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Is honey in hot green tea unsafe?
I used Google to try to figure out what kind of mixture honey has with hot water, and I found several Ayurvedic sources claiming that honey in hot water is toxic.
For example:

Honey – NEVER Put It in Hot Water/Teas
5 Reasons You Should NEVER Cook With Honey
Honey: A Must Read For Those Who Eat It Regularly

What I would like to know is how does heating honey make it toxic?
Is there something that happens at the molecular level that changes the chemical properties of honey when it is heated? If so, are these chemicals harmful, as claimed?
Are there any other reasons other than heating that may make honey toxic?

Could you provide references to your claim?

I assume you are talking about sites like http://markbunn.com.au/honey_never_in_hot_water/ or http://www.mockingbirdmeadows.com/2013/11/19/reasons-you-should-never-cook-with-honey/ ? Basically claiming that heating honey will kill us all (well, maybe not kill, just make us very sick)?

@YviDe, I added some information from an Ayurvedic Research journal that addresses those issues. There concern is an increase in HMF, but HMF is a breakdown product of hexoses, and will be found in anything that contained fructose and glucose that was heated, not just honey. However HMF has not been found to be correlated to any illnesses in humans, so the significance of the find is questionable.

I am voting to reopen this question. In answering the question, I realized that there was a biochemical process at work when honey is heated that transforms hexoses into hydroxymethyl furfuraldehyde. As such, there the question and its answer would be relevant from a biochemistry. I have edited the question to bring it more in line with a question on topic for Biology S.E while trying to maintain the question the OP was trying to find out which is what makes heated honey toxic and is honey in tea safe to drink.

Nice edits @AMR

Heated Honey and HMF
In this paper, Studies on the physicochemical characteristics of heated honey, honey mixed with ghee and their food consumption pattern by rats, by Annapoorani, et.al.;International Quarterly Journal of Research in Ayurveda, 2010 Apr-Jun; 31(2): 141–146.doi:  10.4103/0974-8520.72363, the report finds a statistically significant increase in the compound hydroxymethyl furfuraldehyde (HMF).
The compound was studied by the National Toxicology Program of the U.S. Department of Health and Human Services in Mice and Rats and the results were published in a report dated June of 2010.

5-(Hydroxymethyl)-2-furfural is formed when reducing sugars such as fructose and sucrose are heated in the presence of amino acids. 5-(Hydroxymethyl)-2-furfural is ubiquitous in the human diet and occurs at concentrations greater than 1 g/kg in dried fruits, caramel products, certain types of fruit juices, and up to 6.2 g/kg in instant coffee. 5-(Hydroxymethyl)-2-furfural also occurs naturally and has been identified in honey, apple juice, citrus juices, beer, brandy, milk, breakfast cereal, baked foods, tomato products, and home cooking of sugar and carbohydrates.

- NTP toxicology and carcinogenesis studies of 5-(Hydroxymethyl)-2-furfural (CAS No. 67-47-0) in F344/N rats and B6C3F1 mice (gavage studies).; Natl Toxicol Program Tech Rep Ser. 2010 Jun;(554):7-13, 15-9, 21-31 passim.
HMF is a breakdown product of Fructose, Glucose, and Cellulose (hexoses) and is found in many products, especially high fructose corn syrup, after heating, and is excreted in the urine. However, it has not been correlated to any diseases in humans (4). In the NTF toxicology and carcinogenesis studies, the conclusions were that

under the conditions of these 2-year gavage studies, there was no evidence of carcinogenic activity of 5-(hydroxymethyl)-2-furfural in male or female F344/N rats administered 188, 375, or 750 mg/kg. There was no evidence of carcinogenic activity of 5-(hydroxymethyl)-2-furfural in male B6C3F1 mice administered 188 or 375 mg/kg. There was some evidence of carcinogenic activity of 5-(hydroxymethyl)-2-furfural in female B6C3F1 mice based on increased incidences of hepatocellular adenoma in the 188 and 375 mg/kg groups. Administration of 5-(hydroxymethyl)-2-furfural was associated with increased incidences of lesions of the olfactory and respiratory epithelium of the nose in male and female rats and mice.

- NTP toxicology and carcinogenesis studies of 5-(Hydroxymethyl)-2-furfural (CAS No. 67-47-0) in F344/N rats and B6C3F1 mice (gavage studies).; Natl Toxicol Program Tech Rep Ser. 2010 Jun;(554):7-13, 15-9, 21-31 passim.
As is shown in the NTP report and the other sources above, HMF is not only found in honey. It will be found in any product that contained sugar or high fructose corn syrup that has been heated, such as baked goods. The reason you are likely to encounter it in honey is foremost that honey is 70-80% reducing sugars (5) and also that bee keepers often supplement HFCS for actual flower nectar when there is not enough flower nectar available for the bees to use to produce honey.
Toxic Honey
One thing to note is that there are toxic forms of honey, just as there are poisonous mushrooms and edible mushrooms. Honey derived from rhododendrons can contain Grayanotoxin, however it is rarely fatal in humans. If you are buying your honey from a supermarket or a reputable keeper, then there is almost no chance that your honey will contain grayanotoxin.
Why is Honey Harmful to Infants?
The issue with honey is that it can contain Clostridium botulinum spores. If the spores germinate, the resulting bacteria release botulinum toxin.
Botulinum toxin, which is the cause of botulism, is a neurotoxin that causes dystonia, and can be lethal in minute doses (ng/kg doses).
For most adults, the risk of botulism from the spores found in honey is minute. The gut microbiome and immune system proteins such as defensins will prevent C. botulinum colonization, so even if the spores germinate, they will not grow to a critical mass to produce enough toxin to do harm and will be excreted.
This however is not the case for infants less than six months of age. Their microbiome is still developing and their immune system is not fully formed. Also, as they have less mass, it takes a lesser absolute amount of the toxin to cause illness and death.
C. botulinum spores are heat resistant, though they can be killed by boiling (7), which means that the internal temperature of the spore needs to reach >85°C for over 5 minutes. Pasteurized honey should already have had this treatment, however you will still see the warnings to not feed to infants less than six months to one year of age, as commercial heat pasteurization may not kill all of the spores (7).
So unless you are immunocompromised, have no gut microbiome, are an infant less than six months of age, or your boiled water does not stay at a temperature greater than >85°C for longer than 5 minutes, and are using raw honey, then you shouldn't be at too much risk.
Edit
Information has been reorganized to better reflect edit to question.


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Unilateral damage to vagus nerve
Context:
The vagus nerves supply the neck viscera, heart, lungs and gastrointestinal tract. They join around the oesophagus to form the oesophageal plexus.

