text:
What makes DNA helical?
Why isn't DNA like RNA; why isn't RNA like DNA, that is, helical? Why are RNA chains straight?

The helix shape of DNA molecule is a consequence of its secondary structure. This refers to the bases contained in the molecule which pair, thus determining tertiary structure [1].
Basepairing also occurs in RNA, so it can form a double helix. In fact, RNA is composed of short helices packed together [2]. Base pairs maintain DNA's helical structure no matter the nucleotide sequence [3].
A nucleic acid strand is composed of nucleotides joined together by covalent bonds between the sugar of one nucleotide and the phosphate of the next. Adenine pairs with thymine and cytosine pairs with guanine by hydrogen bonds and form the double-stranded structure [3]. Because covalent bonds are stronger than hydrogen bonds, the double helical structure of DNA is easily broken by heat [4], but the nucleotides remain bonded together.
Here is the tRNA molecule (you can see it has short helices):
"TRNA-Phe yeast 1ehz" by Yikrazuul - Own work. Licensed under CC BY-SA 3.0 via Wikimedia Commons.
Here is the DNA structure:
(source: wikimedia.org)"ADN animation" by brian0918™ - Own work. Licensed under Public domain via Wikimedia Commons.

References:

Wikipedia contributors, "Nucleic acid double helix," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Nucleic_acid_double_helix&oldid=609435163 (accessed June 26, 2014).

Wikipedia contributors, "RNA," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=RNA&oldid=612056511 (accessed June 26, 2014).

Wikipedia contributors, "DNA," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=DNA&oldid=611891356 (accessed June 26, 2014).

Wikipedia contributors, "Nucleic acid thermodynamics," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Nucleic_acid_thermodynamics&oldid=606379256 (accessed June 26, 2014).

RNA (single or double stranded) actually can and does form a helix in the absence of certain complex 3D structures. The RNA helix is typically A-form, as opposed to B-form for typical DNA. The A-form helix is right-handed like the B-form but is more compact (2.6 Å rise versus 3.4 Å) and wider (26 Å diameter vs 20 Å). The differing helices arise from the 2'-OH present in RNA which sterically hinders the formation of a B-form helix (by constricting the ribose to C-3' endo pucker).

[From Wikipedia. Double stranded DNA helices. A-form is on the left, B-form in the middle and Z-form on the right. There are other forms not illustrated here.]

[From Wikipedia. A hairpin loop (the result of intrastrand base pairing in a single RNA molecule) that has adopted an A-form helix.]

[Just emphasizing that a single strand nucleic acid, even without secondary structure, also forms helices.]

The helices of both DNA and RNA form in aqueous solution because of the hydrophobic and aromatic (which also implies planar) nature of the bases themselves. By forming a helix, the bases within one strand come closer together which is thermodynamically more favourable because of stacking interactions between the conjugated ring systems as well as the exclusion of water from their hydrophobic surfaces (which thus increases entropy).


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How do climate and location affect the Pine Processionary moth?
I have statistics on the occurence of the Pine Processionary moth (Thaumetopoea pityocampa); we have the regions that are located in Algeria, infested area in percent, the defiliation degree (small, medium and high) and we have geographical location (longitude, lattitude).
The table is as follows:

Why is there a difference between infested areas, and is there a special pattern for the distribution of this insect? Is it known what the main drivers are for determining the distribution and abundance of this moth, and thereby why some areas are more infested than others?

I think you should merge this question with http://biology.stackexchange.com/questions/19103/classification-of-degree-of-infested-areas-by-pine-processionary-moth-on-regions, since they are very similar and clearly overlap.

source: Stack Exchange

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sort: votes


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Primers on Dystonia
Where can I get a good biochemical overview of dystonia? I will be working in a research lab that focuses on dystonia and I would like to not be clueless.

A good article on the pathophsiology is,
The pathophysiological basis of dystonias, Nature Reviews Neuroscience 9, 222-234 (March 2008)
For a review of the treatment,
Treatment of dystonia, lancet neurology, Volume 5, Issue 10, October 2006, Pages 864–872.
A comprehensive textbook on movement disorders in general is The oxford textbook of movement disorders

this is a bit fragmented and hard to read - can you spruce it up a bit?

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Mode of inheritance - DYT1 Dystonia

Homozygous DYT1 mutation carriers have not been reported in humans.

Does this mean that the mode of inheritance for dystonia (DYT1) is autosomal dominant? This to me implies that if one has both alleles for dystonia, then one must also have the phenotype, as people with both alleles cannot be carriers.

Presumably homozygotes are not viable.

Your description is correct. Most genes do not show complete dominance as outlined in Mendelian genetics and inheritance is almost always more complicated than a simple 1 gene/2 allele system. The mutation you're studying is classified as autosomal dominant but even heterozygotes may not display the phenotype. The proportion of the population that has the mutation AND displays the mutant phenotype is called the penetrance and, for DYT1, has been estimated at around 30%.
http://www.omim.org/entry/128100?search=Dyt1&highlight=dyt1


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What are the ecological effects of moderately high and prolonged concentrations of nitrogen deposition on an ecosystem?
There are many sources of nitrogen which eventually get deposited out of the atmosphere and onto the land/surface.  Typically higher levels of nitrogen compounds are emitted near urban and roadway locations, raising the levels of nitrogen deposited on the nearby landscape.  What are the ecological effects of moderately high (at least double background) and prolonged concentrations (10+ years) of nitrogen deposition on an ecosystem?  Please be specific about which type of ecosystem your comments are intended.

Would help to define magnitudes. Prolonged = decades? Moderately high = 5g/m2/y?

i tried to be more quantitative in some edits, hope that helps

Too much nitrogen can run off during rain and collect in ponds, leading to eutriphication, find more here: https://en.wikipedia.org/wiki/Eutrophication
It's probably also responsible for dead zones: https://en.wikipedia.org/wiki/Dead_zone_%28ecology%29
This is an important question because we've more than doubled the amount of bioavailable nitrogen on Earth in the last 100 years simply because of the haber process and man made fertilizers. This amount of nitrogen has never been available before.


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What are garlic's effects on DHT?
Most antiandrogens inhibit DHT. DHT is connected to testosterone. [1] shows a beneficial effect on prostate cancer which can be caused by DHT. However, according to [2] garlic also increases testosterone.
What are the effects of garlic on Dihydrotestosterone (DHT) or 5α-dihydrotestosterone? Can it be used as an antiandrogen?
[1] Hsing AW, Chokkalingam AP, Gao YT, et al. Allium vegetables and risk of prostate cancer: A population-based study. Journal of the National Cancer Institute 2002; 94(21):1648–1651.
[2] Oi, Y; Imafuku, M; Shishido, C; Kominato, Y; Nishimura, S; Iwai, K (Aug 2001). "Garlic supplementation increases testicular testosterone and decreases plasma corticosterone in rats fed a high protein diet". The Journal of nutrition 131 (8): 2150–6.

This should be migrated to Biology.SE

Welcome to Skeptics! According to the FAQ, Skeptics.SE is for researching the evidence behind the claims you hear or read. This question doesn't appear to have any doubtful claims to investigate. Please edit it to reference a notable claim and flag for moderator attention to re-open (or get 5 re-open votes).

@Oddthinking I think the comment for migration to Biology is accurate and I agree with that. Though, I am not sure how I can migrate it there.

I asked the Biology mods, and got back the response that the question isn't clear enough and it would be closed. I agree; I am not sure what the question really is either.

I added a further explanation in order to be a candidate for Biology.SE. Any help on that is welcomed.

Garlic may affect testosterone metabolism. Its beneficial effect on prostate cancer is not attributed to this, but it is attributed to the direct effect on prostate cancer cells.

What is garlic's connection to DHT?

Cytochrome P450 enzymes. Diallylsulfide, a constituent of garlic, suppresses oxidative demethylation by competitively inhibiting cytochrome P450 2E1, an enzyme that activates carcinogens. Since testosterone metabolism occurs through the mixed function oxidase cytochrome P450 system, garlic may affect the rates of metabolism of testosterone and dihydrotestosterone. The metabolism of testosterone is catalized by inducible P450 1A1, 1A2, 3A3, 3A4 and 3A5 enzymes. These mixed function oxidases can be modulated by a wide variety of environmental facts and dietary constituents. Little is known about the potential for modifying testosterone risk or its treatment modality by administration of garlic constituents [1].

S-allylcysteine (SAC), a potent compound derived from garlic, suppressed the proliferation of PC-3 cells and led to cell cycle arrest at the G0/G1 phases, as well as induced cell apoptosis, which was accompanied by the decreased expression of Bcl-2 and increased expression of Bax and caspase 8. This demonstrates the chemopreventive activity of SAC in vitro, and that SAC may be a promising candidate for prostate cancer treatment [2, 4].
Diallyl disulfide (DADS) is another major component of an oil-soluble allyl sulfide garlic (Allium sativum) derivative. Inhibitory effects of DADS on prostate carcinoma LNCaP cells motility and invasiveness were found to be associated with increased tightness of the tight junctions (TJ), which was demonstrated by an increase in transepithelial electrical resistance (TER) [3, 4].

References:

Paul A. LaChance. Nutraceuticals: Designer Foods III: Garlic, Soy and Licorice. John Wiley & Sons, 2008. Pages 177-180.

Liu Z, Li M, Chen K, Yang J, Chen R, Wang T, Liu J, Yang W, Ye Z. S-allylcysteine induces cell cycle arrest and apoptosis in androgen-independent human prostate cancer cells. Mol Med Rep. 2012 Feb;5(2):439-43. doi: 10.3892/mmr.2011.658. PubMed PMID: 22052207.

Shin DY, Kim GY, Kim JI, Yoon MK, Kwon TK, Lee SJ, Choi YW, Kang HS, Yoo YH, Choi YH. Anti-invasive activity of diallyl disulfide through tightening of tight junctions and inhibition of matrix metalloproteinase activities in LNCaP prostate cancer cells. Toxicol In Vitro. 2010 Sep;24(6):1569-76. doi: 10.1016/j.tiv.2010.06.014. PubMed PMID: 20600798.

