wikipedia), I would expect sexual selection is acting in crocodiles, but how are those phenotypes heritable if there are no sex chromosomes?
I know the sexual dimorphism could be due to differences in gene expression, but that still leaves me with a chick-egg problem. What causes the differences in expression?
I'd like to know if there are any studies that have looked at this kind of question.

Sexes are required for sexual selection, not sex chromosomes

Can sexual selection operate in temperature dependent sex determining organisms?

Yes! Crocodiles are indeed a good example as the sex in determined by the temperature (ref) and they have some traits evolving through sexual selection (ref).
I think you went almost all the way to the answer in your thoughts. Let's categorize things a little bit and talk about Genetic Sex Determination (GSD) and Environment Sex Determination (ESD) separately; that might help.
Note that ESD and GSD are two extremes of a continuum present in nature. Note also that I will talk about sexual dimorphism only and not specifically about sexual selection. Of course sexual selection is one process that can yield to sexual dimorphism. You can replace "locus involved in sexual dimorphism" by "locus involved in selection selection" in what follows and that will work as well expect that we will lose some generality.
Genetic Sex Determination (GSD)
Physical linkage
Indeed if you have sexual chromosomes, then you can have loci sitting on those sexual chromosomes that are affecting only one sex and therefore have genders with different appearances.
Gene expression
As you noted as well, those genes causing sexual dimorphism can also be sitting at different position in the genome and be regulated (directly or not) by the sex determining locus.
Environment Sex Determination (ESD)
If there is no genetic variance for sex but the whole variance is exclusively environmental (ESD), then phenotypic differences between males and females are just determine by whatever environmental variable (temperature for example) is used. In other words, you can have loci being under antagonist selection pressure between the two sexes that is regulated (more or less directly) by the temperature.
In short, you can have sexual dimorphism in ESD just like in GSD that...

the causal agent of the sexual dimorphism is not the sex determining locus but some environmental variable.
sexual dimorphism cannot occur through physical linkage (as there is no genetic variance to determine the sex) but only through regulation of expression.

I recommend this book (although a little expensive).
Do males of all sexual species have Y chromosomes is a somewhat related post but might be too introductory for you.
Here is a nice figure from Bachtrog et al. 2014 that offers an idea of the diversity of sex determination system (thanks @rg22)

See the tree of sex (mark Kirkpatrick,  Judith mank, Doris Bachtrog and many more) for a good figure on the diversity of sex determination systems

http://bbrowse.biol.berkeley.edu/treeV2/files/slide1.jpg


text:
What is pQTL and why do we need eQTL?
eQTLs are genomic loci that contribute to variation in expression levels of mRNAs (wikipedia).
There is data out there that shows that ~60% of the time, the amount of mRNA in a cell is directly proportional to the level of protein coded by that mRNA.[1]
It means that even if the abundance of mRNA is high, we cannot be sure that the abundance of protein is high as well. Why do we still need eQTL if we cannot derive abundance of protein from mRNA transcripts? In the end, the abundance of protein influences the disease rather than the abundance of a transcript.
Does a pQTL implement the idea of a relationship between a genetic variance and the abundance of a protein? I do not understand how a genetic variance can influence the protein level. I assume it is related with a post-transcriptional modification but how?

There is regulation at the protein level ie post-translational modification, autophagy, protein stability etc. Simply knowing total amount of protein does not tell you everything. Knowing eQTL helps to sort out how much of variation in protein amount may be due to the transcription pathway

Genetic variation can affect the levels of protein; consider a variant that reduces the amount of mRNA transcribed, this could have a profound effect on the amount of mRNA available to translate into a protein.
Consider another variant that does not affect the abundance of the mRNA transcribed, but alters one of the many important sequences that are required for translation (co-factor binding sites, ribosomal binding sites, start site, etc.).
These are just a couple of examples that first came to mind, but there are many more. For instance, a variant may increase expression of a particular microRNA that in turn inhibits the translation of another mRNA molecule. I have not included any references as this is more a logical exercise - doubtless there are many more ways a genetic variant can affect protein abundance.

Considering your first two examples and the citation from researchgate about that 60% of the time,  the amount of mRNA is directly proportional to the level of protein coded by that mRNA, I still do not understand why eQTLs are so important in those two cases as we cannot derive the amount of the protein from the amount of the transcript.

The amounts of protein and mRNA are correlated, if not directly proportional. I understand what you are saying, that changes in the amount of mRNA do not necessarily equate to a change in protein abundance, but it seems quite logical to me that if a SNP either changes the mRNA sequence, or changes the abundance of the mRNA, the SNP could affect the amount of protein - this will differ in every case of course, and pQTLs that have been documented presumably do alter the final protein (either in form or abundance), otherwise they would not be reported as pQTLs.


text:
Marker validation using transcriptome and genomic sequences derived from a single cell
I conducted a SSR marker analysis using bioinformatic tool on some RNA-seq data of human tissues. Now, my supervisor believed that we have to validate these SSR on a transcriptomic and genomic sequences derived from single cell.
My question is: why I should do validation on sequences from single cell? Thanks for sharing your idea and experience here.

SSR=simple sequence repeats ?

I think your supervisor wants to see if there is inter-cellular variation in the repeat length and if so, calculate the variation. This may be compared with inter-tissue or inter-individual variation.
Usually when you take a pool of cells for any assay, you would average out the properties of individual cells.
Using sequencing you may actually be able to find the variability in the repeat length if your reads are long enough. According to wikipedia, the SSRs are 2-5bp long motifs that are repeated 5-50 times. So the max length would be 250bp, sequencing which, is an easy task. So you would be able to know the fraction of the SSRs with a certain length from a pooled sample and obtain a length distribution. This is quite easy if you know the locus of the repeats and use specific primers for sequencing.
However, if you do not know the exact locus of your SSRs and you are doing random RNA/DNA fragmentation and total RNA/DNAseq, then you may not be able to do that so easily.
In any case I think that it is easier to determine the locus and do targeted sequencing in pooled sample, than doing single-cell RNAseq (At least if the objective is to obtain repeat length distribution).


text:
What is the antagonist of epinephrine?
Norepinephrine and epinephrine have similar stimulant properties on the nervous system and the body. I was wondering which hormone is the antagonist of epinephrine?

You should understand that it is not the neurotransmitter that is responsible for an effect; it is the neural network that causes an effect and the neurotransmitter is just a mediator.
In CNS, glutamate is generally used in excitatory synapses whereas GABA is chiefly used in inhibitory synapses. Similarly, in peripheral nervous system epinephrine and acetylcholine are used in excitatory synapses whereas glycine is used in inhibitory synapses. Some neurotransmitters always cause excitation in the post-synaptic cell (for example glutamate), however, they can also cause activation of inhibitory neurons and thereby cause inactivation, indirectly. Also, the post-synaptic effect depends on the type of receptor expressed by the post synaptic cell and not the neurotransmitter per-se. For example, α-adrenergic receptors cause smooth muscle contraction whereas the β2- receptors cause smooth muscle relaxation [1]. Similarly, there are both inhibitory and excitatory dopamine receptors [2].
The two divisions of the autonomic nervous system — the sympathetic and parasympathetic systems act in a complementary manner. The former uses epinephrine and norepinephrine whereas the latter uses acetylcholine.

You hit the nail on the head +1


text:
Can dietary monosodium glutamate intake induce restlestness?
The question is all in the title.
More context:
I like phở soup. I have noticed that I get restless after eating the phở soup at some restaurants. The effects are similar to the ones resulting from caffeine intake. (Ingesting a cup of Turkish coffee or a couple of espressos results in my hands shaking badly.)
The phở soups which I think trigger the reaction appear to be the most savory ones. Given that:

Monosodium glutamate (MSG) is a common ingredient in phở
MSG has flavor enhancing properties
Glutamate is a neurotransmitter

I thought there was possibly a connection. (Or perhaps not. Or perhaps it's the intake of MSG together with the consumption of an herb containing caffeine or another psychoactive drug. Phở contains herbs in large quantities.)
I found this paper which states the effects of caffeine result from an increase of glutamic acid (GA) in the posterior hypothalamus which in turns triggers wakefulness.
Thus I guess what I am asking is: does dietary intake of MSG increase blood serum levels of GA and does an increase of GA blood serum level result in an increase of GA in the brain (or in some parts of the brain)?

+1, the question of dietary glutamate consumption has been occupying my mind for a long time :) Below the result of quite some thought on the matter.