Question: Would damage to one vagus nerve in the neck have significant impact on heart rate and gastrointestinal tract function?

Thoughts: If the heart and GIT lie below the oesophageal plexus, which then continue in the inferior direction towards the cardiac and gastric plexuses, then surely a major functional failure in either the heart or GIT would require damage to both vagus nerves (?). I'm trying to make sense of the effect of their fusion, and whether or not this provides a compensating mechanism in the event that one of the two nerves is damaged.

It depends how they're damaged. Pressed on so that they fire continuously and simply severed so that no firing happens have different results.

@Hernandez - it also depends "where" they are damaged. There are branches that we routinely encounter during stomach operations that, if we  damaged, would have very different effects compared to damaging the vague as it descends through the neck in the carotid sheath. More distal injury (i.e. further away from the brain) would likely be less debilitating than more proximal injury.

@Hernandez - how high of a injury in the neck or how low of an injury in the neck?

I was thinking more of damage at the level of the neck. I guess if it occurs before the nerves join to supply fibres to the cardiac and coeliac plexi, parasympathetic functions relating to heart activity and the GIT would remain relatively untouched. Perhaps only the more superior pharyngeal innervations would be affected by such damage.

To qualify that further, I was thinking of damage above the level of the C6 vertebral body.

Would damage to one vagus nerve in the neck have significant impact on heart rate and gastrointestinal tract function?

Not that much, because fibers from both sides are fused, so each nerve carries about a 50% of fibers originated from the one side and about 50% from the contro-lateral. Consider that fibers are rewired after each plexus.
References:
 wikipedia page about vagus nerve
 wikipedia category about vagus nerve

source: Stack Exchange

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sort: votes


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Why does a Urinary Tract Infection cause a strong, persistent urge to urinate?
There are plenty of articles on the fact the a urinary tract infection (UTI) causes frequent and urgent urination. For example; on this National Institutes of Health webpage.
My question is:

Why does a urinary tract infection cause an increased desire and hence, a greater urgency to urinate?

it might be due to irritation of muscular tissue, causing slight disfunction of the mechanism that controls the bladder/urine flow? (the urgency). The frequency might be down to irritation in the urethra and hence the need for release increases but, also the bodies "desperation" to expel the urine in order to excrete the bacteria by the medium, urine.

Nerve endings exist in a more or less homeostatic interstitial fluid medium which when disturbed in certain ways result in depolarization. This is a very simple explanation, but basically correct. Depending on the nerves being discussed, a change in the medium can be the presence/absence of neurotransmitters (serotonin, GABA, etc.), chemicals released from damaged tissue, pH differences, etc. etc.
Very simply put, anything causing irritation of the bladder or urethral mucosa will cause some of the nerve endings to depolarize; these are some of the same nerves that depolarize when the bladder is full, and therefore the sensation is of urgency (the feeling that one needs to urinate). The substances can be substances excreted by bacteria, released by neutrophils, or some other.
Simply administering a topical anesthetic - something that decreases the depolarization of nerve endings by reversibly binding to/inactivating sodium channels - (lidocaine, for example) will instantly alleviate this sensation. In the case of UTIs, a commonly given medication is the bladder anesthetic phenazopyridine hydrochloride.
The more complex answer is that no one exactly knows. The complexity is more important in the treatment of non-infectious causes of urinary urgency and in the investigation of why catheter-related UTI are often asymptomatic.
Edited to add: If you're looking for a more teleological reason (such as, it hurts so that you'll get flush out the bacteria faster, that's not actually what happens. When it hurts to urinate, very many women intuitively stop drinking fluids in an attempt to avoid the pain of urination, allowing the infection to get much worse. The counterintuitive measure is to drink more, not less, to flush out bacteria.

@Medica I presume?  Nice answer, you are well-rounded!

Any links to the sources?

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Can brain damage caused by physical injury affect the social behaviour of a person?
Can a physical injury to the brain, resulting from an accident, and not the result of a diagnosed mental illness, affect a person's social behavior?

If sociability wouldn't have anything to do with the brain, by what other mechanisms would the exposure to the world shape future behaviour?

I didn't say that sociability isn't due to brain. I asked whether brain injury can affect social life or not. :)

So you should edit your question cause now title and first sentence are terrible

oh, sorry about that.. I changed it.. :)

Socialization is a cognitive and executive brain based function that requires higher level thinking mechanisms usually dependent on the prefrontal coretex. A lot of social cues we obtain from our environment when we are young can shape our brains during its developmental growth (infancy-post puberty) and cause our brains to develop social habits and access specific social functions.
A great text book example of altered social behavior due to brain injury is Phineas Gage. He had a metal rod shot through the prefrontal cortex and it caused a severe change in his behavior. He no longer cared about social cues and people often referred to his behavior as becoming "rude" and "out of context." There are many subtle aspects of behavior that are regulated by brain functions and there are many books on the topic.
Source: Wikipedia page on Phineas Gage and
Pyschopharmacology, book by:  Meyer and Quenzer
DSM-5, text book on clinical psychology
Further Reading on Phineas Gage
- What were the symptoms of Phineas Gage after suffering his brain injury?

I was going to suggest that we migrate this question to cogsci, but this answer kept it neatly on topic.

Thanks! I think both sections intermingle nicely sometimes.

Great answer and +1 for including a reference other than Wikipedia. @James - This question is on topic on both sites, regardless the answer.

@Christiaan I don't think it was off-topic, but from the question I thought a better quality cogsci answer would emerge than what our community might provide, but this answer showed me wrong. Cross posting might still be interesting with this question.

Despise the tasteless title, I find this case really interesting: Brain tumour causes uncontrollable paedophilia


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Getting PCR amplification at annealing higher than Tm!
I am amplifying a gene where in a gradient pcr i am getting amplification at an annealing temperature about 5 degrees (67) higher than Tm (62.5)? What is wrong here? Also, I am getting a very strong intense band at wrong size for all the temperatures tried below Tm. Pls help

Are you calculating Tm bioinformatically, because that is just an estimate? If you have a lot of GC content, your melt temp will be higher. It could also be the salt concentration of your buffer. If they are old reagents, you might of had some evaporation and your salt content could be higher than normal... You also do not mention whether the wrong size is smaller or larger. Could be primer dimers or you could have off target annealing. primers do not need to be completely complementary to anneal properly and if you have a primer and a sequence with a lot of GC it could anneal preferentially.

Possible duplicate of Does an annealing temp higher than primer's Tm contribute to primer dimer?