Bhandari P. Dietary botanicals for chemoprevention of prostate cancer. J Tradit Complement Med. 2014 Apr;4(2):75-6. doi: 10.4103/2225-4110.130371. PubMed PMID: 24860728.


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Mechanism of antiperistalsis
What is the mechanism of antiperistalsis that occurs during vomiting? Why the peristaltic waves normally don't propagate in anal to oral direction? Please give logical explanation with authentic sources. :)

What is the mechanism of antiperistalsis that occurs during vomiting?

Emetic agents in the bloodstream stimulate chemoreceptors in area postrema and nucleus tractus solitarius [1].
Nucleus tractus solitarius is connected to motor neurons in ventral medulla and hypothalamus [1].
Esophageal and gastric peristalsis is inhibited. Small bowel peristalsis is reversed. Esophagus and stomach don't have antiperistaltic movements [2].

Why the peristaltic waves normally don't propagate in anal to oral direction?

Because of the mechanism of descending inhibition. Distension of the esophagus and intestine causes a reflex action that leads to circular muscular contraction just above the bolus/chymus. Longitudinal muscle also contracts (shortens) [3].

Reference:

Hornby PJ. Central neurocircuitry associated with emesis. Am. J. Med. 2001 Dec 3;111 Suppl 8A:106S-112S. PubMed PMID: 11749934.
Brizzee KR. Mechanics of vomiting: a minireview. Can. J. Physiol. Pharmacol. 1990 Feb;68(2):221-9. PubMed PMID: 2178746.
AUMSA. Digestive Physiology. May 2012. CC-BY-SA-3.0


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What is the reason behind more severe proteinuria in nephrotic syndrome than in nephritic syndrome?
Why is there less protein loss via urine in case of nephritic syndrome than in case of nephrotic syndrome?

It is to do with the extend of the damage to the glomerulus. In nephrotic syndromes the glomerulus is damaged so that there is death of the podocytes. This happens to sufficiently high number of podocytes so that large proteins such as albumin and clotting factors can leak out causing large proteinuria. Damage to the basement membrane may also occur, such as in minimal change, where there is a loss of charge on the basement membrane.
In nephritic syndrome the damage is as a result of inflammation which does not lead to the same structural damage as in nephrotic syndrome, therefore there is not leakage of protein to the same degree.


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What is the scientific name of such a fungus?
Several days ago, in a bush I found the fungus as attached which is about 25cm in height and does not look like an edible mushroom:

Any one has an idea of its scientific name and other details?

This looks pretty much like a Coprinus comatus (also known as: shaggy ink cap, lawyer's wig, or shaggy mane) to me. You can see the characteristic ring around the stipe of the fungus (see image below from Wikipedia). The fungus is edible and is also cultivated in China for this purpose. See here for more details.


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dbSNP database table desciptions
I am trying to build a local implementation of dbSNP. I would like to know the descriptions of tables listed on ftp://ftp.ncbi.nlm.nih.gov/snp/database/organism_data/human_9606 and on ftp://ftp.ncbi.nlm.nih.gov/snp/database/shared_data/. I tried to use the search on this webpage : http://www.ncbi.nlm.nih.gov/SNP/snp_db_list_table.cgi which is supposed to be a data dictionary for all tables and columns, but I think it is outdated. There are many tables which do not have any definition. Also, there are tables in this dictionary that are not in the ftp site at all. Does anyone know of any better dictionary for the dbSNP database tables?

http://www.ncbi.nlm.nih.gov/books/NBK3855/ ?


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Understanding the Amino Acids
I'm having little trouble studying general relativity or quantum field theory, but remembering all the amino acids and being able to think about them is something that's completely, utterly and absolutely, defeated me...
How do I think about the amino acids, without any memorization, and be able to 'derive' all the names, all the categories they fit into, and their important properties? Memorizing some crazy mnemonic is of no help when it says nothing about the amino acids, I can't memorize it without meaning that explains a lot of things. I ultimately just want to be able to read Albert's Molecular Cell Biology and appreciate it, but I can't without conquering this little issue!
On a side note regarding memorization tricks: is there a mnemonic scheme for the amino acids analogous to the thermodynamical Zhao square, (which gives all the info you need about basic thermo by drawing lines and squares)?
Any help is greatly appreciated, thank you.

Sorry, but I don't understand your question. Can you please make this more precise?

This question appears to be off-topic because it is about memorization techniques - maybe academia.SE might be suitable?

My post explicitly says "without any memorization", the entire purpose of the post is that I'm asking for a way to derive all of the properties of the amino acids in a consistent non-memorization way. Said differently: How would you explain the amino acids and all their important properties (for biology on the level of Albert's) to someone in a way that they can reconstruct what you say. e.g. in physics you can derive the entire theory of electromagnetism by postulating an action principle, using one idea and some obvious rules. Apologies if that wasn't completely clear.

I have amended my response to your question however the short answer, to the best of my knowledge, is that it is not possible since thats not how AA nomenclature works.

you can't learn to even spell without some memorization lol

@bolbteppa ok, sorry. My mistake and badly formulated. I guess I read your Q as asking for a way to structure information in general, and not dealing with biological properties. Either way, nomenclatural Qs are on-topic so my mistake.

understand the chemistry. you'll remember the structures

And yeah Albert's a very readable book. I don't think you really need to "know" the amino acids to appreciate the book ! You could also keep a self made chart nearby when you are reading the book, if you feel that's necessary.

Amino acids have different side chains.If you remember the side chains of each amino acids, and know enough chemistry, you can easily derive almost all the properties of the amino acid.

Maybe this will help? (unfinished currently) https://revolutionarymathematics.wordpress.com/2016/12/18/how-to-memorize-the-amino-acids-without-mnemonics-i-introduction/

I'm sure there are lots of ways of handling this, but there are only 20 of them (more or less).  I really wanted to figure out how the amino acids resulted in the resulting protein structure.  So I started to break them down into categories.  The categories cannot draw boundaries exactly since one amino acid might belong to several categories in a unique way, but it starts to give you a sense of what the sidechains do.

Aliphatic : G A L I V M P
  Aromatic : F Y W H
  Polarizable : F Y W H M C R
  Polar: S T Q N D E K C
  Small: A S T G C
  Large : F Y W H R K
  Strong Structural variation: P G

you still have to memorize them eventually, but you can make it easier to put them in categories and in these groups its easier to bring them to mind.

I don't think methionine and proline are aliphatic compounds, because they don't completely consitsit of Hydrocarbons.

The question is slightly unclear but will do my best to answer it. I'm not a purist as a biochemist and I can tell you when it comes to biology, there are just certain information you have to memorise and one such instance is AA names. You can drive the AA full chemical name (and its properties such as charge, hydrophilic/hydrophobicity) from its molecular structure but such an approach is far far harder than to remember simple names such as A = alanine, S = serine, P = proline etc! There are some odd ones like Y, which is tyrosine but again the only reason they chose letter Y (second letter in tyrosine) was because (the first) letter T was used for threonine. If you want information on AA and their properties look at this page (https://web.archive.org/web/20150302034529/http://www.bio.davidson.edu/biology/aatable.html), but I'm curious as to why you need to know individual AA properties. I don't suggest it is not important but AA property makes more sense in terms of its context in a protein sequence as it interacts with other AA properties and within a 3D protein structure.
Saying that AA names taken at face value do not make sense since it is not telling information about their property, although true, is broadly similar to saying protein names taken at face value do not make sense, again kind of true, because they do not say anything about their function (not true all the time but mostly true). To me this is the wrong way of looking at it. The designations for AA names were made as they were easier to memorise/refer to (and consequently become aware of their properties e.g. Y is capable of becoming phosphorylated) just as it is easier to refer to protein by its name and not its full AA sequence.

Are you telling me that if I derive the molecular structure I can derive all the info on this massive list, as in - if I can picture the structure of Alanine A in my head I'll immediately know a massive amount of info about A? Judging from this page http://books.google.ie/books?id=sZLvdRA_vRgC&lpg=PP1&pg=PA356#v=onepage&q&f=false the molecular structure of Ethylene can be determined by a quantum mechanical variational calculation, can the same thing be done for all 20 amino acids and if I did that would I be able to derive all those properties from knowing the molecular structures?

I do not know much about QM to comment on it but in general, if you know molecular structure of a (complex) molecule and your chemistry is good enough to know what each part entails in terms of its properties towards the entire structure, then yes, you will know many properties of a molecule. That is how people know if a molecule is for example polar or non polar etc. Obviously the more complex a molecule gets, the harder the tasks becomes, which is why we not only use wet experimentations but also computer simulations.

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Can lymph be in peripheral blood?
I read an argument that 1-3% of lymph is in peripheral blood.
However, I am not sure if this lymph is about lymphocytes in peripheral blood; not lymph itself.
Lymph gets exchanged between capillaries through Starling law powered by the heart and Frank-Starling mechanism.
In this way, it makes sense that some lymph is leaking out from capillaries into the bolod.
Can lymph be in the peripheral blood?

Depends if your talking about interstitial fluid or lymph:
As per starling forces: the oncotic pressure of the late capillary plus hydrostatic pressure of interstitial space, would be higher than oncotic pressure of interstitium [though I dunno why since intertitial GAGs are very water hungry and they are responsible for the negative (hydrostatic?) pressures found in interstitium... Read lots of articles, still makes no sense to me] and hydrostatic pressure of the capillary... Thus there would be a net influx of interstitial fluid in the very ending part of the capillary, toward the venous side...
I say interstitial fluid, because it's not lymph yet since the interstitial fluid hasn't yet entered the adjacent lymph capillaries... if the interstitial fluid entered the lymph capillary then it would be stuck there, the mechanism of this one way flow is the junctions between the endothelial cells in these blind ended lymph capillary... These junctions which only opens up gaps between these endothelial cells when the interstitial pressure outside the lymph capillaries is higher than pressure inside the lymph capillaries...
The lymph then goes forward through lymphatic vessels/nodes because external pressure (pulsing of adjacent artery, contraction of adjacent skeletal muscle, changes in thoracic pressuring during breathing, etc) and there is little back flow because of valves (just like venous valves which prevent back flow in the low pressure venous system)... Ultimately the lymph returns by either thoracic duct (in the angle between left subclavian and left jugular vein) or right lymphatic duct  (in the angle between right subclavian and right jugular vein)...
There are some sweet review articles from University of Bergen, Norway that go much more in depth on the physiology of interstitial fluid...
Here is one of their more recent review articles:
http://m.physrev.physiology.org/content/92/3/1005 it's free
IN SUMMARY: the starling forces bring interstitial fluid into the blood (the "peripheral part" right after the capillary)... The thoracic and right lymphatic duct drain lymph into the blood (I'm assuming this does not apply by your definition of peripheral, since this venous blood is about to be drained into the right atrium and is destined for the lungs)...
P.S. aqueous humor (in the eye), endolymph (cochlea aka inner ear) and CSF are also absorbed back into the blood... Also the brain has an interstitial fluid that is different from the CSF found in the subarachnoid spce of the meninges, i actually don't know how that drains... But anyway, the head is so special, I'm sure you weren't wondering about these specifics...