This question made me hungry.

The answer is absolutely. It definitely has the potential for restlessness, and even far worse effects. BIg Food does not want people to know this and the dangers associated with high levels of free glutamates because it is found in nearly every food in the form of "natural flavors" and many other forms including actual monosodium glutamate. The neurotoxic and neuroexcitatory effects of free glutamates is not only well-known, it is exploited by Big Food which puts it into all our food because it tricks our brains into making bland food taste better.

There is no strong evidence for MSG having any kind of neurotoxic/neuromodulatory effect.
However, A 2010 article says that, in a double blind trial, it was found that the people who consumed MSG containing soda, reported headache in significantly more numbers compared to the placebo subjects [1]. The concentration of MSG used in this study was 75-150 mg/kg. Assuming that one serving of soda would be 300ml i.e 300g, the amount of MSG consumed would be maximally 45mg, which is much less than glutamate concentration in some natural food stuffs such as tomatoes (~2000mg/kg [2,3]; a tomato that weighs 6oz/~170g contains ~340mg of glutamate). Therefore, I would doubt the findings of this article. The results could have possibly been observed because of some hidden dependent variable (such as the soda formulation).
In general, the USFDA considers MSG as GRAS (generally regarded as safe) [4].
Finally, a 2014 article concludes that dietary MSG would not lead to increase in either blood or brain levels of glutamate [5].
From the Abstract:

The sodium salt of glutamate (monosodium glutamate; MSG) imparts a
  savory/meaty taste to foods, and has been used as a flavoring agent
  for millennia. Past research on MSG/glutamate has evaluated its
  physiologic, metabolic and behavioral actions, and its safety.
  Ingested MSG has been found to be safe, and to produce no remarkable
  effects, except on taste. However, some recent epidemiologic and
  animal studies have associated MSG use with obesity and aberrations in
  fat metabolism. Reported effects are usually attributed to direct
  actions of ingested MSG in brain. As these observations conflict with
  past MSG research findings, a symposium was convened at the 13th
  International Congress on Amino Acids, Peptides and Proteins to
  discuss them. The principal conclusions were: (1) the proposed link
  between MSG intake and weight gain is likely explained by co-varying
  environmental factors (e.g., diet, physical activity) linked to the
  "nutrition transition" in developing Asian countries. (2) Controlled
  intervention studies adding MSG to the diet of animals and humans show
  no effect on body weight. (3) Hypotheses positing dietary MSG effects
  on body weight involve results from rodent MSG injection studies that
  link MSG to actions in brain not applicable to MSG ingestion studies.
  The fundamental reason is that glutamate is metabolically
  compartmentalized in the body, and generally does not passively cross
  biologic membranes. Hence, almost no ingested glutamate/MSG passes
  from gut into blood, and essentially none transits placenta from
  maternal to fetal circulation, or crosses the blood-brain barrier.
  Dietary MSG, therefore, does not gain access to brain. Overall, it
  appears that normal dietary MSG use is unlikely to influence energy
  intake, body weight or fat metabolism.

Totally false. MSG is proven to have a strong neurotoxic and neuroexitatory effect. One of many: Regarding the mode of cell death, glutamate-induced neuronal cell death has been judged originally as necrotic from the morphological appearance. https://www.ncbi.nlm.nih.gov/books/NBK6108/ This is a well-known scientific fact.

@biology there is a difference between consuming glutamate as food and adding glutamate directly to neurons. Read my answer carefully before saying that it's totally false.

Short answer
Glutamate cannot enter the brain due to the blood-brain-barrier.
Background
You are totally right that glutamate represents the principal excitatory neurotransmitter in the brain (Meldrum, 2000). However, glutamate is a regular amino acid and will be metabolized quickly. More importantly, the blood-brain barrier is extremely effective in keeping polar (hydrophylic) molecules out, and therefore especially ions are not coming through as they are extremely hydrophilic. The blood-brain-barrier is formed by the endothelium lining the blood capillaries in the brain. In the brain, the endothelial cells are coupled through tight-junctions, that effectively keep almost everything out of the brain. The only molecules that can get through are either actively absorbed through specialized channels (glucose transporters for example) or are lipophilic. Glutamate under physiological pH carries two negative charges and a positive charge (Fig. 1), and will hence never make it through the blood-brain-barrier. There are glutamate transporters in the endothelial cells, but these in fact transport glutamate out of the brain, rather than in (Hawkins, 2009).

Fig. 1. Glutamate at physiological pH. Source: WikiWand.
References
- Hawkins, Am J Clin Nutr (2009); 90(3): 867S–4S
- Meldrum, J Nutr (2000) 130(4S Suppl): 1007S-15S

Thanks for adding the molecular explanation. Despite this, there is some scepticism about MSG causing "headaches".

@WYSIWYG - that is likely not through direct entrance, but by some indirect mechanism. Increased glutamate in the brain is potentially excitotoxic and it theoretically cannot enter the brain through the blood stream via dietary intake.

Just a thought: if there are one-way channels for excess glutamate to leave the brain - is it theoretically possible that higher levels of glutamate in the blood outside the barrier could reduce the rate at which glutamate leaves the brain, due to less of a diffusion gradient? So the dietary glutamate never enters the brain, but its presence in blood reduces the rate at which glutamate already in the brain is transported out?

btw. I didn't know about wikiwand. Just installed it in my browser- it's amazing :)

How do you think glutamate gets in the brain? Obviously it enters the brain one way or another. The body doesn't just manufacture glutamate from the air you breathe. It comes in through dietary intake some way or another, indirectly or directly.

@biology - Glu's probably just synthesized de novo, but that wasn't the question


text:
Differing Flow Cytometry Genome Sizes and Sexual Mating Implies Differing Chromosome Counts
Do the fundamental principles of genetics strongly suggest the following is a derived conjecture?
If 2 flowering plant species A and B have widely differing genome size (at a minimum a 50% difference) based on flow cytometry and normal successful sexual mating of A and B is indicated based on the flow cytometry measured genome sizes of the embryo and endosperm of the seeds produced by crossing A and B, then A and B differ in number of chromosomes to a degree indicative of ploidy level differences.
Corn, Cotton, and Rice are three genus where large genome size differences do not mean differences in chromosome counts.
The Vireya in the genus Rhododendron are a group that have large genome size differences between species where multi-generational hybrids between such species appears to be possible at least in some cases. Documentation suggests that all Vireya have the same chromosome counts indicating diploids.

It is not clear to me what you are asking. Clearly there are examples in D. melanogaster, C. elegans, and Z. mays where an autosome contains a relatively large contiguous block that is a tandem duplication. This type of genetic rearrangement would have to increase the length of the autosome. As long as the breakpoint does not inactivate an essential gene, and as long as the increased copy number of the affected genes is not lethal, the heterozygotes and homozygotes would be able to reproduce with the wild type.

I will investigate these 3 examples. I did not realize that autosomes can be widely unequal and normal sexual mating is still possible if the difference in length of the autosomes is due to tandem duplications.


text:
Why are lips covered with specialized skin?
I found out some interesting facts while studying our lips:

They are covered in glabrous skin, while most of the skin surface is hairy;
The outermost layer (stratum corneum) of the skin is far thinner than on any other part of our body;
They lack pigmentation (melanin);
Their pink colour is due to underlying capillaries.
Their only source of moisture is our saliva. They lack sebaceous gland;

What is the reason behind this specialization of our lips?

Why is it not covered with the thicker skin type found elsewhere on the body? The lips are not more sensitive than the fingertips for example (see figures below), i.e., the pressure thresholds are similar (upper graph) and the two-point discrimination thresholds as well (lower graph).

Source: Dreamviews

Source: Institute Balseiro

I edited your question and removed my answer. You're right! Sensitivities are similar on fingertips and lips! That is interesting... I edited your question. +1 Feel free to roll back if you don't like the edits.

No no there is nothing to troll . I respect you mam . Thanks for your support :)

LOL - That was a typo :) I meant "Feel free to roll back" :-)

@Pi5 you need not address people as Sir or Ma'am. One reason is you may not know who is a Sir (male) or Madam (female) just from their profile names. Other reason is that respect can be shown without such salutations as well.