Tm of primers would not tell much about PCR conditions. When you get non-specific bands, it is worth to try higher temperature.
Your temp trying is already close to the temp to extend, so that shuttle PCR is available. Shuttle PCR has just 2 steps: 94 to 96 degrees for melting DNA and 68 to 74 degrees for annealing and extension together.
You might want to add DMSO or betain. They could help to reduce mis-annealing.
If the non-specific bands are smaller and longer than bands you expect, longer and shorter extension times may give you better results, respectively.
And remember, primer design is also important. Check you have sequences repeating in your template and avoid to design primers from such sequences.

Regarding higher annealing temp than Tm, I often use T7 primer of which Tm is 48.3 degrees. The primer works well at 55 degrees of annealing temp. Usually, primers are excess in PCR reaction tubes, pushing the chemical equilibrium toward annealing. That is what I speculate.

It is very common to get annealing at higher than predicted Tm.  If it's a problem in your case, especially if you're getting mis-annealing at lower temperatures, consider using touchdown PCR to find an optimal temperature.  Or, pragmatically, if you have any flexibility in primer design, simply order a set of primers and try them all.  Primers are cheap today, and you'll often find a set that work even where the design programs claim they won't.

The TM of the primer is also influnced of the salt concentration of your mix. Do you try the PCR gradient? Or you try the calculation of Tm and take in consideration the salt concentration.
http://www.biophp.org/minitools/melting_temperature/demo.php

Welcome to SE Biology. It is a good idea to look at the date of posts — easy to miss, especially on a phone — because if you are asking a question of the poster or making practical suggestions in your answer you may be wasting your time. Of course if the question is scientific and you feel it has not been properly answered go ahead. (But not in this case, I think.)

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Are there different species of modern day humans?
I've been watching nature shows on Netflix (Wildest series) and different animals of the same "family" are actually different species.
e.g. Asian elephants vs African elephants. Asian elephants are much smaller than their African counterparts.
Also with monkeys, different locations have their own species. Take langurs for example (see link below)
http://en.wikipedia.org/wiki/Gray_langur
http://en.wikipedia.org/wiki/File:LangurMap.svg
Just in the Indian subcontinent, there are many species of the same "gray langur".
In saying all that, how many species are there of modern day humans? It can't be just 1 homo sapiens it's quite obvious there are differences based on location. (Africans have darker skin. East asians have distinctly-shaped eyes and etc). Monkeys have lots of species even of the same "family" (see example above) and we're also primates.
thoughts? thanks

Nope, all modern humans are one species, even one subspecies (https://en.wikipedia.org/wiki/Anatomically_modern_human). I suggest reading on taxonomy to understand the terms species and family (https://en.wikipedia.org/wiki/Taxonomic_rank). Remember that these distinct classifications are concepts developed by us and appliead to biological entities which actually don't form such discrete structure.

By asking a question and then immediately ruling out a possible answer, which in this case is actually the factual answer to your question, you are giving an indication that you may not be open to an answer that would be contrary to your own ideas. Think about editing your question and rewording it in such a way as to remove the impression that you may not be willing to accept the answer if it is contrary to your view. Thanks.

It can't be just 1 homo sapiens. Guess again. A common definition of a species is that members of the same species group can produce viable and fertile offspring. Think about how that works with humans.

Why would skin color be an "obvious" reason anyway? We don't say that about other animals that come with different skin or fur color. Likewise with eye shape.

Also related: Do humans have enough biological differences to be grouped into races or subspecies?

To James: then you have ligers

Not only is there only one species of human, genetically we don't even divide into different races. Pick any male human on the planet, at random, and any woman from anywhere else on the planet, also at random. They are just as likely to be capable of bearing children as any two people from the same village. The whole concept of a species embraces the concept of 'continuous reproductive continuity', so your 'obviously different human species' is profoundly mistaken.

Nice answer, it could be good to add some sources too which would both allow further reading and offer support to your answer :) though I'm not sure I'd bother in this case if I were you - looks like the question is headed for closure and deletion


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How many genes does D. melanogaster have?
Obviously there is no 100% exact number, but I came across this on flybase, the gold standard for annotation. I am confused now. "Genes located to the genome", is that what I am looking for? If so, what does "Genes not located to the genome" mean?

I guess that the genes not located to the genome are the ones which cannot be mapped to a particular chromosome but are a part of some unmapped contig. You can see that from the GTF file but the figure does not match the stats shown here. In fact the stats page reports a total of 32078 genes records but the GTF only has 17716 (which is same as the genes located to the genome including unmapped contigs and mitochondria). So I guess the other genes are just present in the transcriptome assembly and are not mapped to any genome contig

@WYSIWYG it is related to genes and phenotypes from literature prior to having the sequenced genome.

EDIT
Personal correspondence to representative at FlyBase.org

In FlyBase we have been gathering information about genes and phenotypes for over 20 years including information from papers and resources older than that.  We annotate gene models on the Drosophila melanogaster genome assembly and when possible associate those annotations with other information (eg. phenotype, function etc) that is known about the gene.  However, in some cases, especially for genes and phenotypes that were described in the older literature before the genome was sequenced we still have some information about those genes but have been unable to associate that information with a genome annotation.   Those are what we call unlocalized genes (i.e. those without a annotation on the genome).


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Homework Question: Confused about figure related to cDNA and gDNA

what is the answer in blank?
I think the loop structure for the top blank is an intron.
I think RNA is the answer for the bottom blank, but it is cDNA, so it can't be RNA.
I cannot figure out what the question is asking. Please help me.

I think that the OP has tried to answer the question himself, so why close?

You are correct about the top loop being the intronic region of the gene that would be spliced out of the mRNA that was used to make the cDNA and will not have complementarity to the sequence found in the cDNA.
You are also correct that because it is cDNA, then it cannot be RNA for the bottom box. Remember that the cDNA will contain what the mature, spliced mRNA contained, 5'-UTR, coding sequence, 3'-UTR and Poly-A (Poly T if this is first strand cDNA) tail, so the bottom answer is likely an exon, as there is complementarity between the genomic DNA and the cDNA at that position where the arrow pointing.


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

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

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

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

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

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

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


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Do camels pose an environmental threat to kangaroos?
Camels, once used for transport across the Australian outback, were set free, and are reproducing at an uncontrolled rate in the empty interior of Australia.
Do the ecosystems of camels and kangaroos overlap?
Are camels competing with kangaroos for what little vegetation there is, and if so, what is the impact on kangaroo demography?

Can you please provide a reference to an article that discusses the situation? It may help people who are familiar with ecology but unfamiliar with the particular scenario you are discussing.

@Gordon Stanger: please provide some reference indicating the rise in reproduction rate.