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Pedigree analysis : autosomal or mitochondrial

I have tried a to decide if this is a autosomal dominant, recessive or a mitochondrial disorder.
Is it possible to know for sure, or do you have to use probability?
(English is not my native language)
No other pedigrees have had carriers marked so I did not expect this one had it either.
Auto dominant.
I:1 aa I:2 A-
II:1 aA II:2 aa II:3 aa II:4 aA
II:1 children could have got a from him and a from her the the disorder would be gone.
III:9 children got her dominant A
Recessive
I:1 A- I:2 aa
II:1 aa II:2 A- II:3 A- II:4 aa
Mitochondrial disorder
I read "transmission only accours through females"

Could you please share your findings/rational so far on the matter and what makes you think it is autosomal or mitochondrial? This will show that you have thought about the question and will encourage others to contribute and point you to the right answer.

Since other pedigrees we have used have not had carriers marked I presumed this would not either.

Mitochondrial because all the offsprings have the same trait as that of the female parent. Lets go through the possibilities one at a time. Assuming you have no carriers (you do not have any carrier symbols) we can work out the following.
Autosomal Recessive?
This might be the case if we assume the male in the first generation is a carrier.
Autosomal Dominant?
This might be the case but it is unlikely. Looking at the first generation possibly yes, as 50% of offspring have the trait. Looking at the second generation however only 3 out of 9 offspring have the trait. Making autosomal dominant unlikely (but it is still a possibility.)
In the test, if you have to go with one option, mitochondrial inheritance is the best because there are no assumptions at all but if multiple options may be correct, you can have any of them.

Actually, all offspring of females with the trait are affected ...

ah yes sorry my mistake, i read the female in the first generation as a daughter not a wife. so it is mitochondrial. Thanks

As Rory has pointed out, there is no incomplete penetrance if we accept it as a mitochondrial trait. Besides that, your "Sex-linked?" point seems to be incorrect. In this case we can rule out the case of a dominant X-linked locus based on the observation that males didn't pass the trait to their daughters (decisive argument) and that sick heterozygous mothers transmitted the trait to all of their progeny (in statistical terms).

It cannot be X linked dominant. If it were then the male in the top left corner would always have daughters who had the trait as they need to inherit one X from their mother and the other trait X, X_T from there father. Resulting in XX_T and if X_T was dominant they would show the trait.

Please read my comment again. Your argument was: it's not a sex-linked locus, "because both males and females are effected."


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What I can do in order to improve the folding of the protein?
I am struggling with the expression of the certain protein. It seems that it is not properly folded and thus, it is not active. I tried to express it at the lower temperature and for the longer time, but it did not help. Can anyone give me a clue what I can try to do?
The size of the protein is around 55 kDa. I know that I have some soluble protein as I run western blot. The protein contain His-taq on the C-terminus so I started with Ni-NTA column chromatography. Steps of purification:

Incubation the lysate with resin (30 min/4°C)
Unbound proteins were collected as the ‘Flow-through’ fraction
Wash 1 with buffer: 50 mM NaH2PO4, 1M NaCl, 10 mM Imidazole
Wash 2 with 10% buffer B in buffer A
Elution with buffer B: 50 mM NaH2PO4, 1M NaCl, 250 mM Imidazole

Because the protein is co-purified with something else in size around 57 kDa (which might be a chaperone protein) I tried also:
1. add ATP to first wash in concentartion of 2.5 mM and incubate column for 1h/4C
2. add ATP to first wash in concentartion of 2.5 mM and incubate column overnight in 4C
3. add ATP to first wash in concentartion of 2.5 mM and incubate column overnight in room temperature
4. add ATP and glycerol to first wash in concentartion of 2.5 mM for ATP and  4M for glycerol and incubate column for 2h in 4add ATP to first wash in concentartion of 2.5 mM and incubate column overnight in 4C
All the method end up with two close to each other bands (only one of them is my protein) and protein is not active.

What kind of protein? Is this a membrane proteine? Probably even a helical? Or is it toxic? What conditions did you try?

DNA binding protein. I tried express it in 37°C /4 hrs, 20°C/4hrs and 20°C /overnight

You'll have to add a lot more detail if you want to have a chance for any proper advice. All the known properties of the protein as well as your exact expression and purification protocols at minimum. Otherwise you'll only get some guesses and vague advice.

If you have over-expressed an eukaryotic full length protein or the enzymatic part, then E. coli does not necessarily provide a good environment for its folding so you need to express it in the same system which the original protein came from, e.g. mammalian or Drosophila etc. E. coli over expression is mostly used to generate wast amounts of protein for the purposes of protein sequence based Ab generation amongst other things. Look at this review for some of the solutions it offers for proteins not folding correctly in E. coli when over-expressed (http://www.biomedcentral.com/1472-6750/4/32).
The remainder of your question is a duplicate of this question (Ni-NTA purification, problem with the chaperone protein), which I have provided an extensive answer/comments to!
In addition, since the lack of enzyme functionality is a potential indication of errors in its state/3D structure, it is however not a definitive reason. Could you provide some explanations as to what experiments you have conducted to reach that conclusion and how this second point about chaperone eluding with your protein relevant to the first and the last section of your question?

Also, to make it easier on yourself. If it is a soluble protein, use a leader sequence that translocates out of the cell. Then there will be no need for lysis


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Muscle force/energy relationship
I found the Hill muscle model, which helps relate the force a muscle can generate to its change in length over time (its "contraction velocity").  Is there a similar model to get an idea of the energy consumed during a contraction as a function of the force generated?

You can calculate the energy consumption using basic physics formulas.
Work = Force x Distance
and the unit of work is the Joule. Therefore if force is a function of change in length then substituting this function in for force in the above calculation we have that work is a function of length.
If you want to talk about energy consumed in terms of calories rather than joules,
1 calorie = 4.184 joules

That's part of it, but what about isometric exercise?

The same physics applies, you are buttressing your muscles but they will still be exerting a force. The resulting distance of movement is small so that you don't notice it, however the force is greater. Work is still force x distance.

But that doesn't help in building a mathematical model for muscle activation.  I want a predictive model for the energy consumed during a muscle contraction, whether it's isometric or isotonic.  Even for only isotonic contractions, if you only account for mechanical work you're entirely ignoring the heat generated.  You'll only get a lower bound on the amount of energy consumed.

Your question asked for energy as a function of force generated. Not as a function of heat and force generated. If you want the total energy used then yes you would have to take into account the inefficiencies of muscle contraction which generates heat. The question then is how efficient are myocytes in converting energy from ATP to force. This a variable quantity see the following paper http://www.ncbi.nlm.nih.gov/pubmed/11350777

Yes, I asked for energy as a function of force generated.  Because muscles can produce force with no net movement, mechanical work is simply not a complete answer to the question :(  Did you read the body of my question, or just the title?

Yes I read the body of your post, and was trying to help with sarcastic comments like that I am sorry I tried.

I wasn't being sarcastic; I'm sorry if you read it that way.  I was pretty specific about what I was looking for in the body of the post, so I was trying to understand where the disconnect was coming from.


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Should the sum of RPKMs be constant over experiments
I have cufflinks data from 18 different RNA-seq experiments.
I've noticed that if the sum all the RPKM values for a particular experiment, are vastly different between experiments. How could this be? I was under the impression that RPKM was normalized by the total number of reads. If that is true then the sum of RPKM values for a single experiment should be the same?

I recommend that you ask this question in biostar. This is a valid question and neither biostar nor seqanswers have addressed this issue yet.

I think it might have something to do with reads that do not get aligned. unaligned reads might affect the normalization factor in RPKM, but since it is not aligned it dosen't contribute to the sum of RPKM values.

I guess this arises because of the default cufflinks option --total-hits-norm in which it normalizes the FPKMs with total reads including the ones that are not mapped to a known gene or a predicted gene from the assembly. In the genes.fpkm_tracking file the FPKM values are reported for known/predicted genes. It is certainly possible that the number of genes are different in a certain sample compared to the other and perhaps therefore the sums are different. If you are not interested in finding new transcripts then you can run cufflinks with a reference GTF/GFF file provided using --GFF along with using --compatible-hits-norm.
You can also try this:
Assemble with cufflinks, merge the GTFs with cuffmerge and run cuffquant with the merged GTF.
You can subsequently use cuffnorm to normalize the expression values. It has been observed by me and others that the FPKM value reported by cuffdiff and cufflinks are different which is most likely because of differences in default parameters (see this). The inner operations of cufflinks are not very clearly documented; so I cannot conclusively answer your question.

I fell like the --total-hits-norm must be it. but I cannot confirm either. thanks!


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Questions regarding Scapulohumeral Rhythm
I'm actually an artist, but I wanted to ask this because it will help a lot in my figure drawings.
My artistic anatomy teacher taught me about the Scapulohumeral Rhythm. He said that in during the first 30 degree of rotation of the humerus, neither the scapula nor the clavicle moves. But after that, for the next 60 degree of rotation of the humerus, its rotation is distributed in a 2:1 ratio to the Scapulathoracic joint.
He said that beyond that, the Humerus is locked into the socket with Acromium and Coracoid Process. So the Glenohumeral Joint is frozen. Additional elevation comes from the Clavicle.
My first question is how true is that?
My second question is what happens to the Scapula after the 90 degrees rotation of the Humerus? I noticed that the Scapula keeps rotating even after the Humerus is rotated beyond 90 degrees, but is there any consistent ratio?
My third question is what is the maximum elevation of the Humerus in degrees?
Forgive me if I looked liked an annoying dumbass, I'm just an artist. So, please explain in a simple and understandable way.