What did I say about cell differentiation? Same reason. Specialization of cells for a specific purpose so they express different genes than skin cells. They are the begin or the alimentary canal. This differentiation occurs very early on in development.


text:
How do roots absorb water instead of presence of waxy - material suberin in the form of casparian strips on the wall of endodermis?
I found that in the endodermis, the tangential and radial walls have deposition of the waxy, and hence water-impermeable, material suberin in the form of casparian strips. The endodermis comes before the vascular bundle so how is water absorbed in roots?

Read this (especially the function part):
https://en.m.wikipedia.org/wiki/Endodermis


text:
Are all pathogens parasites?
If parasites are organisms that feed on other living organisms, then aren't all pathogens parasites?
I've emphasised on 'feed' because I guess the pathogens just eat us (i.e. take nutrients to reproduce and sustain their lives), right?
But then there's another question.
If, pathogens need us (a host) to survive, then why do they eventually kill us? I mean, why did they evolve to become an organism that exploits their food to the extent that even they, themselves die? Isn't it disadvantageous for pathogens to kill their hosts, because they will eventually die?
Or I'm totally wrong, do those pathogen sustain their lives even when host has died?
Or perhaps they don't care if they, as individual organisms die, because they can survive as an species by infecting other.

Welcome to Biology.SE. Parasites usually don't kill their host, parasitoids do. Parasites don't necessarily feed on other living organisms. There are two (or three) definitions of parasitism causing the debates under the current posts. I don't really understand the relationship between the question on the first line (which is a semantic issue) and the question(s) in the last paragraph.

The post "Why do parasites sometimes kill their host?" will probably answer your last paragraph.

Not all pathogens are parasites. Many opportunistic infections can be caused by organisms that are normally commensal or even mutualistic.
For example, this paper describes how multiple bacteria species can be pathogenic as well as mutualistic.

Despite its generally innocuous nature, over the past 20 years S.
epidermidis has emerged as a frequent cause of nosocomial infections.
Several extrinsic factors contribute to the conversion of S.
epidermidis from a member of the resident microflora to an infectious
agent. The bacteria primarily infect compromised patients including
drug abusers, those on immunosuppressive therapy, patients with
acquired immune deficiency syndrome (AIDS), premature neonates and
patients with an indwelling device.
...
Recent studies can be interpreted to suggest that S. epidermidis is a
mutualistic organism, much like the bacteria of the gut. Many strains
of S. epidermidis produce lantibiotics, which are
lanthionine-containing antibacterial peptides, also known as
bacteriocins (Fig. 3). Among the several identified bacteriocins are
epidermin, epilancin K7, epilancin 15X, Pep5 and staphylococcin
1580.37–39 Additional antimicrobial peptides on the surface of the skin have recently been identified as originating from S. epidermidis.
...
The removal of S. epidermidis (i.e. through overuse of topical
antibiotics) may be detrimental to the host for two reasons. Firstly,
removing S. epidermidis eliminates the bacterium’s endogenous
antimicrobial peptides, allowing potentially pathogenic organisms to
colonize the skin more effectively. Secondly, without bacterial
priming of the skin, the host may be less efficient in warding off
infection.

When they are being pathogenic, they are parasitic. Parasitism may not be exhibited all the time. You may say that they exhibit facultative or conditional parasitism. But they cannot be pathogenic and non-parasitic. The only case where that could be true is when the microbe itself dies but also causes harm to the host (like in case of endotoxins).

@WYSIWYG Your statement is absolutely correct. I was intending to show that parasitic (or mutualistic) relationships are not fixed, and can change from time to time.

The question is a matter of definitions.

A parasite is an agent that causes harm to another agent
A pathogen is an agent that causes disease to another agent.
A disease is bad.

Therefore, all pathogens are necessarily parasites. Note that some definitions of parasites, imply that the parasite benefits from the relationship. In which case, then the above sentence (in bold) is true only if all pathogens benefit from being pathogenic.
However, it is important that classifying all living things into one or another category is not feasible. organisms from many species can sometimes be called mutualist, commensal and parasitic (to another agent) depending on the ressources and the life-cycle. For example, "symbiotic" algea are mutualistic when there is light but are parasitic in the absence of light.

As I mentioned in WYSIWYG's answer, from an Immunology perspective, while pathogenic bacteria act parasitically, the classification of an organism being a parasite is limited to Eukaryotic protists or multicellular organisms. The distinction is important as there are much different protocols for treating infections by Eukaryotic organisms than there are for Prokaryotic ones.

The Wikipedia article on parasitic disease goes into more detail. https://en.wikipedia.org/wiki/Parasitic_disease

I wasn't aware of this semantic gap between ecology and immunology. Reading fully the OP's question (I eventually just read the title before :)) I realize that there are a bunch of misconceptions. parasite vs parasitoid, species survival thing, fate of the host, etc... I am too tired to write a complete answer on that now. And I guess there's the issue of the several definitions of parasitism.

Not only active parasitism by pathogens, but any kind of interaction that leads to advantage of one species while causing disadvantage to the other species is considered a parasitic interaction. In this post, Remi has explained why even Batesian mimicry can be considered a parasitic interaction. The only case where a microbe could be pathogenic but non-parasitic is when the microbe itself dies but also causes harm to the host (like in case of endotoxins released after death of the bacterial cell).
Now, as you pointed out, killing the host is like wasting the food but killing of the host is an inevitable consequence of the infection. In fact not all successful pathogens kill their hosts (such as influenza; people die of influenza but it generally has low mortality rate). You can think of this as an optimization problem. The pathogen has to maximize the growth with a constraint on available resources. If the host population size is very large and the pathogen has a decent infectivity, then killing the host would not matter as long as the host population remains more or less stable.
Some pathogenic microbes can even grow for a while inside the corpse. Most of these pathogens are of the opportunistic types. They would thrive on the body of the host better when the immune system has collapsed (which happens at the time of death). These microbes also assist in the decaying of the body.

From an Immunology standpoint parasites are viewed as worms or protists. The discipline of Parasitology focuses on unicellular and multicellular Eukaryotic organisms, where as Prokaryotic organisms are the purview of Bacteriology. While the strict definition of the word would allow for bacteria to be considered parasitic, one could also make the argument that a fetus can also be parasitic, especially if the result of the pregnancy is gestational diabetes or the death of the mother in childbirth.

@AMR from an ecological standpoint, parasitism is any interaction that has a +/- effect. Did you have a look at the linked post?

Yes, however as the question is asked from the perspective of a pathogen, then the definitions of immunology, parasitologist, an bacteriology have more relevance and have a more specific definition of terms.

Fetus, parasitic? I don't know the definition, but my logic says that an organism using another organism of the same species can't be parasitism.. It was a consequence of an effort to continue a particular species, using the organism of same species. It was not effort made by another species, to continue living, by using another one... But this is not the case with microbes. A worm is a parasite because it's multicellular, and a microscopic pathogen is not, because it's unicellular, that doesn't seem reasonable!

@Perceptioner. I wasn't trying to make a case for fetuses being classified as parasites, I was simply pointing out that using the strict definition of a parasite, (see Remi.b's answer) then a fetus could be viewed as a parasite in a woman who develops gestational diabetes during the pregnancy or if the pregnancy results in the death of the pregnant woman.

@AMR the immunological terms, I would say, are a bit obsolete. I am not an ecologist per se but I think that the definition of parasite as mentioned by Remi is the correct one, which is also applicable in any context. Parasitism refers to a relationship and not a class of organisms. Oh yes foetus is parasitic, and I too have once mentioned this elsewhere.

Look at my comments to Remi.b's answer below. Parasitic disease are not considered bacteriological in nature, though bacteria can act parasitically. The definition of parasite and parasitism likely predates the discipline of immunology, so I would hardly say that the immunological term is obsolete. Also as I pointed out, there is an important distinction as bacterial infections have different treatment protocols that those of infections derived from Eukaryotic organisms. Modern antibiotics actually exploit those differences to kill bacteria while leaving the eukaryotic host relatively unharmed

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

While all pathogens act parasitically, a definitional distinction is made between Eukaryotic parasites; protists, worms, and ectoparasites such as lice, and pathogens such as bacteria, viruses, and even eukaryotic fungi.
The Center For Disease Control's resource on Parasites states:

A parasite is an organism that lives on or in a host organism and gets its food from or at the expense of its host. There are three main classes of parasites that can cause disease in humans: protozoa, helminths, and ectoparasites.