Feral camels have environmental, economic and cultural impacts in Australia's Northern Territory (Dept of Land Resource Management, Australia).
In central Australia, camels feed on more than 80% of the available plant species. Feral camels severely defoliate and suppress the recruitment of some shrub and tree species, with such impacts being greatly exacerbated in drier years (Dept of Land Resource Management).
Feral camels have a noticeable impact on fragile salt lake ecosystems and waterholes, which are important sites for Aboriginal people and for native fauna (Dept of Land Resource Management).
However, its impact on kangaroos may be the last of our worries. There are other, typically smaller, marsupials that cover the endangered species list in the NT, including the Western quoll, bandicoots and wallabies (Dept of Land Resource Management). Kangaroos thrive in the agricultural farmlands that now dot the nation.

Oh... I forgot there was an honorary Aussie in the room.

@AMR - that's why I am here ;-)

@AMR - with the interesting side note that OP lives in Adelaide, while I am back in the Netherlands ;-)

That's strange... there is an anagram somewhere....


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Can people with AIDS get tattoos?
When I do a Google search, most of the results are about whether or not people can get HIV / AIDS from getting a tattoo through dirt needles. I am, however, curious whether or not it is possible to get a tattoo if you have AIDS.
Quoting wikipedia's entry on tattoos:

Tattooing involves the placement of pigment into the skin's dermis,
  the layer of dermal tissue underlying the epidermis. After initial
  injection, pigment is dispersed throughout a homogenized damaged layer
  down through the epidermis and upper dermis, in both of which the
  presence of foreign material activates the immune system's phagocytes
  to engulf the pigment particles.

If your immune system is not working properly, I can imagine that the phagocytes might never respond to the tattoo ink and that the pigment might not ever enter the fibroblasts?

AIDS affects T-cells, I have never heard of it being particularly damaging to macrophages/neutrophils... So I would imagine AIDS would have no effect on the tattooing process.

@TheNightman. AIDS is the disease that is caused by the Human Immunodeficiency Virus, so AIDS is the result of HIV infecting T-Cells. The mechanism that it does this by is by glycoprotein 120 binding with high affinity to the CD4 surface receptor. It then binds to the CCR5 co receptor and fuses with the membrane to deliver the viral nucleocapsid and associated proteins. CD4 T-Cells, Macrophages, and Dendritic Cells all have CD4 and CCR5 (barring a mutation) and thus HIV can infect all three cell types.

@AMR - I edited my answer

@AliceD I saw, thank you for the acknowledgment. Was there something you wanted me to do further? This comment was related to The Nightman's comment...

@AMR - all is fine! Thanks for clearing matters up.

One of my interests is immunology, and I spent a good amount of time this Spring looking at the adaptive immune system and how HIV infections occur at the cellular level... I was actually kind of disappointed that I had to look some things up... What is it, we lose 70% after the first month?

Short answer
People with HIV can get tattoos.
Background
In Africa there are countries that tattoo people identified with HIV (Source: Kenya Today) and some people with HIV find comfort in tattooing biohazard symbols and related images on themselves to express their illness (Source: CNN).
However, as rightly mentioned by @AMR, macrophages  which are mainly responsible for ink fixation express CD4 and therefore can be infected by the HIV virus targets.
Hence, while I don't think HIV affects tattooing given the fact that HIV-infected people get tattoos, in theory HIV could reduce the ink fixation.

While it may not affect the ability to get a tattoo and have it fix in the skin, The HIV virus infects T-Cells, Dendritic Cells, and Macrophages. gp120 binds with high affinity to CD4 and then needs CCR5 to fuse with the cell membrane. Both CD4 and CCR5 are present on those three cell types and thus the virus can infect all three.

Posted due to certain inaccuracies in comments and answers provided to this question regarding the Human Immunodeficiency Virus.
It should be noted that while it may not affect the ability for macrophages in the dermis to phagocytose the heavy metals found in the inks used in tattooing, and thus not interfere with the fixing of a tattoo in an HIV+ person, the Human Immunodeficiency Virus, the virus responsible for Acquired Immune Deficiency Syndrome (AIDS) does in fact have the ability to infect any cell type that expresses the cell surface glycoproteins CD4 and CCR5.
Cells that express CD4 and CCR5, barring mutations seen in the bone marrow received by the Berlin Patient (Timothy Ray Brown), among them CD4 "Helper" T-Cells, Macrophages, and certain Dendritic Cells, are all capable of being infected by the HIV virus.
Glycoprotein 120, found on the surface of the HIV envelop, binds with high affinity to CD4. The coreceptor CCR5 then binds to the gp120 CD4 complex and allows the HIV envelop to fuse with the plasma membrane of the host cell. The fusion then delivers the viral nucleocapsid and associated proteins into the cytoplasm of the cell and the infection takes place.
If I had to venture guess, I would say that as Macrophages tend to be present within the dermis of the person for extend periods of time, there is likely enough of a population present in the skin to have the macrophages necessary to fix the inks used in tattooing.

+1 thanks for your careful analysis. I adapted my answer to be in line with yours.

Yes.. If I am not wrong HIV strains are classified as M-Tropic (macrophage) and T-Tropic (T-cell).

The same infection in initial stages is more m-tropic and later turns in the late stages, more t-tropic


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How is a bacterial strain defined?
When a species of bacteria is referred to by its strain, are they a clone of single founder or is a certain amount variation allowed?

In theory they're clones, but depending on the age of the strain(some strains are surprisingly old: ~40 years) there's variation inside strains.
The reverse is also true. Bacteria from a single species are isolated twice and named different things by different labs and the mistake can take years to even find, much less correct.

Whereas a clone (or clonal population) is the current population of individuals descended from a single particular ancestral individual, a strain can be understood as the whole line of individuals down and up to that single particular individual.
But as noted in the other answers, even though the isogenic character is often taken as a more or less tacit approximation, none of those two concepts forbid genetic variation or assume that all the individuals of the said clone or strain are isogenic.
The concept of species for microbial organisms is more intricate.

Bacteria effectively clone themselves so theoretically all clones are identical. However like every organism they're subject to Darwinian evolution so there's always a chance a random mutation happens. Since bacteria usually reproduce fast the rate of these mutations can happen fast resulting in the strain evolving to a (slightly) different strain.


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Why do humans masturbate?
Why does masturbating seem to be like an addiction?
What controls or initiates the urge to masturbate?
Is it good or bad or both and why is it so? I have heard guys who say that the do it regularly. Also there is a relaxing feeling; what generates that?

You probably mean masturbate instead of masterbate. I edited it. I also remove the triple interrogation mark, remove the spaces around interrogation marks and points and not use both interrogation mark and point.