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Ancestral Allele explanation
I'm having some trouble understanding the concept of ancestral allele. What exactly does it mean? What does it have to do with Identity by descent/state? What does it have to do(if anything) with SNP's? Also, how is the concept useful in genetics/evolution? I've tried reading these up on various websites, but I'm not satisfied with my understanding yet.

SNP
Let's start with the definition that has nothing to do with the rest of the question :). A Single-Nucleotide-Polymorphism (SNP) is a kind of genetic variation that you find in population. This genetic variation is defined as a variation caused by only one single nucleotide (as its name indicates it). For example if you have in the populations the two following variants at the same locus: AGCCGT and AGCTGT, then you have a SNP at the position of the C and T. This type of variation is very common. We estimate that there are about 10 millions SNPs in the human genome. We often use these SNPs as genetic markers.
Ancestral vs derived alleles
An ancestral allele or an ancestral trait (depending on whether you look at the phenotype or a t the genotype) is the trait/allele that was carried by the common ancestor of the taxon you consider. For example: as you may know the taxon Reptilia includes lizards, snakes, turtles, birds, mammals and some other lineages. In the taxon Reptilia, the scales is the ancestral state (still exist in lizards for example) and the hairs and feathers are derived states. Usually, the ancestral state is the one that carried by the most basal lineages.
Identity by state (IBS) and Identity by descent (IBD)
If two sequences are exactly identical, then we say that they are identical by state (IBS). Such identity can occur either through convergent evolution or through common ancestry.
To understand the concept of "identical by descent" (IBD) it is important to understand the concept of coalescence. A coalescent event is, when looking backward in time, an event where two sequences were actually the same sequence. Often IBD is defined relatively to a given threshold in time. If the coalescent event occurs after this event then the two sequences are not IBD. If the two sequences coalesce before this time threshold and that the two sequences are still IBS, then the two sequences are IBD
Bridging everything together
So, if you look at sequences in a given group of lineages and see that they are all exactly the same then they are identical by state. If you know that all these sequences come from a common ancestor and even they all coalesce to a single individual in the common ancestor, then all sequences are identical by descent. But some mutations may have occurred since the last common ancestor resulting in some SNPs, then all the sequences are not IBS anymore and therefore not IBD either. You can use such sequence variance in order to create a phylogeny for example.
Hope that helps.

According to you, Identity by descent does not imply identity by state. But according to wikipedia https://en.wikipedia.org/wiki/Identical_by_descent it's the other way round. I realize wikipedia could be wrong in a lot of cases, but could you read what it has to say? My initial confusion arose from this article.

@Venkat You're right it sounds wiki and I don't totally agree! To my understanding, IBD does not imply IBS because of recombination (I ignored this point in my answer above for the moment) and mutations. I don't mean that IBS implies IBD either. IBS without IBD may occur due to convergent evolution. I haven't read the wiki article but indeed this citation from the wiki article "DNA segments that are IBD are IBS per definition" sounds wrong to me! I'd appreciate to have the opinion of some other people to confirm or invalidate my point of view.

I believe I have seen both ways of defining IBD before, but I guess it makes sense to require alleles to be indentical (ie IBS) in order to be "indentical by decent". This is also the definition John Wakeley uses in his Coalescent Theory Book.

Is it really what John Wakeley's says in his book? I'll check this out tomorrow as soon as I'm back home to my library. If indeed some (or all) authors defines IBD such that it implies IBS, I will modify or remove my answer.

On page 11, it says "The concept of identity by decent [...] posits that two or more gene copies are descented from a common ancestor without mutation. That is, their identity is a direct reflection of their common ancestry, as opposed to the more general case of identity by state [...]."

This definition of IBD is counter-intuitive to me. But I'll have to accept it I guess as you show that John Wakeley uses this definition. So I updated my answer to fit John Wakeley's definition. Thanks a lot @PaulStaab for your help! Feel free to edit my question to improve it if you want!


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Identifying a spider from my childhood memory
Once, as a child, I found a spider in my parents' garden. I remember catching it in a jar because I thought it looked unusual, but I never figured out what kind of spider it was and unfortunately didn't get any pictures. I've been looking for it in books and on the Internet since, based on memory, with no luck.
This was twenty years ago now, and I realize my memory of it may not be good enough to identify it now, but here's trying.
What I remember best was its abdomen, which was a dark metallic blue and sort of rectangular in shape. Its body was probably about 1.5 cm long, without the legs, and maybe 1 cm wide or a little less (I was a child, things look bigger when you're small.) It was found in a garden in the suburbs of Copenhagen, Denmark, sitting on a bed sheet drying in the sun. It left only a few strings of web, almost like a bridge, from the bottom of the jar to the lid where it had escaped during the night because the lid wasn't sealed. I never found it again or saw another spider like it.

black colour with blue abdomen in a rectangle? Also on top of the abdomen or was it the underside that you saw this mark?

@TheLastWord Rectangular, blue abdomen, yes. I'm sure the rest of it (head, legs) was probably black.

anyway you can go through these internet images and find any similarity with the one you saw. https://www.google.co.in/search?q=spider+black+blue&client=ubuntu-browser&es_sm=94&source=lnms&tbm=isch&sa=X&ei=DWmhU_-UOYi0uASZ2oGIAg&ved=0CAYQ_AUoAQ&biw=1215&bih=911#q=spider+black+blue+mark+abdomen&tbm=isch&imgdii=_

@TheLastWord Mark? It had no mark. The abdomen was dark blue and sort of rectangular instead of round. Looking through images on Google hasn't turned up anything

This may be what you are searching for:

It's actually a male purseweb spider (Atypus affinis), the color fades to black, eventually.
Source: http://www.spiderzrule.com/purseweb2.htm

This is definitely close. Colors, geography, and everything seem to fit. I remember the abdomen being bigger and less rounded, but maybe that's just my memory.

Was it this? This is another purseweb spider species.


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Simultaneously using both hands - How does that work?
Is some part in one hemisphere the decision maker and "calling the shots" - controlling the opposite side's hand "directly" and controlling its own side's hand through the corpus callosum. Or: is there some "Gestalt" of parts in both hemispheres working as one making the decision?
If the latter - it would seem counter intuitive to have a deciding part which is not "unified" in one region, having to go back and forth through the corpus callosum for deciding.

Why can't the hemispheres coordinate? Even though control of muscles on one side of the body may primarily originate in the opposite hemisphere, inter-hemisphere communication and coordination is vital to proper functioning of the body.

@MattDMo Yes. I can't seem to formulate the question clearly. Perhaps better phrasing would be to ask: Is one side dominant in the decision and "calling the shots" or is it some "Gestalt" of the two hemispheres working together on the same "level"?

@user133943 This article should interest you http://faculty.washington.edu/chudler/split.html

@MattDMo I edited my question. Thank you for your response.

@TheLastWord I edited my question. Thank you for your response.

I am not sure I fully understand your question, it's a little unclear. But if I understand the question correctly it is how to we coordinate movement on both sides of the body?
Well this can occur because we have connections between both hemispheres of the brain. The major connection is called the corpus collosum, this is a white matter tract that allows signals from one side of the body to pass to the other side of the body.
In some rare cases there have been individuals who have had this connection severed, for these individuals each side of the body may perform tasks of which there other side of the body is unaware.

I tried upvoting your answer because it answers my question as originally posted. But I don't have enough reputation for upvoting. I have also edited my question.


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Are harmful gases abiotic or biotic factors in our environment?
As we all know, harmful gases play a negative role in our society and our environment. Are these gases playing as abiotic or biotic factors in our lives?

About what gases do you think?

The harmful ones such as Carbon dioxide and Carbon monoxide. @Chris

Isn't definition of biotic a living thing? gasses are not living (i.e. abiotic) harmful or non-harmful, or am I missing something? (http://en.wikipedia.org/wiki/Biotic_component). If so, could you clarify the question? If you mean whether bionics can use harmful gasses, then it depends on the species. e.g. plants can use CO2 but mammals can't.

I'm voting to close this question as off-topic because it is about the English language rather than Biology.

Bez is correct, biotic and abiotic refer to the nature of the agent performing the stress.

biotic = living thing (lion that is actively engaging in catching you as food)
abiotic = non-animated (far from optimal temperature)

Now the example "shade" is trickier; because it depends on the perspective you choose.
There's always a context. Does the element creating the shade matter in your context?
If so, and this element happens to be animated/living:  stress = biotic (though you should reference at some point that the object at hand is animated).
If it doesn't matter what object generates the stress since you are only interested in the effect of the shade on a system: shade = abiotic
Pipeline: Analyze the context, choose and communicate your choice of perspective/angle and then remember what biotic and abiotic literally mean.
Coming back to "harmful gases": What is your context meaning harmful for whom? Specify that first. Carbon Dioxide is an example of something that may be deleterious at a specific concentration for one system and at the same time beneficial for another.
Does it matter how these gases were produced? CO2 may be a product of an animated system's metabolism and thus may be called abiotic. It may also be a product of oxidation of a multitude of carbohydrates.
I don't know of an example where Carbon Monoxide is produced by living things.
You could of course circumvent this discussion by analyzing what harmful effect the gases have on your system of interest. For example: they generate respiratory stress on humans, and then you use the effect of the gases on the system to characterize them.


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Blosum matrix with probabilities instead of the positive and negative scores
I am trying to find a version of the BLOSUM matrix that has the frequencies instead of the scaled log-odds. i.e. instead of the common version that tells us that the score LEU/ASP is -4, I would like to know the probability of LEU replaced by ASP.

Download the BLOSUM data and source-code from here. Unzip the archive which has several files.
The file called blosum'XX'.qij will have the co-occurence probabilities, and the subsitution probabilities can be calculated from them.
Also have a look at this article.