The World Health Organization fact sheet on Antimicrobial Resistance refers to parasites separately from Bacteria, Viruses, or Fungi:

Antimicrobial resistance threatens the effective prevention and treatment of an ever-increasing range of infections caused by bacteria, parasites, viruses and fungi.

The American College of Physicians makes the same distinction on its page describing the specialty of Infectious Diseases:

ID specialists have expertise in infections of the sinuses, heart, brain, lungs, urinary tract, bowel, bones and pelvic organs. Their extensive training focuses on all kinds of infections, including those caused by bacteria, viruses, fungi and parasites. Many ID physicians specialize in treating patients with infections due to human immunodeficiency virus (HIV), the cause of AIDS.

Even the Wikipedia page on Parasitic Diseases points out the distinction:

Terminology
Although organisms such as bacteria function as parasites, the usage of the term "parasitic disease" is usually more restricted. The three main types of organisms causing these conditions are protozoa (causing protozoan infection), helminths (helminthiasis), and ectoparasites.(1) Protozoa and helminths are usually endoparasites (usually living inside the body of the host), while ectoparasites usually live on the surface of the host. Occasionally the definition of "parasitic disease" is restricted to diseases due to endoparasites.(2)

In my opinion this is an important distinction to make. The treatment protocol for prokaryotic organisms and eukaryotic organisms are different. Evolutionarily, eukaryotic organisms are far closer to us than prokaryotes, and so strategies such as disrupting the ability of a ribosome to translate proteins, a method that some classes of antibiotics employ, would not only affect the protist or worm, it would more than likely affect our own cells ability to produce proteins. In bacteria, the ribosomal subunit is different enough that it can be targeted by medicines, yet similar enough that we can use them in recombinant DNA technology to reproduce mammalian genes. The closer we get evolutionarily to the pathogen, the more alike their molecular machinery is to our own.
Even our own immune system makes a distinction. Leukocytes such as eosinophils are usually only raised to combat parasitic infections. Organisms that are medically termed as parasites also pose a problem in that they are often larger, protists, or much larger, worms, and our phagocytic cells such as macrophages and neutrophils are unable to phagocytose them as a way of clearing an infection.
From your question, you ask

If parasites are organisms that feed on other living organisms, then aren't all pathogens parasites?
I've emphasised on 'feed' because I guess the pathogens just eat us (i.e. take nutrients to reproduce and sustain their lives), right?

There are a host of organisms that live in and on the human body, that feed and reproduce in us and on us that do not do us any harm, known as commensals, and might even be symbiotic, gut flora. However commensals and even symbionts can do harm if they gain access to areas of the body other than their niche locales.
In fact, immunologists often view commensal organisms as part of the bodies innate immune defenses against pathogens. Because they take up space and use resources that would otherwise be used by pathogenic organisms, then serve to limit the ability of pathogens to reproduce and to gain access to tissue that would be vulnerable to the pathogen.
Commensal organisms can become opportunistically pathogenic if they gain access to sterile environments within the body that have not evolved to live "in harmony" with these organisms. An example of this is peritonitis. We can live our lives perfectly fine when our intestinal bacteria remain within the intestines and the colon, however if those tissue are damaged and perforated, these organisms that posed no risk to our health, and actually probably provide a benefit can lead to serious infection and possible death.
There are also commensal Eukaryotes, such as mites and fungi that either do no harm or are kept in check by a properly functioning immune system.
You also ask:

But then there's another question.
If, pathogens need us (a host) to survive, then why do they eventually kill us? I mean, why did they evolve to become an organism that exploits their food to the extent that even they, themselves die? Isn't it disadvantageous for pathogens to kill their hosts, because they will eventually die?
Or I'm totally wrong, do those pathogen sustain their lives even when host has died?
Or perhaps they don't care if they, as individual organisms die, because they can survive as an species by infecting other.

I think where you might be going wrong here is that you are thinking in terms of sanitary and clean forms of death and burial that is a social construct of human primates. Through much of the evolutionary history of multicellular organisms, when organisms died, they died in place and decomposed. This decomposition allowed the pathogenic organisms a route to go on and spread to other organisms. Other living organism came in contact with the decomposition and the pathogen had a way of spreading.
Also many bacteria and viruses can survive outside of their host for extended periods of time, so they in effect are dormant in the environment until they come in contact with a new host that they have the opportunity to infect. In this case, the most important thing for them is to escape the host until another suitable host comes along that can sustain an infection.
Though there are pathogens that have evolved the ability to circumvent our social norms. The body of a victim of the Ebola virus is highly contagious and can infect those that ritualistically tend to the body for burial. The WHO has developed guidelines to try and respect the cultural customs of burial while also preventing the spread of the disease. You could also think of Cholera. Vibrio cholera reproduces extremely rapidly in the host, and the toxins that it produces cause the host to expel the pathogen at a rate that can kill. This serves cholera as it can then go on to infect a new host.
You also have to remember that there are pathogens that are pathogenic in one organism but commensal in others. The parasite that causes malaria is commensal in mosquitos. The vector for Ebola is thought to be bats, but bats do not succumb to the disease. So for pathogens like this, the strategy would be to find a reservoir vector, then find a host where they can replicate, then escape that host either to reinfect another host or find another carrier where it can survive commensally.

The sites that you have mentioned and the classification that they make is more like a layman classification. It is not in strict sense based on any particular convention. These sites may be of credible institutions but the sites themselves are not standard sources of reference. Plus, I again emphasize, parasitism is an ecological relationship and not a classification of organisms. Phylogenetics is there for the classification.

The audience for ACP is prospective physicians.... It is how Janeway Immunobiology, the textbook recommended by many graduate Immunology and medical schools refer to it. It is how Parasitologists refer to it. It is how Bacteriologists refer to it. You seem to be the only person that I can find that has a problem with it. If I go to a doctor and they diagnose me as having a parasite, they will never be referring to viruses or bacteria... If my dog' vet tells me he has a parasite, I guarantee that 100% they are referring to a protist or worm, not bacteria or a virus, not even fleas or ticks.

Yes because your doctor or vet is supposed to interact with laymen and not give scientific discourses to their patients. The very definition of a parasite as you quoted is general. If parasite means only certain organisms then the definition should say it explicitly. You seem to justify a wrong usage simple because a lot of people do it. You also seem to hold a view that textbooks are infallible.

The majority of professionals that are responsible for the definitions have made that distinction. You have three distinct branches of study, Parasitology, Bacteriology, and Virology. The Immunology professor I had makes that distinction, and she corrected me when I did not use the term renature to describe proteins refolding into their proper conformation after denaturation. The people whose careers, research, and livelihoods are in these fields make the distinction. If I was quoting one obscure source, I could see being doubtful, but you are being like The Black Knight in The Holy Grail.


text:
How do neurons receive the ions needed for creating electrical pulses?
I really wonder how ions are transported into the brain and the neurons for creating electrical potentials - how do ions get from our digestive system to the neurons? Or are the ions just freely released into the brain like hormones? Or are they transmitted during neural signalling somehow (via neurotransmitters maybe)?

There are voltage-gated ion channels in the cell's plasma membrane that controls the release of ions. https://en.wikipedia.org/wiki/Action_potential

I voted to close because the title asks for a cellular/molecular approached answer pitched to neurons, the body text asks for a tissue-level answer. It's unclear what you are after. Feel free to edit. It can be an interesting question.

Short answer
The sodium-potassium pump in the epithelial cells lining the brain capillaries pumps Na+ and K+ into the brain.
Background
The blood-brain-barrier is formed by the endothelial cells lining the capillaries in the brain. Not many compounds can pass this lining, especially not when they are hydrophilic, such as charged metal ions. However, as you rightfully state, somehow these metal ions, and especially Na+ and K+ need to get access to the brain because they are crucial for membrane potentials and action potentials, and hence for neuronal survival and function. And indeed they can, albeit the exchange between blood plasma and brain is slow compared with other tissues.
Intravenously administered K+, for example, exchanges with muscle K+ in 1 hr, but K+ exchange in brain is only half completed in 24 to 36 hr. Na+ exchange is somewhat faster, with half-exchange into brain occurring in 3 to 8 hr. Despite its relatively slow entry into the brain, Na+ exchange across the blood—brain barrier appears to occur by mediated transport. This occurs, in part, through brain capillary Na+,K+-ATPase (the sodium-potassium pump). The Na+,K+-ATPase in the brain also may mediate removal of interstitial fluid K+ from the brain and thereby aid in brain K+ homeostasis.
Reference
- Laterra et al. In: Siegel et al. eds. Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th ed. Philadelphia: Lippincott-Raven; 1999

The cells/neurons themselves have Na+ and K+ channels in their cell membranes that allow for passive movement of these ions between the outside and inside of the cell. If you're wondering how the gradient gets established in the first place, simply put, these channels are built to open/close at the right amounts in their environments. Additionally, the cell uses a Na/K ATP-ase pumps in the cell membrane, which uses the chemical potential energy of ATP, to help regulate and establish that gradient.