The question is more on-topic on Health.SE. But before you ask your question over there, note that if you google your questions you will find millions of hits because you are very clearly not the first one to ask this kind of question.

I searched on google but most of time i get only one answer that it is good...

Maybe you should using the word masturbate instead of masterbate and try with a more accurate question. There is definitely loads of information. Way more than what you could read. For example, in your question you do not specify whether you are interested in physical or mental health. In its current form, I am voting to close the question as too broad.

I think it's on topic, there are Evolutionary hypotheses for masturbation and studies of how it affects sperm and ejaculate quality, and how that in turn can affect fitness

One word. DOPAMINE
See this article on Reward System and this one on Dopamine Those basically answer your question as to addiction, urge, and feelings of relaxation.
There is absolutely nothing wrong with masturbation, so long as you realize that it is a healthy expression of one's sexuality, that is observed, quite frequently, in our nearest relative, the Bonobo. There is no shortage of the study of primate masturbatory practices in the literature, and one could make a career out of its scientific study and analysis, so if you are interested in learning more, conducting a Google Scholar search on Primate Masturbation should give you literally years worth of reading material.
As for an actual addiction, it would only develop into a pathology if it became disruptive to one's life and was pursued at the exclusion of other basic activities.

Masturbating can yield to a strong addiction that can be bad for health just because it prevents one to have a normal social life. Also some are masturbating so much that they can injure themselves. So it is not as easy as to just say There is absolutely nothing wrong with masturbation.

@Remi.b I agree that that statement should be qualified, but I think AMR was speaking to religious/cultural conservatism that frowns upon masturbation as some sort of "sin" or social ill.

@Remi.b If you notice I had qualified my statement as to when it can become pathological. However, as with alcohol, or shopping, or food, or sex, or gambling, most can maintain a healthy balance and control without developing an addiction to the stimulus.

@Remi.b Scientific literature would contradict your impression. http://www.tandfonline.com/doi/abs/10.1300/J056v14n02_02 and http://link.springer.com/article/10.1007/s10508-010-9722-0 as examples.

Oh... I guess I missed your last sentence. Sorry about that. +1

@MattDMo More cultural than religious. Just as antivaccine ignores the scientific data to support an agenda, so to do those spreading superstition when it comes to sexual development. The scientific reality is far different from Remi.b. Yes, there will be a few that can become addicted, as it is linked into the neurological reward system, but for most it is a healthy part of development and coming to terms with their sexuality. Also physical injury is a fallacy, perpetuated with the same agenda looking to suppress the behavior.

@AMR I agree. I was raised in a fairly conservative religious environment, which is why I read religion into your statement.

@MattDMo, Don't need to be conservatively religious to have been sold an unhealthy view of normal sexual development. Just think of Seinfeld's Master of My Domain episode.


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Is there a model perennial plant species?
Most of plant science is conducted on small annual species with short life cycles; predominantly Arabidopsis thaliana, but also a handful of others like Oryza sativa and Medicago truncatula etc.
Is there a model perennial species? And, if not, is there a good candidate that is relatively small but fast growing and able to be grown in lab/glass house environments that someone could recommend?

To my knowledge, Populus is one of the main model species when it comes to perennials and trees. It is for instance used in several sequencing projects, and to study accelerated breeding in strains that are promoted to flower at a very early age.
Excluding trees, other perennial species that has been described as model species are Panicum virgatum (Switchgrass) (see Lu et al. 2013. Plos Genetics) and Solanum lycopersicum (Tomato) (see Sato et al. 2012. Nature.
For a closer description, and arguments for Populus as a model species, see e.g. Taylor (2002. Populus: Arabidopsis for Forestry. Do We Need a Model Tree?. Ann. Bot.) or Jansson & Douglas (2007. Populus: A Model System for Plant Biology. Ann. Rev. Plant Bot).

Here it is argued that Populus is rapidly becoming accepted as the ‘model’ woody plant and that such a ‘model’ tree is necessary to complement the genetic resource being developed in arabidopsis. The genus Populus (poplars, cottonwoods and aspens) contains approx. 30 species of woody plant, all found in the Northern hemisphere and exhibiting some of the fastest growth rates observed in temperate trees. Populus is fulfilling the ‘model’ role for a number of reasons. First, and most important, is the very recent commitment to sequence the Populus genome, a project initiated in February 2002. This will be the first woody plant to be sequenced. Other reasons include the relatively small genome size (450–550 Mbp) of Populus, the large number of molecular genetic maps and the ease of genetic transformation. Populus may also be propagated vegetatively, making mapping populations immortal and facilitating the production of large amounts of clonal material for experimentation. Hybridization occurs routinely and, in these respects, Populus has many similarities to arabidopsis.

(from Taylor, 2002))

With the completion of the Populus trichocarpa genome sequence and the development of various genetic, genomic, and biochemical tools, Populus now offers many possibilities to study questions that cannot be as easily addressed in Arabidopsis and rice, the two prime model systems of plant biology and genomics. Tree-specific traits such as wood formation, long-term perennial growth, and seasonality are obvious areas of research, but research in other areas such as control of flowering, biotic interactions, and evolution of adaptive traits is enriched by adding a tree to the suite of model systems.
  ...
  The development of Populus as a model system for tree and woody perennial plant biology has been largely driven by the rapid development of genomic and molecular biology resources for this genus, as discussed below, culminating in the completion of a draft sequence of the Populus trichocarpa (black cottonwood) genome (106). This information will facilitate studies on the comparative biology of Arabidopsis and Populus as representatives of two angiosperm extremes, enabling discovery of mechanisms conserved among eudicots.

(from Jansson & Douglas, 2007)

Thank-you for your answer, and yes Populus trichocarpa is an interesting species. However its not quite what I'm looking for as it is difficult to study it like one would study Arabidopsis.

Being a large tree and (relatively) slow to reproduce mean that you cant control enviromental variables (light duration, quality, temperature, humidity, etc) to a satisfactory level of accuracy to avoid systemic noise in any molecular experiments and genetics can't be done very quickly. I'm looking for an Arabidopsis type plant amenable to such experimental approaches.

@G_T I've now added two non-tree examples as well. However, note that you cannot find a long-lived perennial that is as as easy to study on a short timeframe as an annual such as Arabidopsis (almost by definition). This is sort of the point of looking into perennials as well, to get a different perspective and a comparison to short-lived annuals.


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How can hyperthyroidism induce osteoporosis?
It says in my physiology notes that hyperthyroidism can cause osteoporosis.
I've been trying to figure out how this could be possible for a little more than an hour now. Every article that I look at seem to agree with the fact, but I can't find the explanation as to why it is that way.
In MarieB, it says T3 and T4 favor bone growth. Calcitonine also favors bone formation.
How can.... too much of an hormone that favors bone growth, cause bone resorption?