Thank you for the answer and the link. For the benefit of anyone reading this: the frequencies in .qij files still need to be normalized before they can be used as substitution probability since they don't add up to 1 for each column or row (they add up to 1 for the entire matrix). i.e. If I want to know the probability  of ALA being replaced by HIS, the table will say it is 0.0011 but actually it is 0.0011/0.0741 (the sum of the frequencies in the ALA column) = 0.014844804318488529

So perhaps they are more called cooccurance probability than substitution probabilities. The probability of ALA substutited by HIS is p('His'|'Ala') but the table gives the joint probability p('His', 'Ala'). So we get the conditional probability p('His'|'Ala') = p(His,Ala)/p(Ala) and p(Ala) is basically p(Ala,x) for all x. so it is the sum of the Ala column.

oh yes you would need the $p_i$ for the calculation. I have not checked if that file exists in this archive.


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Quantitative Comparisons of Phylogenetic trees
I am working on a broad phylogenomic analysis of proteins involved in one particular cellular process.  I have constructed a phylogenetic tree for each protein.  I am now working on comparing those trees in order to extract categories (i. e., allele a of protein a occurs most frequently with allele b of protein b, etc.).  I have attempted to construct a super tree using clann, but the tree is extremely difficult to interpret.  I would therefore like to carryout a quantitative comparison (and subsequent categorisation) of each each tree, but it is unclear to me how to even begin this analysis.  Is there a standardised method for comparison of phylogenetic trees?

I don't know whether it's exactly what you need, but there are formal algorithms for tree comparison.
There are basically two approaches: one utilizing tree lengths (branch score distance) and the other one dealing with topologies only (symmetric-difference metric): details and references can be found in the manual to treedist from the phylip-package, which implements both.
PAUP* has a command under the same name (treedist), which calculates the symmetric-difference metric only. This metric is very intuitive: it describes the total number of partitions (= splits) present only on one of the two trees.


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What is the difference between "cistron" and "gene"?
I'm asking after reading the cognate wikipedia.en article on "cistron". I am still not sure about the difference between the two terms.
To me it seems valid to picture a "cistron" as the genome wide set of a specific gene's alleles ?
Thus if all copies of a gene bear recessive mutations all generating the same phenotypic trait (not necessarily the same mutation) no complementation is observed in a cis-trans test?

off the top of my head:
cistron and gene are equivalent to each other but cistron is a bit old-fashioned. Consider two phenotypes in different individuals belonging to certain organism; let's say both of them are recessive and you cross these phenotypes with one another. If you see wild type phenotype in the next offspring then it means your phenotypes reside in different regions in the genome and these regions were first defined as cistrons. Of course it then turned out to be much more complicated than that and people started using the term gene more often

A cistron is a gene - here's how the word came about:
It's 1955. The proposed double helical structure of DNA has been published and the race is on to understand the implications of this for genetics. Geneticists have been working with genes for decades, but they don't know what genes are. Sanger has sequenced the two polypeptides of insulin, so the idea of a specific sequence of amino acids is established. The emerging molecular geneticists believe that genes will be explained by a feature of DNA, probably a sequence of nucleotides, but they don't know how. Crick and others are theorising about coding (i.e DNA > protein), but at this stage there is no genetic code, no mRNA or tRNA.
Seymour Benzer, at Purdue, is working on fine structure of a genetic region in bacteriophage and in this year he publishes a key paper with that phrase as the title. Without going into a lot of detail about his experimental set up, he is studying a region of the bacteriophage T4 genome called rII. Wild-type T4 can form plaques on E. coli B or E. coli K12. Mutations in the rII region cause a large plaque phenotype in E. coli B so it is easy to isolate them, but these phage cannot produce plaques on E. coli K12 which sets the scene for a powerful assay for rare recombination events.
Benzer used this system to do very fine mapping of thousands of rII mutations because he was able to use the system to measure recombination frequencies, but what matters in the present context is that he was able to do a kind of complementation test (he called this pseudo-allelism). He was able to assign the rII mutants into two groups according to whether, in a mixed infection, they produced lots of progeny. So if he mixed two phage with different mutations and didn't get many progeny he put these in the same group. On the other hand if he did get a lot of progeny he placed the two in different groups. He called this approach a cis-trans test.

"The application of the phenotype test to pairs of rII mutants leads to the division of the region into two functionally separable segments."

This is as close as he dared to go to claiming to be studying genes. He refers to 'functional units' but never uses the word 'genes' because at this stage that word belonged to classical genetics in higher organisms. In 1957 he proposed the word cistron for the functional unit defined by this type of test, and the word caught on, particularly because of its incorporation into the operon model with the idea of polycistronic mRNA. His other coinings, muton and recon were not adopted.
The two T4 genes/cistrons in the rII region of the phage genome are now called rIIA and rIIB.

Benzer, S (1955) Fine structure of a genetic region in bacteriophage Proc. Natl. Acad. Sci. USA 41:344-354

Really nice answer.

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


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Reusable microarray chips
Microarray chips allow us to conduct many expression experiments in parallel to each other but they can be used only once as far as i know. Are there reusable microarray chips? Have people ever tried it? If there are, are they becoming more common? If people do not choose to use them even though they are in the market, what can be the reasons?

As far as I am aware, there are no commercially available re-usable microarrays. The reason for this is most likely that the arrays are really sensitive and you run into the trouble with false positive signals. I have once seen a microarray which has been stripped and still delivered quite some signals in areas which had a strong signal before.
You have to make sure to strip all the hybridized samples from the chip without damaging the probes which are bound on the surface. I think the trade-off between "everything is off" and "some sample is still bound" is not good enough. Who wants to risk false positive signals and possibly retract publications on this basis? You may also loose weak signals which are hidden under false-positive signals.


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Where do butterflies sleep?
Do butterflies (insects) sleep, and if so, where??
I have googled for information but didn't get an exact answer.

It would be better to say that they go into an inactive, low metabolic state. This low metabolic state is often driven by the temperature in the air itself; ectothermic butterflies require outside heat-energy to become active. Basically they use this time to digest their food and produce sperm/eggs. (reference). At night, or during inclement weather, most butterflies perch on the underside of a leaf (this provides them with a bit of shelter from the rain and makes them less noticeable to prey), crawl deep between blades of grass or into a crevice in rocks, or find some other shelter to rest (reference).  In short, I would not call it sleeping but just a state of rest. Butterflies cant even close their eyes from the lack of eyelids (reference).


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How Behind is the Human Mind (Latency of the Senses)
I would like to know if there is any research into the latency of human perception.  Particulary:

What is the minimum time for various inputs (vision, touch, sound) to be recognized by the conscious mind?
How different are these times?  (Loud sound vs sense of touch in your toe)
Given the above, is there a number we can put on how many milliseconds behind reality the human mind is?

are you the same person from the youtube channel that makes the picture videos or are you just using his name?

I'm the guy from YouTube.

awesome to know.. i am subscribed to ur channel.. fan of ur work..  this probably is ur next project.. will try and answer ur question if i get good references..

There is a huge amount research into this subject. It is vast and nebulous as such I cannot give you an overall picture of this. I can however illustrate some of the complexities to this.
Firstly I would say that what you mean by human perception is extremely complex, there are different modalities of perception. For example in terms of a visual stimulus, we may simply perceive its basic shape, outline, colour, whether or not it is moving. We then may also perceive higher levels of information such as the function of the object. Similarly there are different aspects to other stimuli.
These different components of perception are transmitted by different neurons leading to the brain and then processed by different areas of the brain suited to specific tasks and then are integrated together to give us a conscious idea of what the object is.
Therefore when measuring the latency of human perception you would first have to decide what exactly you mean by this?
The other aspect is that a lot of study has occurred in this area as we are aware that perception can be altered by states of illness (for example audio evoked responses in schizophrenia, or visual evoke responses in multiple sclerosis). The perception of pain is yet another huge area of study.
Again this is such a vast area of research that I wouldn't really know where to point you to. However for a entertaining read on how perception can change in neurology I would recommend reading the books of Oliver Sacks, in particularly "The Man Mistook His Wife for a Hat" and an "Anthropologist on Mars".
I am sorry I haven't provided you with more detail but good luck in reading around this subject. If you are more specific about what perceptions, (e.g. perception of faces, perception of danger etc..) then maybe you will receive more specific answers.

If I had to pin it down, my question is really 'how far behind the current moment is the conscious mind?'

Again that is very difficult, first of all there is no real understanding of what consciousness is, and we also know that we become consciously aware of different things at different rates. This conscious awareness is highly variable. Take the conscious awareness of pain, this is highly dependant on type of pain, where it happens, what your underlying state of mind is. How would we ever measure such a thing? What we do know are things like reaction times, how long it takes for various stimuli to reach the brain, how we process input on different levels, etc.


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Thrombus and Embolii
Can treatment of thrombus cause embolism, in case of very high blood pressure, that may even lead to a heart attack ?
As the very high Blood pressure may cause some of the enzymes not act completely on the thrombus and release emboli in the blood stream ?

Which treatment of thrombus are you talking about? Angioplasty or thrombolytics?

Yes, treatment of thrombus can cause embolism. Hypertension favors hemorrhagic complications.
Thrombolytics:
Yes, they can cause paradoxical embolism, although it is a rare complication [1]. The most fearful complication of thrombolytic medication is major hemorrhage. And hypertension favors bleeding [2].
Catheter-directed thrombolysis:
Hypertension (more than 180 mmHg and associated with congestive heart failure) was found to increase hemorrhagic complications [3].
Angioplasty:
Angioplasty produces some embolic particles [4]. However, using embolic protection is disputed [4, 5].