So they all are pumped into our brains while we are in the uterus? I meant more like how do the neurons get it (the way of the ions from our digestive system to neurons) than how do they get into the correct place in the neuron.

We absorb ions through our GI tract. Those ions are then in the blood. The blood is separated from the brain by the blood-brain barrier, but the endothelial cells can regulate the flow of the necessary ions into the brain, specifically to the cerebral spinal fluid, which bathes the central nervous system with all its neurons.

@Biomed_guy And how does the ATP pump work?


text:
Is there a way to prevent an HIV infection after exposure to HIV infected Blood?
If a person is accidentally injected with blood from an HIV+ person, is there a treatment option that can keep the person from developing an HIV infection?

Is this a serious question.. ?

I must add that it is not possible to save someone by sucking venom from a bite.

@Macedon93 I don't think this comment will help the OP in any way. The comment might actually feel a little offensive.

I think that the spirit of this question, Is there a way to prevent an HIV infection after exposure to HIV infected bodily fluid, is a valid one that deserves an answer.

@Macedon93 and March Ho's comments refer to the question in its unedited form and are out of context with the edited form of the question. Look at the edits to see the question in its original state.

The standard protocol for treating a healthcare worker that accidentally comes in contact with HIV infected body fluid is to receive HAART treatment.
HAART is an acronym that stands for Highly Active AntiRetroviral Therapy, and is a multi-drug cocktail that acts on a number of pathways to block the HIV virus from replicating.

There are early inhibitors which seek to block the binding of gp120 to CD4/CCR5.
There are Nucleoside analogs that are able to block the activity of Reverse Transcriptase.
There are Reverse Transcriptase inhibitors that can bind to allosteric sites on the enzyme, thereby effecting its ability to catalyze the reaction which produces the viral cDNA.
There are protease inhibitors which inhibit the viruses ability to make the necessary post-translational modifications, thereby causing the viral proteins to be non-functional, as they are produced from a single, long mRNA transcript.

UPDATED
This is the link to the CDC guidelines from prophylactic treatment for occupational exposure to HIV. http://www.cdc.gov/mmwr/PDF/rr/rr5409.pdf with an update to the guidelines here http://stacks.cdc.gov/view/cdc/20711
After confirmed exposure to HIV infected bodily fluid, it is recommended that HAART begin as soon as possible after exposure, that toxicity be monitored, and that the treatment be continued for 4 weeks.
The recommendations weigh the toxicity of HAART with the HIV status of the person. Even in cases where the status is not known, but the risk factors of the source are low, HAART is often not recommended.
Note that post-infection prophylaxis is less effective than preventing exposure in the first place. That is why barrier protection during intercourse (in the general case), proper handling of sharps, screening of the blood supply, and barrier protection to mucous membrane for healthcare workers is vitally important in preventing an HIV infection from taking hold.
These are the CDC guidelines for Prophylactic treatment from non-occupational exposure. http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5402a1.htm
UPDATE
In the original, unedited question by the OP, they asked

Yes It is possible to save a person when snake bites him, by sucking the poison from the bite region. so sucking AIDS Virus like snake's poison, will he get cured?

I do not know the answer to this question, nor do I think that there would be any published information regarding the efficacy of trying to suck out HIV infected blood, but given the nature of the virus and how a subcutaneous injection works, I think it is safe to say that it is highly doubtful that attempting to prevent the infection in this way would be an effective treatment option.
Also note, as March Ho stated in the comments, attempting to suck the venom of a snake bite from a wound is an ineffective method of treatment as well.

This seems an excellent answer to the question after you edited it! You might want to make sure to address the OP's point of whether one could get HIV viruses out by sucking the blood. +1 in the meantime

@Remi.b Better? I actually think that this is an important question to have on the SE, not necessarily in its original form, but in the spirit of the question; can something be done in the event of accidental exposure to HIV. I actually wonder if HAART is offered prophylactically to victims of sexual assault and rape. I was familiar with the protocol for healthcare workers and accidental exposure, but don't know what the standards are to victims of a crime.

Yep, perfect! Thnks

AMR's answer is excellent and deserves praise.  I only want to add that, scientifically (NOT therapeutically) there may be other ways to prevent infection.  A Nature letter from 2012 examined the role migratory T-cells play in HIV infection. They used a drug, FTY720, also known as fingolimod, which essentially kept lymphocytes from moving out of lymph nodes.  In a humanized mouse model, use of the drug limited infection, providing evidence that infection could be potentially halted if caught quickly enough before disseminating systemically.

Thank you Amory, I appreciate your evaluation and insight. The Nature article is interesting. Then again the mechanisms that HIV uses to infect us are pretty astounding as well; even to pulling down CD4 receptors off of infected cells so they will not interfere with gp120 in the viral envelope as they bud off. I think that I will follow the motto of an ounce of prevention is worth a pound of cure.


text:
What were the symptoms of Phineas Gage after suffering his brain injury?
Phineas Gage was a construction worker who suffered a head injury due to an explosion at a construction site. A metal rod was pushed up his cheek and through his head.
I have heard he demonstrated six symptoms after the accident. What were they?
I have researched this for a while but all I can find is that he was very inappropriate in social situations.

He wasn't just inappropriate , he had a complete personality change. Only his frontal lobe was damaged, similar to a lobotomy. It was the section that allows you to be rational and make clear decisions, the part that has our conscious, so I was told. We studied it a bit in Psycology 101. I don't believe he had any physical ailments from this, but I could be wrong.

I don't see  any question here. You are asking for the case study reference. I am afraid questions on such a kind of reference request is off-topic. Moreover, the question itself is not about any biological mechanism but is just about "listing" the observations. An example of an on-topic question on this area would be: "Why does injury in the X-lobe of the brain result in symptom-Y ?" This may be suitable for [hsm.se]. Also have a look at this.

Gage suffered a massive injury to the frontal cortex due to his accident in 1848 (Fig.1). Recent work using computer assisted tomography (CAT) has shown that contrary to popular belief, the injury was probably not bilateral, but confined to the left-lateral frontal lobe (Ratiu et al, 2004).

Fig.1. Original drawing of the wound sustained by Gage (left). Source: Harlow (1869) and the reconstructed injury using modern CAT scanning techniques on the original tamper and Gage's skull (right). Source: Ratiu et al., (2004).
The question of OP is not very particulate about the nature of symptoms (physical or psychological symptoms), or about the time window of interest after the accident (acute or chronic symptoms). I assume that OP is asking about the behavioral changes of the subject after he was physically fully recovered. The following is a formatted quote from the original publication written by his treating physician (Harlow, 1869) describing the subject's behavior approximately 6 months after the incident:

His physical health is good [...], but says [he] has a queer feeling [in the head] which he is not able to describe. [...] His contractors, who regarded
  him as the most efficient and capable foreman in their employ previous
  to his injury, considered the change in his mind so marked that they
  could not give him his place again. The [...] balance [...] between his intellectual faculties and animal propensities, seems to have been destroyed. He is fitful, irreverent, indulging at times in the grossest profanity (which was not previously his custom), manifesting but little deference for his fellows, impatient of restraint or advice when it conflicts with his desires, at times pertinaciously obstinate, yet capricious and vacillating, devising many plans of future operation, which are no sooner arranged than they are abandoned in turn for others appearing more feasible. A child in his intellectual capacity and manifestations, he has the animal passions of a strong man. Previous to his injury, though untrained in the schools, he possessed a well-balanced mind, and was looked upon by those who knew him as a shrewd, smart business man, very energetic and persistent in executing all his plans of operation. In this regard his mind was radically changed, so decidedly that his friends and
  acquaintances said he was "no longer Gage."