T3 stimulates osteoclast formation. Osteoclasts are cells that break down bone tissue. They are essential for bone growth in children, because they allow bone remodelling. However, elevated stimulation of osteoclast formation leads to osteoporosis in adults, where bone remodelling is not necessary.
In hyperthyrodism, T3 levels positively correlate with levels of calcium ions in blood, which confirms the break down of bone tissue. Calcium ions are then excreted in urine, because they cannot be efficiently reabsorbed. This constant loss of bone tissue cannot be reduced with high calcium diet, only by drug treatments that affect T3 levels.
Definitely can recommend further reading, especially regarding different types of thyrodism:
DOI: 10.1002/jcp.20041


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What are flagged primers?
I'm interested in amplifying a sequence for further use with Gibson Assembly. I want to create overhang regions in my DNA fragment so there would be complementarity to the plasmid I'm trying to insert it in.
I was informed by a colleague to work with "flagged primers" though I can't find any literature online.  Can anyone explain this concept to me?

Are you sure they didn't mean labeled primers. The Oligonucleotides become part of your DNA, so if they are labeled, then the label will be incorporated into your amplified sample.

they described them as forward and reverse primers with overhang regions

The only place I could find a reference to flagged was on what appeared to be an personal journal from someone at UCSC. This is the Addgene protocol. If has a link to the Gibson's original 2009 article, and that doesn't mention flagged either. Nor does Janet B. Matsen:Guide to Gibson Assembly

There is nothing, in my knowledge, called flagged primers. What your colleague must have meant is perhaps "flanks". If you clarify your objective then this question may be answered. Since the real question is unclear as of now, I am putting this on hold.


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Is it painful for the hen to lay eggs?
My little son just asked me this question. His mother used to complain about the excruciating pain she suffered when she gave birth to him. He is a compassionate kid and wonders whether the hen goes through this pain everyday. Not being a hen, I am not sure if chickens experience pain that is close to the pain associated with giving birth.

By the way, taking your son to a farm that has laying hens might be really nice. As anongoodnurse said, there is a lot of squawking when the egg is laid, but nothing he would associate with pain.

I see why you would ask this question AMR, the do squawk after laying an egg

We really don't know - we can't really ask the chicken. At least, it's unlikely it's as painful as it can be with humans.
The reason human birth is (or can be) very painful is that the human baby's head has to fit through the woman's pelvis. Since splitting from chimpanzees, human heads have gotten bigger, while the pelvis has gotten more narrow due to adapting to walking on two legs. While chimpanzees give birth in an average of around 2 hours, humans can take over a day to do so, and the baby being too big can lead to maternal and natal death.
Back to chickens, while there are different sizes of eggs,  the larger eggs come from larger chicken breeds. If it does hurt them, at least it takes a lot less time - only a few minutes. From personal experience, the hens do not appear traumatized even seconds afterwards and just go about their day as soon as the egg is out.

YviDe, there is another part of the OPs question that is of interest. Without the introduction of hormones in feed, will a hen lay an egg daily? Are commercial farms affecting the hormone balance to increase output? +1 for not ignoring the question!

@AMR - hormones don't make chickens lay eggs; breed, light and temperature do. A mature chicken will lay 300+ eggs a year given long days (that means artificial light in the winter) and enough food and some help with temperatures (less energy lost to maintain body heat), Some lay ~360 (obviously referred to as layer breeds, like white leghorns.) There is another question answered already on hormones and eggs. Chickens don't need them. When they slow down, they get replaced. It's just cheaper.

@AMR - If you want to ask that (separate) question, though, since I answered for broilers but not layers, I'd be happy to answer it.

@anongoodnurse Interesting... So conditions affect nesting behavior and nesting behavior drives egg production.

@YviDe - +1. I used to have laying hens (I'm not exaggerating when I say I've had hundreds). They cluck and might squawk a bit when they lay, but they don't need bed rest after, and I never had one bleed to death from the experience.

@AMR - Yes, that's safe to say. Light affects the pituitary gland, which affects egg production. Usually regardless of age (within reason), my chickens all started to lay eggs at about the same time in the Spring once the days were long enough.

@anongoodnurse "If you want to ask that (separate) question, though, since I answered for broilers but not layers, I'd be happy to answer it." I tend to research on my own instead of ask questions, I just saw a quick tack on that's always been in the dark recesses of my mind. Thank you for the enlightenment. I would not have guessed that.

@anongoodnurse  "They cluck and might squawk a bit when they lay," I know I am anthropomorphizing, but I always found it rather adorable :-)

@YviDe - I can't even say why they cluck and sometimes squawk; they might well be warning me (or other chickens, seen or unseen) to stay away from their preciousssss. ;)


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Determine which seed will germinate first
I recently studied about plant physiology for a test. Strangely, there was this question which I had no idea how to approach.
The question is,
Which seed will germinate first?
a) Castor
b) Wheat
c) Mung( Vigna radiata )
The answer is (c). I want to know how do we determine if which seed will germinate first? Which factors does it depend upon?

Mung germinates over night, doesn't it ? Think of sprouts..

It does. But that wouldn't be the correct way to answer. Right? I mean, It'll be pure hunch and no scientific reason.

Yes that's true. But maybe the question is just targetting that general knowledge. Anyway, it isn't a very good question. Typical of exams that just test your cramming capacity :(

It was asked in a model test for a medical institution ug admission. There was a separate gk section. This question was in the bio section :P

Catcha ! AIPMT/AIIMS treachery ;)

Ah! You know!!!

Well, I am giving them this year. Best of luck to you too ! Hope we survive the craziest exams on the planet :P

The odds.  Such low is the probability.  Yeah,  hope we do survive it! Hope to see you in aiims Delhi xD

You'd have to know the individual germination times for each family.  I'm linking a table for vegetables, but it doesn't include the three plants you're looking at.  A google search for each one individually shows that yes Mung does have the shortest germination time.  It's a memorization question.
To add to that here is a paper where they review variation times between over 600 seeds and find that the variation in time is mainly constrained within families.

I'm wondering if there's a more general answer, like if it's a general property of that subfamily of Fabaceae to have fast germination times, so they wouldn't expect students to know the germination times for those three exact plants but rather general patterns of germination across grasses, Euphorbs, and legumes

@CactusWoman excellent point, I found a paper that shows you are correct and edited appropriately.