References:

Liu YF, Bayliss M. Paradoxical embolism: a rare complication of thrombolysis. Emerg Med J. 2008 Mar;25(3):180-1. doi: 10.1136/emj.2007.053934. PubMed PMID: 18299379.
Meneveau N, Vuillemenot A, Bassand JP. [Complications of thrombolytic therapy in pulmonary embolism]. Arch Mal Coeur Vaiss. 1995 Nov;88(11 Suppl):1769-76. PubMed PMID: 8815838.
Agle SC, McNally MM, Powell CS, Bogey WM, Parker FM, Stoner MC. The association of periprocedural hypertension and adverse outcomes in patients undergoing catheter-directed thrombolysis. Ann Vasc Surg. 2010 Jul;24(5):609-14. doi: 10.1016/j.avsg.2009.12.011. PubMed PMID: 20413257.
Malik RK, Landis GS, Sundick S, Cayne N, Marin M, Faries PL. Predicting embolic potential during carotid angioplasty and stenting: analysis of captured particulate debris, ultrasound characteristics, and prior carotid endarterectomy. J. Vasc. Surg. 2010 Feb;51(2):317-22. doi: 10.1016/j.jvs.2009.08.063. PubMed PMID: 20006918.
Divani AA, Berezina TL, Zhou J, Pakdaman R, Suri MF, Qureshi AI. Microscopic and macroscopic evaluation of emboli captured during angioplasty and stent procedures in extracranial vertebral and internal carotid arteries. J. Endovasc. Ther. 2008 Jun;15(3):263-9. doi: 10.1583/07-2326.1. PubMed PMID: 18540698.

Those complications which the above mentions is not necessarily talking about due to embolic events, the tPA interferes with clotting and as such can lead to events such as haemorrhagic stroke. But yes thrombolitics can cause emboli. Using the treatment is weighing up the effects of ischaemia due to the thrombus vs risk of the treatment.


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Source of hydrogen in reduction of oxygen in electron transport?
What's the source of hydrogen in the reduction of oxygen to water in metabolism?

Is this implying that half the hydrogen comes from NADH and the other half from lone protons?

I don't think they're implying that; they've just combined the two half reactions. NADH doesn't interact directly with oxygen (it is oxidized at complex I). I think that the protons used in the conversion of oxygen to water are, ultimately, free in solution.

The equation you've shown is similar to other cellular respiration equations that I've seen, in that, it is trying to simplify a pretty complex process.
My guess is that you're doing first year cell biology like I am, so you probably know that there is a difference between the pH of the mitochondrial matrix (7.8 - making it alkaline) and the inter membrane space (roughly that of the cytosol - usually about 7). The lower the pH of a solution, the greater the concentration of H+. My point is that the solutions on either side of the inner mitochondrial membrane both have a concentration of H+.
So even though, when NADH is oxidised, it loses a H+ to solution, thereby contributing to the pH of the mitochondrial matrix, what is the likelihood that that particular H+ will be the H+ that is part of the molecule that takes the electrons at the end of the electron transport chain? I think low.
Indirectly, NADH does contribute H+ to the overall pH of the mitochondrial matrix but it doesn't directly give the H+ to "half an oxygen gas molecule".
Check the video below which is from the publisher of the textbook my course uses.
http://www.garlandscience.com/garlandscience_resources/resource_detail.jsf?landing=student&resource_id=9780815344544_CH14_QTM02

So the proton source is water? Also I'm not doing first-year bio. If I showed you the rest of the slide you'd be scared ;).

So what are you doing? :)
Proton source is not water its the solution in the mitochondrial matrix.

What do you mean the proton source is the solution?

I'm not sure I can explain it any better than I did in my first answer. Sorry I can't help.

It's okay; the problem is that the proton is not found alone in water; it's hydrated. If you are suggesting that the proton source is in the solution, then the most likely source is water, and not hydronium ion or any hydrated derivatives of the protons because heteroytic bond clevage is less costly when it only has to be performed twice - i.e. on water - rather than thrice - i.e. with hydronium ion.

But isn't a hydronium ion a lot less stable than a H2O molecule? Did you look at the video I linked? At the end, a molecular oxygen combines with four protons to form two water molecules. Wouldn't it make sense for four protons to come from 4 hydronium ions? I don't know though, I'm just a first year Biomedical Engineering student :) and I definitely wouldn't say I have my chemistry down.
Based on your question, I thought a more simplified answer about the proton source would be sufficient, but obviously its a higher level chem subject you're studying..?

Hydronium is much more easily ionized than water. Thus you could expect that that four hydronium ions would each donate a proton as oxygen is reduced.


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Is WIFI safe for humans?
I have wifi on at my home almost all the time. I learned that the frequency of visible light is around several hundreds of THz, while the frequency of wifi is only several GHz, which is only 1:100,000. But I'm not sure how the amplitude of wifi wave compares to the amplitude of the visible light? Are the frequency and the amplitude the only concerns when we talk about the radiation? Can someone educate me to quantify the effect wifi radiation could have in our life?

Welcome to BiologyBeta.SE. Your question is off-topic here. It would be on-topic on Skeptics.SE. But before asking, notice that this post probably already answers your question.

what is being said here is that there is not enough evidence to sustain a conclusion here, and so its not a great question for this site.  on the other hand you can also take that as the answer to your question.

so digging a little more into your question , this might also be a physics question.  there are two aspects of electro magnetic radiation which are good places to start.  first is the power of the signal, which is related to amplitude and frequency of the wave, but is on the order of Watts usually. The second is how often the frequency of the radio wave is absorbed by the body and what.  that is much more controversial.  1 GHz waves are have a wavelength of about 30 cm - or about a foot.  this is why radio waves tend to pass through walls and through bodies.  Can this still be harmful?

its not a strong number. but small amounts of power concentrated in tiny spaces can be harmful.  so that's the controversy.  Its hard for many of us to believe that a fraction of a watt deposited extremely rarely in the body can be harmful in an extraordinary way.  (say more than commercial radio transmissions)  but its very hard to say it isn't with enough confidence to shut off speculation. so that might give you an idea of what sort of answer you might get.

Thanks @shigeta, actually I asked the same question at http://physics.stackexchange.com/questions/119806/is-wifi-safe-for-humans before I asked here, but unfortunately I met a group of politicians.

@shigeta thanks for your idea. So how do you think if we are exposed to our home lamp vs to the home wifi? Can I say the radiation from the visible light from home lamp is much stronger than it from the wifi?

yes but also visible light does not penetrate the skin (much).  there's really no way to definitively end the argument. that's why you might have gotten some static here.  although that is also true for most scientific questions too - very few scientific papers definitively come to a proof of one thing or another.  a lot of people ignore this when calling questions 'subjective'.


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Could an annual plant be genetically modified to be a perennial?
My chives, asparagus, oregano, and rhubarb come back every year like clockwork.  Suppose I want my bok choy to join the party - is there an "I'll be seeing you next year!" gene that can be modified to be turned on to be like my hardy chives, or is it more complicated than that?

It is definitely more complicated than that.

@Chris But they just need a rhizome system to store nutrients for the winter right?

the plant's genes are all adapted in countless ways to optmize the out come for the annuals for their current lifestyle.  it would take a lot of effort, re-engineering many aspects of the plant's genome.  In the end you would have a very different plant if you could do it.  it sounds almost like a manhattan project of plant biology in scale.

Researchers at Ghent University have made a discovery that downregulation of the proteins CONSTANS 1 (SOC1) and FRUITFULL (FUL) lead to the development of many perennial traits in annual plants (in the study Arabidopsis thaliana is used) (reference).
The CONSTANS gene controls flowering in Arabidopsis thaliana (reference).
FRUITFULL (FUL) is an MADS box gene that functions early in controlling flowering time, meristem identity and cauline leaf morphology and later in carpel and fruit development in Arabidopsis thaliana (reference).
The process is complicated and would need many genes to be manipulated but this research proves that it is possible. Another article of interest.


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Ion Channel gating
I have been studying ion channels and there is one thing i am confused about, gating between open and closed states in channels.
Am i right in thinking gating is so fast that it is effectively always open for ion flow? So that if ten ions flow through a channel, then one can imagine that the channel opens and closes so quickly it is basically always open for the flow of the ten ions, or does a channel open allow one ion through, close and then open again for the next ion?

There are several types of channels, but probably the type you are referring to is voltage gated ion channels.
The state in which these channels are, open or closed, depends on the action potential across the cell membrane.
If the potential is at the correct energy for the channel to be open it will remain open allowing a steady flow of ions through. Once enough ions have passed so that the potential across the membrane changes to meet the deactivation energy, the channel will close. It then enters a refractory period which requires repolarisation across the cell membrane so that the ion is reset ready to open and let ions through again.
Different ion channels have different activation potentials, deactivation potentials and different refractory periods. This results in different rates of opening and closing.
So based on the above, in answer to your question, no gating is not so fast that it is always open. There are significant periods of time where channels are closed allowing no flow of ions and significant periods of time where they are open allowing continuous flow of ions.


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What's the difference between diuretic veggies and alcohol that make the latter bad?
So I'm reading this article to Treat Fluid Retention and it suggests

Eat foods with diuretic properties.

But also

Avoid drinks that will dehydrate the body such as tea, coffee and alcohol.

As I understand, tea, coffee and alcohol are plenty diuretic. So what makes those veggies's diuretic nature better than alcohol's?
I know alcohol is more harmful than veggies, but I mainly wanted to know how do diuretic veggies help you when infact the diuretic alcohol actually makes you dehyderated? How's veggies' diuretic nature more helpful than the alcohol's (disregarding other side-effects of it)?

This question is primarily concerned with the mechanism behind a supposed effect of certain vegetables, and does not ask for any treatment suggestions. Voting to reopen.

Firstly I would suggest if you have concerns about suffering from symptoms fluid overload you should consult your doctor. Self diagnosis and self treatment is not a good option.
In terms of alcohol being used as a diuretic, you have to bear in mind that there are many deleterious effects of excess alcohol. By consuming alcohol as a diuretic you would most likely cause more health problems than you solve.

I was just researching remedies for Puffy face, nothing too serious. I know alcohol is more harmful than veggies, but I mainly wanted to know how do diuretic veggies help you when infact the diuretic alcohol actually makes you dehyderated? How's veggies' diuretic nature more helpful than the alcohol's (disregarding other side-effects of it)?


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What is doubling of genetic material invented in flowering plants?
David Attenborough in his Kingdom of Plants 3D said, that flowering plants made two inventions: (1) doubling of genetic material and (2) symbiosis with animals.
What was meant by "doubling of genetic material"? Appearing of diploidy or something else?
UPDATE
Let me explain my doubts. Inventing of ploidy I regard as inventing of sex and syngenesis. This was done ~500 million y.a. in Ediacarian, if I am not mistake. Hence, this can't be done 140 m.y.a when flowering appears. I.e. both plats and insects had sex 140 mya.