The symptoms of Gage indeed match the current understanding of the functions of the frontal lobes. The frontal lobes are thought to be involved in a multitude of cognitive processes, such as executive function, attention, memory, and language, affect, mood, personality, self-awareness, as well as social and moral reasoning (Chayer & Freedman, 2001).
References
- Chayer & Freedman, Curr Neurol Neurosci Reports (2001); 1(6): 547-52
- Harlow, Bulletin of the Massachusetts Medical Society (1869) and see wiki page
- Ratiu et al., J Neurotrauma (2004); 21(5): 637-43

"…it was proven to have been confined to the left-lateral frontal lobe" sounds like the injury occurred on the lateral side of the left frontal lobe. Did it? Because the tamper looks like it's going right through the middle of the lobe.

@canadianer - they reconstructed the injury using the original tamper and Gage's skull using CAT scans. Sounded convincing to me.

@user117852 - my pleasure, thanks for the interesting question. It took me a while because it needed some detective work :)

Phineas Gage actually recovered from his personality change.
A recent study was just published suggesting that most of what we thought we knew about Gage is incorrect, and he recovered from this extreme personality change. An emeritus professor, Richard Griggs, analysed over 23 books on Gage and came to the conclusion that he made a miraculous recovery, which people rarely discuss in textbooks. Griggs states that Gage ended up immigrating to Chile where he "worked as a horse-coach driver, controlling six horses at once and dealing politely with non-English speaking passengers." The importance of understanding and acknowledging this recovery is an important step towards understanding the plasticity of the brain.
Also, as explained in another answer, recent CAT scans suggest that the injury was confined solely to the left frontal lobe. Therefore some un-updated publications on his personality changes will also be incorrect because they will discuss the effects of bilateral frontal damage rather than left frontal damage.
Griggs, R. (2015). Coverage of the Phineas Gage Story in Introductory Psychology Textbooks: Was Gage No Longer Gage? Teaching of Psychology, 42 (3), 195-202 DOI: 10.1177/0098628315587614

+1 for this answer - It would be really interesting to know how much time had passed since he moved to Chile? My answer deals with 6 to 7 months after the accident. When did his full recovery set in?

I think he moved to Chile around 18 months after the accident. It is really unknown what kind of recovery he made, but he did make some kind of recovery. The problem is that all of this happened in the 19th century and only comments from doctors can be used as evidence for his changes in personality and recovery. There is a really good article on the entire story here: http://www.slate.com/articles/health_and_science/science/2014/05/phineas_gage_neuroscience_case_true_story_of_famous_frontal_lobe_patient.html


text:
Why is chemotherapy-related hair loss temporary?
Chemotherapy kills cancer cells by targeting rapidly growing cells. That is why patients lose hair as well. Why is chemotherapy-related hair loss temporary?
The doctors say it is because healthy cells are able to repair themselves. But, if that is true, then people should not even lose their hair, as the damaged hair cells would repair themselves before patients lost their hair.

Related: https://medicalsciences.stackexchange.com/q/20545/12704

Its less that the cells repair themselves and more that the tissue can repair itself. Rapidly dividing tissues have reservoirs of stem cells waiting to replace the cells that are rapidly lost. For instance, histologically, there are stem cells just waiting at the hair follicles and intestinal lining, waiting to replace the old cells that rapidly die off. But those are killed off during chemo.
Stem cells at the follicles:

Most chemotherapy drugs targets DNA replication in some way, which damages not only cancer cells but normal replicating cells as well. But normal cells are typically more resistant, and stand a better chance of survival. It is thought that this is because normal cells respond to DNA damage by "arresting" the cell cycle, and not dividing until the damage can be repaired. Cancer cells, in contrast, have lost these safety mechanisms, and will continue to divide despite having damaged DNA, which can cause serious problems and lead to cell death. This difference is exploited in chemotherapy.
There are of course large variations between individual cells. Some normal cells will die of chemotherapy, and some cancer cells will survive. But statistically, normal cells stand a better chance, and so chemotherapy dosage can be adjusted to a level where the drug effectively kills most cancer cells, but spares at least some normal cells. (Provided the cancer is sensitive to the particular drug used, of course; in many cases this strategy unfortunately does not work.)
After a course of chemotherapy, many normal proliferating cells will also be damaged, causing problems like hair loss and other unpleasant side effects. But given some time, normal cells will recover and repopulate hair follicles and other tissues.

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


text:
What species is this?
We found this on a beach in the Bay of Lannion, Brittany, France. What is it? About 6 cm long.

It is  the skeleton of Sea Urchin or sea hedgehog.

There are a lot of species (nearly 1000), so it is very difficult to identify just in five minutes, but in general you can start from knowing the Subclass Perischoechinoidea.


text:
Why I don't feel pain when I press the skin on my knee and elbow?
Does the muscle on our knee and elbow have some speciality ? Why are we unable to feel any sort of pain when I pinch it ? I also did it with my Mom and Dad and result was same .

I think the skin is what you are pinching, and its mostly dead skin. I could really find a valid source though. Sorry

There are no muscles (except smooth muscle in the skin) under the skin at the knee or the elbow. You are pinching skin, not muscle.

There is several types of nerves in the body.
Some nerves are specialized in sensing cold or hot temperature, some other to cuts and cell damage and others feel pressure and touch.
The answer to your question is that the nerves in your elbows and knees have less pain detectors and are in fewer number, thus with they are less sensitive.
Here's a funny little poster on BBC: Can you pinch yourself without it hurting?


text:
Whole Genome Sequencing and Chromosome Counts
In general, do standard whole genome sequencing techniques rely more on known chromosome counts, independently arrive at chromosome counts, and/or not directly address issues such as base number, aneuploidy, and polyploidy?
For example would have normal whole genome sequencing techniques detected that humans have 46 rather than 48 chromosomes?
Maybe a better way to put this question would be as follows:
Given the whole genome sequence for humans and a belief that chimpanzee had 46 chromosomes would whole genome sequencing of the chimpanzee most likely say
1) Here are the sequences for those 46 and by the way there was material left over.
2) Here is the best representation of all the chimpanzee's DNA mapped onto 46 chromosomes.
3) Here are the sequences for those 46 and chimpanzee's appear to have 48 chromosomes.

What Biomed_guy says is basically the answer, I just wanted to clarify a bit. When you sequence DNA, you do something during the preparation of your DNA library to turn it into small fragments if it isn't already, like shearing the DNA. This gives you very small pieces of DNA that should still be quite unique when matched to reference genome.
But as previously answered, the determining factor for how DNA is then mapped is the reference genome you are using. So the answer is what you state in both 1 and 2. When trying to figure out what DNA you have, you start with a reference sequence which is all of the genomic DNA 'layed out' so that your fragments can then be compared against it and matched to a best fit region based on matching sequence. Anything that does not match the ref genome gets dumped into a 'junk' output file.
So conceptually, many gene sequences are highly conserved between humans and chimpanzees. This would mean that you could successfully align your sequences fragments to either genome. Importantly, this is number of chromosomes agnostic. It is the genes that matter.
Imagine that if Ras, Myc, and Erk are all on human chr 12 in humans, but split up in chimps so that Ras is on chr 12, Myc on Chr 13, and Erk on Chr 24, this would make no difference when you map back to the genome assuming the genes are conserved between human and chimp. If you have a sequenced fragment from human Myc that is the same as Chimp Myc, it would align to a location on chr 12 if you use human DNA as ref, or it would align to a location on chr 13 if you use Chimp as ref. Make sense?

I'm pretty sure that it relies on a reference genome. As in, since the original human genome sequencing, most of the techniques used today rely on that original construction (with modifications).
That's how people use it to detect copy number variations (CNVs) and single nucleotide polymorphisms (SNPs) with these sequencing techniques (and aneuploidy as well).
The reads from the sequencing run are compared to the reference genome and if statistically significant differences in the number of reads are seen, then they are noted as differences in the genome. If there is extra unmapped DNA, then it would likely just not know where to put it and call it "extra material".
So #1.

You understand, it's not that chimps have lots of extra DNA that humans do not, they have two chromosomes which are fused in humans.
Theoretically, discrepancies between the reads and the reference could be discovered.  Practically, with current short read technology, it would be difficult to sort out a discrepancy that involved a region of the genome that was repetitive, which the telomeres of the chimp 2A and 2B and the telomeric-like sequences in the regions where those fused in humans, would be.


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Whole Genome Sequencing and B Chromosomes
Do whole genome sequencing techniques detect B chromosomes if such chromosomes are present?
My understanding is as follows:
How the DNA material in a B Chromosome is mapped depends on the reference map and not on how the material is packaged into chromosomes for the sample being sequenced.
Is this correct?