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Do biological phenomena follow Gaussian statistics?
I have recently entered the life sciences (from physics).  I am concerned about the use of p values in the life sciences literature.  For example, in this article, they test 9 - 12 rats in a control group and compare it to an experimental group.  They use p values to claim that their results are statistically significant.  This type of use of p values seems to be very common in the literature.
So here are my concerns :

Why is it so often assumed that biological measurements follow a normal distribution?  To my knowledge, this isn't known a priori.
From my physical intuition, it seems quite challenging to claim "statistically significance" when using such low sample sizes.

Yes, if/when you can apply the central limit theorem. Things like body mass/size etc are influenced by many relatively independent atomic factors, hence you can apply the theorem. But don't fool yourself into thinking that normal distribution is all we've got in biology. Binomial, Poisson, beta and gamma distributions are highly common in genetics and bioinformatics.

1) this is really an emprirical question; sometimes it is, sometimes it isn't. Even if the "real" process is poisson, a normal distribution can still be a fairly accurate approximation. 2) intuition based "significance" and the technical concept of "statistic significance" needs to be clearly separated. If assumptions are met, an analysis might produce statistically significant results, while still being weak with rather shaky results.

Healthy skepticism is a great thing, especially in biological research. Also remember that in Biology, models are often imperfect approximations for the questions studied. That doesn't mean they aren't the best that we can do given the current limits of technology, but it is something to always have in the back of your mind when you read biological publications. There are countless examples or studies that produced significant results in rodents but collapsed in human trial. Also, in vitro tissue cultures can be fraught with assumptions that cannot be extrapolated to the organism.

Answers to this question are right, but I miss someone mentioning that there are tests to assess if your data follow a normal distribution, although those test aren't powerful if your sample is small.

kmm's answer is correct; I just want to add some of my points on what kind of data should follow Gaussian distribution.

Unless you know from observation that a process doesn't follow a
  Gaussian distribution (e.g., Poisson, binomial, etc.), then it
  probably does at least well enough for statistical purposes.

I won't fault kmm for this statement because what they said is what happens prevalently. This is practically what all biologists do, but this is an incorrect approach.
Gaussian should not be considered a default distribution. This may lead to incorrect inferences. Usually the experimenter has an idea of what kind of data they are measuring and what distribution is the data likely to follow. If you are unsure of the underlying distribution then you should go for non-parametric statistical tests.

What kind of data follow Gaussian distribution?
According to the Central Limit Theorem, the distribution of the mean (expected value) or sum of several samples of independent and identically distributed (IID) random variables would follow Gaussian distribution. The random variable itself can follow any distribution but if you measure the mean several times using repeated experimentation, then the distribution of the mean would be Gaussian.
From the Wolfram site:

Let $X_1,X_2,...,X_N$ be a set of N independent random variates and
  each $X_i$ have an arbitrary probability distribution $P(x_1,...,x_N)$
  with mean $\mu_i$ and a finite variance $\sigma_i^2$. Then the normal
  form variate:
$$X_{norm}=\frac{\displaystyle\sum_{i=1}^N x_i-\sum_{i=1}^N \mu_i}{\sqrt{\displaystyle\sum_{i=1}^N \sigma_i^2}}$$
has a limiting cumulative distribution function which approaches a
  normal distribution.

The wikipedia page on CLT is also quite good. You can have a look at it too.
Usually in biological experiments we measure some property, lets say expression of some gene. When you do several replicates, and there is no specific underlying mechanism that would generate variation (i.e. the errors are purely random), then you would get normally distributed values. Note that this applies only for the sample means. In certain cases, we assume that the variation in the value of a variable is because of some random fluctuation and therefore consider these variables to be normally distributed (not their means but the values themselves); for e.g. the weights of mice which are fed and raised equally. This is just your assumption which constitutes the null hypothesis.
Another point to note is that the variable that is expected to follow normal distribution should essentially be continuous in nature. Some discrete variables can be approximated as continuous but one should have a good reasoning of doing so. For example population sizes, though discrete, can be assumed continuous if the sizes are large.

Poisson distribution is unique and is a discrete distribution. Certain kinds of phenomena result in Poisson distributed RVs. These phenomena should basically be Poisson processes. See this post for details. Poisson distribution basically models the probability of N events in a given time interval for some given rate of events ($\lambda$). This rate is also called the intensity of the distribution.

Binomial is another unique discrete distribution. Genotypes resulting because of Mendelian segregation of genes, for example, follow this distribution. It basically models the probability of N number of events in some M trials. In binomial distribution there are only two possible outcomes. Multinomial distribution is a generalization of binomial distribution with multiple outcomes.

Since both Poisson and Binomial are discrete distributions they should not be confused with normal distribution. However, under certain conditions especially when the number of trials in Binomial distribution is high and binomial probability = 0.5 then it can be approximated as a gaussian with same value of moments. Similarly, if the intensity (rate) of Poisson distribution is high or the time interval is large, the distribution of the Poisson RV can be approximated to Gaussian (with same value of moments). In these cases, the value of the mean goes up significantly, thereby allowing a continuous approximation.
Many datasets show power-law like/skewed normal distributions and people often make the mistake of assuming them to be normal. An example (from my experience) is the expression of all the genes in a cell. Very few genes have high expression and many genes have low expression. This also applies for degree distribution of nodes in some real networks such as gene regulatory network.

In summary you should assume Gaussian distribution when:

Variable is a measurement of a value which is repeated several times from identical samples
Variability is expected to be random in the control case (in t-test, when you reject null hypothesis you are actually saying that a certain variable does not follow the normal distribution assumed under the null hypothesis)
Variable is continuous, or discrete with large sample size

You raise two issues, both of which might be better suited for stats.SE, but I think the questions are suitably biological to warrant an answer here.
Do most biological processes follow a Gaussian distribution?
Unless you know from observation that a process doesn't follow a Gaussian distribution (e.g., Poisson, binomial, etc.), then it probably does at least well enough for statistical purposes. While ~10 observations isn't enough to test the distribution accurately (and those tests are pretty flawed anyway), as long as the values are approximately normally distributed, then you probably meet the assumptions of most general linear model-type statistical test (t-test, ANOVA, linear regression). These tests are fairly robust to deviations from normality, so in a sense, as long as the values are close enough to normal, the test is fine (which says nothing about the interpretation of the results).
Is the pervasive use of p values warranted? Is there problem with small sample sizes?
Although certainly not the first to raise the alarm about p values, Ioannidis's (2005) paper sounded most loudly. The central idea is that, in science, there is a strong tendency to only publish "significant" (but whatever definition of significance you use) results. Thus the literature is rife with false significant results. For example, if only 1 in 20 experiments yield significant results, the other 19 are not likely to be published. Yet those 5% might represent 95% of the literature, and thus we have a strong bias in the literature. All of those "significant" results can't possibly be correct.
Statistical inference from small sample sizes are also quite problematic (e.g., in neuroscience; Button et al., 2013). There has been a recent push toward including effect sizes for estimated parameters and simply reporting confidence intervals (which will be suitably wide for small sample sizes).
Many of the failings of statistics are summarized in Statistics Done Wrong: The woefully complete guide, which I don't have any affiliation with except that I enjoyed reading it.
The paper you link is pretty deficient in what you might call modern statistical analysis. What they could improve:

Run (and show the results of) an a priori power analysis to establish that their sample sizes are adequate
Include effect sizes of the estimated parameters
Include confidence intervals for estimated parameters
Use one of the many available multiple comparisons procedures to control familywise type I error rates.