Yes, D. Attenborough probably refers to ploidy number
Ploidy number
Humans for example are 2N (except during the spermatozoid and ovule phase of human existence) meaning that they carry two copies of each autosome (=non-sexual chromosomes). Some species are 1N (haploid), some are 3N (triploid), etc… It would actually be more correct to talk about the time a species spend in each of its phase or talk about the number of cells in each of its phase because many species undergo change in chromosome number during their existence as it is the case for humans. Humans are 2N most of the time but they are 1N when they are ovules or spermatozoid. The correct word to describe the human lifecycle is diplontic. Some species are diplontic, some are haplodiplontic and some have phases when they have a greater number of chromosomes. Those species are said to be polyploid.
Ploidy number, chromosomes and chromatids
To make sure one don't mix up things... One chromosome is made of one or two chromatids (depending on the cellular phase). The chromatids of the same chromosome (called sister chromatids) are (almost completely) identical. A given "chromosome type" is either alone (1N) or accompagnied by one very similar chromosome (2N) or two other very similar chromsomes (3N), etc.. Considering the case of a 2N individual: If at a given locus (position in the chromosome) the two alleles (gene variant) are different than the individual is said to be heterozygote for this locus. The ploidy number describe "this number of chromosomes"! Now there may have different number of different "types of chromosomes". Humans for example have 23 different types of chromosomes and in its haploid phase has therefore 23 chromosomes (23 or 46 chromatids depending on the cellular phase) and has 46 chromosomes (46 or 92 chromatids depending on the cellular phase) in its diploid phase
Ploidy number in angiosperms and other plants and non-plants organisms
Yes, D. Attenborough (who I don't know and I haven't read anything of his work) probably means doubling, tripling, quadrupling, .. the number of N of chromosomes. And, yes indeed polyploidy (3N, 4N, 6N, 8N) is relatively often observed in flowering plants. There are many crop species that are polyploid. According to this article an important part of the speciation that occurred in plants is accompanied by a change in ploidy number but this is not only true for angiosperms.
Polyploidy is also found in many fungi species and some animal species as well. There are lots of terminologies linked with the discussion of chromosome number and reproductive system and many articles discuss these mechanisms and also the evolution of polyploidy. I found the work of Sally Otto to be of the greatest interest for example.
Notes
The words inventions are not really used in evolutionary biology but rather in popular books. Also, there are many non-angiosperm plants that have symbiotic relationship with animals. For examples: some angiosperms and the squirrels or birds. But it is true that angiosperm have particularly important symbiotic relationship with animals, in particular insects and this probably allowed an important diversification in both angiosperms and insects. As already said angiosperms are not the taxon of plants to include polyploid species. There are other characteristics that allow to tell an angiosperm apart from other plants. The number of aperture on pollen grain or the positions of the meristems (tissue where mitotic division of unspecialized cells occur allowing the growth of the plant) for examples.
You may be interested in reading this post on the effect on fitness of ploidy number

I haven't seen this particular film, but other documentaries by Dr. Attenborough are very accurate and well done.
In contrast to Remi.b, I'm pretty sure Attenborough referred to the ancient whole genome duplication event in land plants recently discovered in angiosperm genomes by the presence of multiple paralogous genes. The scenario is that at a certain moment either a hexaploidization or a genome fusion event occurred and was followed by gene losses, chromosomal reorganizations and gene diversification. In Selaginella, a spikemoss, no traces of this event were found.
A similar event, a tetraploidization, is hypothesized for vertebrates.


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How is information sent from the skin to the brain?
Say you have a needle, and you poke a very specific area on your left thumb.
A signal gets sent from that nerve up your spine and into your brain.
How does the brain know exactly where this signal has come from to such accuracy?

Does each nerve in every conceivable part of the body have a unique path that goes up the spine and into the brain, so that's how the brain knows where it came from?
Or does the nerve encode the signal as data which travels up a generic nerve, and the brain decodes the information, which contains the "address" of the particular spot that was stimulated? If this is the case, how are the data encoded? Binary?

For a quick primer, see http://en.wikipedia.org/wiki/Receptive_field#Somatosensory_system, but hopefully I (or someone else) can come along and fill in the gaps in a bit.

Ok so that explains the receptors and their surface area. How do these signals then reach the brain and how does the brain know exactly where the signal comes from?

Cross-posted on Cognitive Sciences...

@user2721465 I will try to address some of these questions in my answer.

In addition to what Spinoral has said, and in response to your comment above, I will add a bit more about the mechanisms.
Essentially, in some form or another it's receptive fields all the way up.
A brief outline of the anatomy:
The cells from the spinal cord are pseudounipolar and have their cell bodies in the dorsal root ganglia in the spinal cord.  The other "leg" of the sensory neuron projects to the medulla, which has cell bodies which send axons to the VPL thalamus, which then has cell bodies that project to the primary somatosensory cortex.  There are points of decussation (crossing over the midline), but I'll ignore those for now.
The receptive fields:

The receptive fields of somatosensory neurons share much in common with the receptive fields of visual neurons. As for visual neurons, the somatosensory receptive fields comprise a restricted 2-dimensional region of space where a stimulus can evoke a neuronal response. In somatosensory neurons, however, space refers to a region of the body and the stimulus can be touch, vibration, temperature or pain

(from Scholarpedia)
Essentially, the somatosensory input is "filtered" at all of those stops along the way and refined in terms of things such as whether the sensation came from the center or the edges of the receptive field, etc.
Cells in the cortex (the waypoint for the sensory information) are organized in microcolumns, which are representative of a particular location on the body (and arranged topographically into the "homunculus", as the other answer mentions).
All of this follows what is called the "labeled line" theory, which is getting a bit outmoded due to new knowledge about ensemble coding in neurons, but for purposes of the somatosensory system it still holds up pretty well.

This is a bit of a work in progress, but it should give you some terms to google, etc.

Great, thanks this is exactly what I was looking for. So there's 2×10^8 minicolumns in the cortex corresponding to places on the body. Does that mean that there's roughly an equal amount of sensory neuron pathways in the spinal cord correlating to these minicolumns?

@user2721465  It's not necessarily a 1-1 relationship between skin receptive field and column in the cortex (there are higher level "abstractions" in the cortex such as orientation of the stimulus, etc.).  Since the information is being "filtered", there are complex relationships between the thalamic cells, and there's some degree of consolidation that goes on.  The bundles of axons are converging on the cord at different levels (see a map of the dermatomes for the mapping), but the tracts are quite thick anatomically, so there's many thousands of axons in one nerve bundle.

(for example, the roots for the arms enter between the vertebrae of the cervical region -- http://en.wikipedia.org/wiki/Dermatome_%28anatomy%29, legs in the lumbar, etc.)

If this is something that you are interested in, the rat whisker system is the model used for decoding some of these pathways.  The earlier connections are different (it's a nerve that goes directly to the brainstem), but the cortical layout is similar.

The accuracy of sensation is actually quite variable depending on the region of our body. Highly innervated areas such as our fingers have a higher degree of accuracy than sparsely innervated areas such as our legs.
There is a simple experiment you can do to illustrate this. Close your eyes and then get a friend to lightly and slowly run their finger from your wrist, up towards the bend in your elbow on the inside of your arm. Try to guess at what point the reach the joint of your elbow.
In terms of how the brain knows where it came from,  there is part of your brain called the sensory cortex. This sensory cortex has a pattern that corresponds to areas of the body. This pattern is known as a the sensory homunculus (google images will find this). As signals pass up the various different spinal pathways and into the brain they are sent up to this sensory area and the appropriate region of the homunculus is stimulated thereby giving the sensation in the appropriate body area.
Interestingly in some brain surgery a patient may be kept conscious so that these areas can be directly stimulated by electric current and the patient will experience sensations.
There is also a matching area, called the motor cortex, which corresponds to movement rather than sensation.
The above is a simplified version of what goes on and there is lots more detail which would be covered in neuroanatomy books

Ok, so the signal from the nerves travels up the spinal pathways into the sensory homonculus.
Does the sensory homonculus know where the signal came from because a specific spinal pathway is used which is unique to each area of the body or is it because the signal is encoded in a particular and unique way?

Due to specific spinal pathways, but my point with the experiment and the arm is that this is not as accurate as you may perceive it to be.


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TB disease - treatment and infection
Background: I'm currently performing research in mathematical biology,
specifically on the treatment dynamics of HIV and TB co-infection.
Question: Can a person infected with TB disease, who are undergoing treatment for it, infect a person with no history of TB bacteria in their body?
Reformulation: In other words, is there a similar analogue for TB as for HIV, wherein an HIV+ person undergoing treatment for HIV will have a lowered viral load and thus have negligible chances of infecting a person with no history of HIV?
Please note that my model does not incorporate latent TB because it would become too complicated to analyze. I am focusing only on TB disease because only it is infectious.
Thanks for any help.

Is the focus of your model also referring only to respiratory TB or TB infection in general?

First there is one major difference between HIV and TB: As long as the TB bacteria are still susceptible to treatment (which is developing into a major problem in some regions of the world) there is a effective treatment which can eradicate the infection. For HIV this is not possible. Here we can only lower the viral load (sometimes under the detection limit), but when the treatment is stopped, the virus will return.
Then it seems that patients under treatment of a drug susceptible TB are infectious for a longer time than previously thought. Until now they have been isolated at the beginning of the treatment (typically around the first two weeks) until three consecutive sputum samples had been negative. Then they were released from isolation and thought to be non-infectious. At this point they are not cured, the treatment has to go on for several weeks.
Now there is newer research indicating that patients can still be infectious although they are under treatment and have negative sputum samples. It seems here that the currently used detection method is not sensitive enough. See these references for more information:

How Many Sputum Culture Results Do We Need To Monitor
Multidrug-Resistant-Tuberculosis (MDR-TB) Patients during Treatment?
High incidence of tuberculosis, low sensitivity of current diagnostic
scheme and prolonged culture positivity in four colombian prisons. A
cohort study.
Prolonged infectiousness of tuberculosis patients in a directly
observed therapy short-course program with standardized therapy.