You can use differences in coverage (number of reads mapping to certain regions in reference) to infer if there is a B chromosome.

The analysis of NGS reads coverage rate can give information on B chromosome genomic content. Have a look at the article mentioned below:

 Valente GT et al. (2014). Origin and evolution of B chromosomes in the cichlid fish Astatotilapia latifasciata based on integrated genomic analyses. Mol Biol Evol. 2014 Aug;31(8):2061-72

Can you add a little explanation on how coverage can be used to infer B chromosome genomic content. An illustrative figure from the mention reference would also do. We would greatly appreciate some explanation in addition to providing a link to the reference.

The attached figure shows the Illumina reads coverage for two 0B, two 1B and one 2B samples. Note that the figure shows a specific genomic regions with a higher reads coverage for the 1B and 2B samples compared to the 0B ones.

Welcome to Bio. Could you provide sources to your data and answer? References are encouraged here.


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Junk DNA and "random" mutations
I'm somewhat irritated by "mutation" generally being described as a fully random factor in evolution: pure randomness does not seem like something that can survive in a long evolutionary process.
And some basic evolution in some long-lived organisms appears to happen in quite fewer generations than one would consider plausible considering just natural selection over an unbiasedly mutated genetic base.
So I'm wondering whether there have been attempts to view mutation itself as a process influenced by evolution.  For example, couldn't "junk DNA" result in a susceptibility to certain mutations that is determined by environmental factors, like amount and constitution of nutrients, ambient temperatures and others.
The overall discussion of mutagenesis I can find focuses entirely on "damage", again basically assigning all mutations a negative or at least undirected character (like more mutations occuring under stress, with the "aim" being more likely to have more random mutations where one offspring might be more successful than the stressed parent by chance).
In a similar vein, I don't see not much of anything about evolution and competition of gametes: how different environmental factors influence which of an abundance of eggs mature and which of the (asexual) male gamete reproduction mutation in the testes will be favored over time or under environmental conditions.
Basically all of evolution and natural selection seems about how to survive into fertility and select a partner, and that's it as genes are constant apart from random cosmic radiation or toxic substances.
I think that this kind of viewing the message in the DNA as isolated from its medium just does not sound like something that would survive billions of years without something less random replacing the pure randomness.
So are there any major studies trying to figure out whether certain mutations leading to better adapted phenotypes occur in a non-random manner (namely not just affecting mutation rate but also direction) in response to environmental circumstances?

I'm a bit unclear what your question is. Are you asking what the general mutation rate is of genomic DNA, if anybody has looked at this, and if certain base pair changes are more common than others?

Welcome to Biology.SE. There is a mixture of different concepts in your post, most of them seem to be a little unclear to you. I recommend that you take some time to follow some introductory course to evolution. Understanding Evolution for example would be a good fit.

I am voting to close as the question reveals several misconceptions that cannot be fully addressed in a post (although I gave it a short try).

Biology SE is not the place to come and just throw out an opinion like this, if you have a proper biology question then please focus on that. The effect of a mutation is random - a species cannot will itself to produce a mutation with specific effect

I agree with the above. Mutations are random. Selective pressure provides direction.

"pure randomness does not seem like something that can survive in a long evolutionary process." This is the "argument from incredulity". Just because it doesn't seem that way to you doesn't mean it isn't that way.

"that's it as genes are constant apart from random cosmic radiation or toxic substances." That's totally wrong. Genes mutate without external influences like radiation or toxins--in fact they mostly mutate without these, due to occasional replication errors. It's incredible how little the DNA machinery screws up, but it's not perfect, either.

pure randomness does not seem like something that can survive in a long evolutionary process.

I think this is because you don't quite understand (no offense) the interplay between mutations and natural selection. You should have a look at Understanding Evolution.

The overall discussion of mutagenesis I can find focuses entirely on "damage"

This is because the vast majority of mutations are deleterious (=damaging). But obviously, not all mutations are deleterious, otherwise no adaptation would be possible (only purifying selection would occur).

In a similar vein, I don't see not much of anything about evolution and [..]

I don't understand this paragraph.

Basically all of evolution and natural selection seems about how to survive into fertility and select a partner [..]

No! There is much more to evolution than that. Note that the semantic of evolution and natural selection is wrong as they are used in your sentence. Again, check out an introductory course.

I think that this kind of viewing the message in the DNA as isolated from its medium

No! The environment is a fundamental tenet in evolutionary biology. The association between genotypes to fitness is a function of the environment as well.
Are mutations random?
The mutation rate varies dramatically among species and along genomes (roughly speaking from $10^{-2}$ to $10^{-10}$). For example microsatellites (repeated sequences) are highly mutable. Note also that the probability of a given nucleotide to mutate depends also on the exact nucleotides that are around it (Rob Ness; Personal communication). The mutation rate is also a plastic trait (and is therefore under selection) in some species (of plants typically). The environment affect the mutation rate and the environment can be chosen by some species (avoidance) or even constructed in some species (niche construction). In multicellular organisms, the age of the father correlates with the number of new transmitted mutations as well. However I have never heard of any studies showing such behaviours in order to affect the mutation rate. Epigenetic changes (does not concern all species) can also the mutation rate and even into what new nucleotide the old nucleotide will be mutated into (with a given probability). Mutations are more likely to be transitions than transversions. If a specific region is under environment-depend selection, then a mutation that would allow to drastically increase the mutation rate at this nucleotide whenever the organism has a low fitness (or even whenever the trait of the organism is unfit for the specific environment) could reach fixation. This process (and maybe others I am not aware of) are I think encapsulated within a hypothesis called (and it is a horrible name as it can yield to confusion) adaptive mutation hypothesis. But really don't start studying any field of science by jumping into an advanced subject (or even worst, a controversial subject). You should start with an introduction.
However, the impact on fitness (and on phenotype) of a new mutation is essentially random. An organism has absolutely no way to know what protein will be caused by a given new mutation. Selection then select upon the variance created by the mutations, the variance decreases and adaptation occurs. The impact of new mutations seem to follow more or less two weighted gamma distributions (added to which a bump of probability density for lethal mutations).

The studies you cite seem focused on short-lived organisms with a high reproduction rate.  I did explicitly mention longer-lived specimens.  Some correlations like a higher male birth rate for older first parents are well-known and not attributed to destructive mutations.  It's also established that the number of birth defects for old fathers is not explainable by mere random mutation but rather by higher competitiveness in replication of gametes with a certain defect inside of the testicle issue.  But all of that is always focused on defects and not on correlation with desirable features.

I don't actually cite any studies. Not all what I am talking about is specific to short lived vs long lived organisms. I don't fully understand why the short-lved vs long-lived distinction metters for your question but I guess I don't really understand the question.

I think I am also confused about the low level of understanding of evolutionary processes that your post shows and am even more confused now that I see that you actually have some knowledge...but in the same time things like number of birth defects for old fathers is not explainable by mere random mutation but rather by higher competitiveness in replication of gametes with a certain defect inside of the testicle issue really doesn't seem to be related to the question. Also I don't understand the use of the concept of "junk DNA" in your title. I guess I just don't understand the question.

junk DNA is an obvious contender for contributing to tertiary molecule structures and/or hydrogen bonds that make the neighboring non-junk DNA more or less susceptible to certain environmental influences.  Those can be either direct influences of factors like acidity or other ion concentrations, temperature, viscosity, osmotic pressure or more specific organic substances potentially generated by the body itself in response to external stimuli.  When people "turn grey with grief overnight" (no, hardly overnight) does the responsible change in body chemistry also affect gene mutation?

Did you hear about the historical Luria-Delbrück experiment where they demonstrated that in Escherichia coli mutations conferring resistance to antibiotics are essentially random?
Also, discussions and some references on the phenomenon of (directed) adaptive mutagenesis, which I think you are asking about, is mentioned in the Wikipedia article. But I don't know much about the debate.

Most antibiotics are essentially "random" environmental factors since the substances in question don't as a rule occur in massive amounts in nature (penicillin being a notable exception).  Escherichia coli also is not exactly a higher organism with slow reproduction and long life.

As Rémi.b, I don't see why slow reproduction and long-life are relevant for your question. You seem to be surprised about mutations appearing quickly, but a mutation can and does actually appear in one generation because it appears in an offspring. What takes time then is just the "propagation" of the mutation to the population through successive new offsprings, but this has nothing to do with the complexity or life expectancy of the organism.

Also, whether an environmental factor is "random" or predictable is independant from whether the mutations that occur in an organism experiencing those factors would be random or targeted, so I don't see the relevance here either.

slow reproduction and long life are relevant for the question since there is not much of a necessity for adaptive genetic changes bypassing the selection process of phenotypes when phenotype selection already happens fast enough to follow typical environmental changes.


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Role of microvilli in cell volume regulation
Does the presence of microvilli on a cell's surface ensure that it's more resistant to cell swelling or lysis in a hypotonic solution, as compared to a normal cell?

Microvilli, are cellular protrusions on the membrane and hence they increase the total surface area of the cell in context.
If we evaluate the characteristics of microvilli and the structural appearance, we know that; they have many small folds; strengthened and lined by the protein filament actin; bedded in a terminal web of alpha-actinin and keratin. All of these characteristics, work in harmony to support its ability, for it to do its function. That being, to allow greater diffusion whilst controlling the cells integrity. Evidently, the microvilli do help resist the hydrostatic pressure within a cell as a result to the distribution of pressure and the microfilaments present.
Most animal cells have microvilli so, there is a huge excess of factual evidence to support what happens to them in under specific conditions. Knowing this, it confuses me why you even asked this question. It just takes a simple comparison.
I'm presuming, a normal cell is a cuboidal cell, too. So, yes, if they were both placed in a variable hypotonic solutions, with gradual increases in concentrations for comparison, the cuboidal cell would rupture much earlier rather, the cell with the microvilli would be still standing at a further stage (concentration). However, the cell with the microvilli will nearly all of the time still lyse despite it's additions. Microvilli don't sorround the entire cell, if they did, the integrity of the cell in greater hypotonic solutions would be more applaudable vs a plant cell (cell wall containing pectin).
Yes
References:
**
http://www.histology.leeds.ac.uk/cell/cell_cytoskel.php ; 'keratin is a type intermediate filament in cells' [...] 'The nucleation of actin fibers occurs as a response to external stimuli, allowing a cell to alter its shape to suit a particular situation.'
**
http://www.westfield.ma.edu/personalpages/draker/edcom/final/webprojects/sp10/cell/Ross44.jpg; 'A hypotonic solution has decreased solute concentration, and a net movement of water inside the cell, causing swelling or breakage.'
**
http://www.histology.leeds.ac.uk/cell/cell_cytoskel.php ; 'Intermediate filaments are inserted into desmosomes at cell-cell junctions, and help to maintain cell-cell connectivity, as well as the structural integrity of the cell itself.'
P.s. Most of the answer was achieved by the application of knowledge so, direct references cannot be found!

Can you add few references to your answer ?

Yes! I will add some now (it was late).

Most animal cells have reservoirs of membrane, including microvilli (Sheetz et al, Annu. Rev. Biophys. Biomol. Struct. 2006. 35:417–34). This can help preventing lysis in hypotonic conditions, but has other functions as it allows the cell to take varied shapes without being constrained by its membrane area.
This is not volume regulation, by the way, but rather accomodation of volume changes. There is evidence that volume is regulated, but some osmotic challenges can be too great or to sudden for the volume response.

You can add example of insect photoreceptors where increase in surface area of membrane due to microvilli is needed to increase probability of hitting photon on rhodopsins.


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What techniques can be used to link environmental conditions to crop yield?
Im interested in how we can determine what are the optimal conditions for crops and how deviations from these optimal conditions affect yield. In the literature I have found two main approaches and I was interested if there were more ways that are used or if anyone can think of a more creative way to test the link.
Approach One
Use a greenhouse experiment to isolate all variables bar one and vary it. Measure the change in yield based on that variable.
But this approach is time consuming and it is difficult to include interactions.
Approach Two
Use a model that relies on some base knowledge of that plant - i.e. the base temperature at which growth is zero, and a rough idea of optimal ranges. But requires this base knowledge already.
Potential Approach Three
Use multiple linear regression in combination with field data to create a linear or polynomial model of each variables effect on yield. Interactions can be included easily. But relationships are unlikely to be linear and without prior knowledge it is hard to decide on non-linear models.
Can anyone think of other ways that could be used to test these links?


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White blood cell transfusion
Some patient who have low White blood cells need  WBC Transfusion do resist infections.  What is interesting, doesn't transfused WBCs cause temporary autoimmune disease ?   Like recognising patients organs as foreign ?
just like in the organ transplantation.
Regards.

I do not think that the white blood cells received in a whole blood transfusion would be enough to cause a problem, as most WBCs are only raised during an active infection, so would likely be too low to cause problems. The WBCs are likely killed off soon after the transfusion. The problem with organ transplants is that the hosts immune system attack the foreign cells, not the other way around... Also it is funny answering this question as I have a friend named Armin who has a PhD in Immunology... I almost feel like it is a trap.

http://www.cancer.org/treatment/treatmentsandsideeffects/treatmenttypes/bloodproductdonationandtransfusion/blood-transfusion-and-donation-types-of-transfusions I don't think they are used much anymore, as there efficacy was questionable, but it does appear they had the ability to produce a fever in the host.

@AMR  Great explanations.  I have found  out, a guy in this link states that "There is also a process called transfusion-associated graft versus host disease in which the donor white blood cells will attack the host cells; this mainly occurs in immune-compromised individuals" http://biology.stackexchange.com/a/10126/17583
Wiki https://en.wikipedia.org/wiki/Transfusion-associated_graft_versus_host_disease


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Extending a small fragment of DNA
Is there a way to extend a small fragment of DNA, say 150 bp, by making copies of itself and attaching each copy of that small fragment to the end of that 150 bp sequence?
For example, I want a 1 kbp+ DNA fragment made up of copies of that exact 150 bp sequence.
I am performing optical tests on DNA strands, but the issue is that the DNA fragments that I am targeting are too small.
However, if the DNA fragment is just a repeated sequence of the DNA fragment I am testing, the tests will yield the same results. For that reason, I am trying to create a long strand of DNA from just one DNA fragment copied over and over.
Is there a procedure that I can follow to accomplish this?

well you can use PCR in conjunction with some ligation technique...

What exactly are you trying to do? If you give a clearer explanation of your experimental setup and goals, we might be able to help you further. As it is, this question is rather vague.

@MattDMo Hi, basically I am performing optical tests on DNA strands but the issue is that the DNA fragments that I am targeting are too small. However, if the DNA fragment is just a repeated sequence of the DNA fragment I am testing, the tests will yield the same results. For that reason, That I am trying to create a long strand of DNA from just one DNA fragment copied over and over.

If the both ends satisfy the condition under which ligase works, you just treat with ligase. But you get various length of ligation products. You can cut from agarose after electrophoresis if you think the yield is enough.

Could you provide some more details? Does your fragment have blunt ends? Is the entire fragment important or could you cut in a little bit if need be?

If what you trying to get is 1kbp of repetitive 150bp sequences, then synthesis as a large chunk might be better idea. It costs ~150-300$ but will potentially save tons of time. (see gBlock from IDT in US)
PCR and ligation with repetitive sequences is pain the butt. It might be true that you save money, but time and frustration could be more expensive.

IDT doesn't like highly repetitive sequences, they become hard to do quality control on. It depends on your exact sequence though, so put your sequence in their form and see if it comes back with a problem. If not, this is probably a good cheap way to do it. Be sure to get PCR primers for your sequence too, so you can make more.

Given the cost or DNA synthesis you could probably order the two single strands and anneal them together. Engineer two complementary restriction enzyme overhanging ends onto the sequence. For example, at one end engineer a partial Bam HI site and on the other end engineer a Bgl II site.  Those sticky ends will anneal but the resulting ligation product cannot be cut by either enzyme.
By alternating cycles of ligation, digestion, and ligation, you can build up concatemers of your starting fragment. Then you can gel purify the longer pieces and sub-clone them into a suitably prepared vector.

Instead put adaptors? (if orientation is not an issue)

If orientation is not an issue you can use a blunting enzyme or a blunt-end-polymerase during the PCR (like Phusion polymerase) and then go for a blunt-end ligation. N.B. primers need to be phosphorylated!

I suggest you to try Recursive Directional Ligation. It is meant to do exactly what you are aiming for, i.e. to "polymerize" short DNAs into a longer one.
You can find the protocol here http://pubs.acs.org/doi/abs/10.1021/bm015630n