I think its a bit difficult to compare HIV and TB this way because TB is transmitted mainly through respiratory droplets whilst HIV is mainly through contamination of blood products/sex, etc but not via the respiratory route. As far as I know, there's still a likelihood of TB transmission from a treated patient to an untreated patient. TB is quite complex, treated patients can still undergo reactivation later in life and still infect other people-the mechanisms are not fully understood. Treated patients can also develop drug resistance and then relapse which will make them again highly infectious.


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Which part of human eyes is getting tired?
It's a thing of common sense that if you read, drive or look at computer screen for too long your eyes will get tired. They burn, itch and try to close all the time.
But I was wondering which part(s) of them need rest so much... Blinking muscles? Lense muscles? Or the eyeball is drying out?

These symptoms have a name: Computer vision syndrome.
Basically our eyes are made to look at longer distances from 1-6 meters without much accommodation. Typically computer screens are located at a much closer distance (30-50cm), which requires constant accommodation by the eye. This leads to high stress on the muscles in the eye which subsequently get tired. Additionally less blinking leads to drier eyes.
One of the common recommendations against this is to regularly focus further located objects to give the eye the chance to relax. This is sometimes called the "20-20-20" rule, every 20 min focus on a 20 feet (about 6 m) far object for 20 seconds. See the article in the Wikipedia and here for more information (and probably also the linked references in the articles).

Was there any success using lenses to make screen appear 6 meters away?

This would be like you sit 6m away from you screen: It would most like be too tiny to read anything.

You could sure make it look 6meters high using proper optics. I heard screens in fighter aircrafts are on the cockpit and appear to be on the sky, so that the pilot does not need to change focus.

Then you need to turn the head quite a lot to read everything. And my guess for the screens in fighter jets is that they are further away than the typical computer screen.

This doesn't answer the question of which muscles are getting tired.

I haven't found any specific information on that. Otherwise I would have added it to the answer.

Wouldn't the muscles that allow the eye to focus be the ones getting tired?


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Is epimysium same as fascia?
I have read that epimysium is dense regular connective tissue made covering the a muscle like bicep brachi. at the same time we have fascia that is made of dense regular tissue and covers muscles. so are they same or different how can we describe it and differentiate it?

Epimysium is the specialized fascia located at the muscle.

Epimysium is a layer of connective tissue, which ensheaths the entire muscle. It is composed of dense irregular connective tissue. It is continuous with fascia and other connective tissue wrappings of muscle including the endomysium, and perimysium [1].

The fascia that covers muscle is named deep fascia:

The deep fasciae envelop all bone (periosteum and endosteum); cartilage (perichondrium), and blood vessels (tunica externa) and become specialized in muscles (epimysium, perimysium, and endomysium) and nerves (epineurium, perineurium, and endoneurium) [2].

References:

Wikipedia contributors, "Epimysium," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Epimysium&oldid=540536396 (accessed June 27, 2014).
Wikipedia contributors, "Deep fascia," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Deep_fascia&oldid=593605746 (accessed June 27, 2014).

As I understand it epimysium is not only fibrous but also contains more elastic fibres than fascia. As such it is more 'loose' than the 'dense' fascia.  It lies immediately on the surface of the muscle (epi = on, mysium = muscle) below the fascia. The deep fascia which is denser lies on top of this.

Fascia is a widely used yet indistinctly defined anatomical term that is concurrently applied to the description of soft collagenous connective tissue, distinct sections of membranous tissue, and a body pervading soft connective tissue system. Inconsistent use of this term is causing concern due to its potential to confuse technical communication about fascia in global, multiple discipline- and multiple profession-spanning discourse environments. The Fascia Research Society acted to address this issue by establishing a Fascia Nomenclature Committee (FNC) whose purpose was to clarify the terminology relating to fascia. This committee has since developed and defined the terms a fascia, and, more recently, the fascial system. This article reports on the FNC's proposed definition of the fascial system.
Reference:
http://www.bodyworkmovementtherapies.com/article/S1360-8592(16)30259-5/fulltext

"A fascia"
A fascia is a sheath, a sheet, or any other dissectible aggregations of connective tissue that forms beneath the skin to attach, enclose, and separate muscles and other internal organs.
"The fascial system"
The fascial system consists of the three-dimensional continuum of soft, collagen-containing, loose and dense fibrous connective tissues that permeate the body. It incorporates elements such as adipose tissue, adventitiae and neurovascular sheaths, aponeuroses, deep and superficial fasciae, epineurium, joint capsules, ligaments, membranes, meninges, myofascial expansions, periostea, retinacula, septa, tendons, visceral fasciae, and all the intramuscular and intermuscular connective tissues including endo-/peri-/epimysium.
The fascial system interpenetrates and surrounds all organs, muscles, bones and nerve fibers, endowing the body with a functional structure, and providing an environment that enables all body systems to operate in an integrated manner.
Reference: http://www.bodyworkmovementtherapies.com/article/S1360-8592(16)30259-5/fulltext


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Where do trees get their shape?
Does anyone know any good resources dealing with shapes of trees?
For example, pine trees are cone shaped for optimal absorption of sunlight, but lone pine trees growing in isolation (and other commonly cone shaped conifers) often grow very high above ground and have no well-defined shape. Presumably, when there aren't neighbours to compete with for sunlight or space, the optimal shape is..well, whatever shape absorbs most sunlight; less constraints = more possibilities.
Looking for an answer that explains this sort of phenomenon. Thanks.

Dr Karl Niklas from the Cornell University has written a book about the effects of factors that influenced the shape of early trees. He created a computer model in which he drew trees in the shape that favored particular characteristics.

When Niklas favored plants that could gather light from the sun, they
  had non-overlapping horizontal branches. When reproductive success was
  favored, the plants grew tall, in order to spread their seeds. When
  the trait selected for was mechanical stability, the plants had few
  horizontal branches.

When he combined these three favourable traits, he noticed that most of the trees today are in a form that favors these three traits (reference).

L is light favourability, M is mechanical stability and R is the shape of trees that favor reproductive ability.
Explanations for a few shapes found commonly with examples can be found in this article.
Illustration for the common tree shapes Columnar, Pyramidal,Vase, Round, Spreading, Weeping and umbrella with a few more examples can be found in this article (reference).
Another interesting thing about trees is the way in which their shapes can be influenced for the purpose of landscaping (reference).
What you mentioned about pine cones in isolation having no definite shape at all, I would like to see a reference that this is a fact before I can elucidate on it further (I couldn't find any articles that mentioned such a phenomenon).
The reason you felt so could be because it were two completely different species of pines. Counting varieties and subspecies, the plant list of the Royal Botanic Gardens, Kew and Missouri Botanical Garden accepts 175 names of pines as current(reference). Here is a list of different pine species (reference).
Here is an article on how tree shape and light available influence yield in cherry trees.

Nice visuals. I was looking for a resource like that, but couldn't find one.

Please accept this answer with a checkmark

Note lone pines can also be subject to high winds which can further distort their shape, sometimes  extremely so, wind twisting or knee wood can nearly unrecognizable as the same species as specimens not under windy conditions.

Plants are genetically programmed to grow in certain shapes; many are subject to apical domination, but it's a very complicated subject, involving exterior influences such as extreme wind causing different growth, and a host of other environmental factors, together with auxin and other plant hormones impacting within the plant itself. The basic tree shapes are columnar, weeping, pyramidal, horizontal branching, vase shaped, round or globular, and all these shapes are programmed in the genetics of the plant. There is a book I know of called Dynamic Models of Plant Growth by Nikolai Bessonov, but it contains an awful lot of scientific biology stuff - I don't know of any simpler books.


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Carbon Monoxide and High-Oxygen-Affinity Varieties of Hemoglobin
I recently learned about the concept of "affinity" in regards to hemoglobin. For hemoglobin in humans, carbon dioxide has a lower affinity than oxygen, which allows gas exchange to occur in our lungs.
Carbon monoxide is problematic for us because it has an even higher affinity to hemoglobin than oxygen does. This means that our red blood cells will not exchange carbon monoxide for oxygen in our lungs.
My question is: for high-altitude-adapted organisms such as the bar-headed goose, whose hemoglobin has a higher affinity to oxygen than ours does, is carbon monoxide still poisonous?

As carbon monoxide binds to the same place in the heme as oxygen, I would expect that. The question is if the difference between a "normal" hemoglobin molecule and one from a altitude adapted bird does really matter.

I don't know about the makeup of bar-headed goose haemoglobin, but fetal haemoglobin (HbF) has a higher affinity for oxygen and a lower binding of carbon monoxide than HbA (http://bloodjournal.hematologylibrary.org/content/bloodjournal/33/1/37.full.pdf?sso-checked=1). If the goose haemoglobin behaves similarly it may also have lower affinity for carbon monoxide.

My question is: for high-altitude-adapted organisms such as the bar-headed goose, whose hemoglobin has a higher affinity to oxygen than ours does, is carbon monoxide still poisonous?

Yes. To put out a few other facts from the Stritch School of Medicine:
CO has 250 times the affinity for hemoglobin than O2
Hb becomes 100% saturated with CO at PCO = 0.6 mm Hg
Hb becomes 100% saturated with O2 at PO2 = 600 mm Hg

What does that mean? Well, that means that when the partial pressure of CO is 1mmHg, you're well and truly dead. So if the bar headed goose could survive in an environment more than 1% CO its hemoglobin would have to bind to molecular oxygen very, very tightly below 1mmHg. If this was true you would expect their binding curve to reach a high % of O2 saturation below a partial pressure of 1mmHg. Does it exhibit that?

Nope. At 1mmHg (remember, CO has 100% binding at 0.6mmHg) the bar headed goose hemoglobin's saturation is less than 2%. In fact, they're pretty similar to humans:

Is this casual glance conclusive? Well... Not entirely. I couldn't find any carbon monoxide data for the bar headed goose, but to overcome the 250x higher affinity for CO the goose's hemoglobin would have to be very, very different from that of humans while still exhibiting a similar binding curve. I've not received the education to determine if that's possible or how it would occur, but it is a very remote possibility.
Erring on the side of "most likely", however, I think it's safe to say that given a room filled with 1% CO you'd end up eventually killing anything that relied on hemoglobin to move necessary oxygen to tissues.

Do you have references for your images and graphs?