It's incumbent on reviewers of papers to ask for these things if the authors do no supply them willingly.
There is no way around the small sample size in many studies, so it's possible that there isn't much they could do to change the sample size. Those who work with humans or animals are under pressure to keep sample sizes as small as possible while maintaining adequate power. However, they could show that what they have is sufficiently powerful.
Button, K. S., J. P. A. Ioannidis, C. Mokrysz, B. A. Nosek, J. Flint, E. S. J. Robinson, and M. R. Munafò. 2013. Power failure: why small sample size undermines the reliability of neuroscience. Nature Reviews Neuroscience 14:1–12.
Ioannidis, J. P. A. 2005. Why most published research findings are false. PLoS Medicine 2:e124.

I really don't agree with the first part of your answer, "Unless you know from observation that a process doesn't follow a Gaussian distribution ... then it probably does".  The burden of proof should be the other way around: unless you can clearly motivate why your data should be normal distributed, you should concede that it might not be, and use a nonparametric method.

You are right to be suspicious. I would contend that, in most situations, hypothesis tests based on the normal distribution are not appropriate. If hypothesis testing is needed, a permutation test should almost always be used.
As WYSIWYG points out, there is no reason to assume a measurement is normal distributed without strong a priori knowledge. The central limit theorem is the standard argument for assuming that the mean is approximately normal distributed, but I would say that it is not very helpful in practise, because the convergence can be very slow: if your data distribution is far from normal, you need a large number of samples for the mean to be approximately normal. How many? Impossible to tell, since we don't know the data distribution! So in practise, the approximation can be very bad, and then the test will be completely off. This applies not only for the t-test, but for many parametric tests that rely on the normal approximation, such as chi-square tests.
Fortunately, there are better tools nowadays. The permutation test does not require the normal distribution assumption; the results are always valid, regardless of the data distribution. It is easy to carry out with today's computers, and simple to understand. This is a good book on permutation tests (and other resampling methods).
Ronald Fischer and his contemporaries that developed the normal theory in the early 1900's were perfectly aware that permutation test was a much better solution, but it requires extensive calculations, which was simply not possible back then. So the normal test was developed as a poor man's approximation to the exact permutation test. But today, we have no need for this approximation anymore, as our powerful computers can perform even large permutation tests in the blink of an eye.
Then why do people stick to the approximate normal tests still? Sadly, I think they are routinely used only because most biologists know of no other tools, and simply follow tradition. A historical reason behind the normal assumption in biology is a classic argument by Fischer, concerning population genetics: if a phenotype is affected by a large number of genes, and their effects are additive, then the phenotype variable is a sum of many random variables, and by the central limit theorem it should be approximately normal. The classic example is height, which is indeed closely normal distributed in the population. But this reasoning applies to genetics of natural populations, not laboratory experiments.
Then there is the whole debate about whether hypothesis testing (and p-values in particular) should be used at all, regardless of which test you use. Other answers touched upon this. I won't go into it, but it is a very important topic, and I would recommend this excellent article from Nature, and references therein.
http://www.nature.com/news/scientific-method-statistical-errors-1.14700f

The willingness to publish only significant results has a second consequence to add to bias on publications. Since power of parametric tests is usually larger than power of equivalent non parametric tests, often results are significant only if parametric tests are used - usually needing to assume a Gaussian distribution. Therefore, researchers willing to publish are highly incentived to assume normality.

Can you please justify shortly the benefit of permutation tests? What do you want to answer with them? How can they help to identify the possible distributions in biological data?

Permutations tests are commonly used to test difference in mean / median / etc between two sample groups. They require only very mild assumptions (e.g. independent sample) and are applicable to virtually all data distributions.  Estimating the actual underlying distribution is not necessary (and rarely feasible).


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How many diseases can be linked to disruption in the microbiome of a human?
I was listing to the radio and heard recent research found a link between children and higher cases of asthma when certain bacteria are missing from the microbiome. How many other diseases can be linked to a disrupted microbiome and are there ways in repopulating missing bacteria?

It is an open question and an active area of research. You will not be able to get a definitive answer to your question of number, as each new discovery will add to the total.
As for repopulating, we have not even determined all of the strains of microbes that populate us, many are very difficult to culture in vitro, and we do not know of all the functions for each species, so we do not have a clear picture of which need to be there, which don't, and whether or not some species work together to provide us with a benefit. For certain conditions such as Irritable Bowel Syndrome, one of the treatments that has been tried is fecal transplant.
Do a literature search for recent reviews. Nature Reviews tend to do detailed reviews, especially on topics as in the news as the Human Microbiome. That is probably the best first place to start. Then you can start to drill down into the reference papers that are cited in the review. That will generally give you a good state of play in the field.

Thanks for the reply I will definitely take a look at some of the literature out there, I was very surprised to find out how many bacteria live on and inside of us. And I was told all this time growing up that "germs" are the enemy!

@DanTerry They are actually a very important part of the innate immune system. One aspect of immunity is keeping pathogens out. One way we do that is mucus. Another way is to provide a favorable living environment for microorganisms that don't harm us. The term for these is Commensals. Basically commensals, yeast, bacteria, etc, that are non-pathogenic to us, grow on our exposed surfaces, i.e. skin, respiratory tract and our gastric tract. The are there to basically just take up space that would otherwise be populated by pathogens. There are 10x more microbes than human cells making up a human


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Red fox with blue legs
On the Wikipedia I found this photo of a red fox, labeled as being taken at Quesnel Lake, British Columbia:

Why would the fox have blue legs? Is that normal for a Red Fox?

It is black skin and fur. The blue is just a problem with the White Balance of the photograph. Remember the Blue Dress thing on Facebook earlier this year?

I suppose one could expand on @AMR to make an answer.

I find it kind of hard to believe the legs appear blue because of "white balance". The nose and upper part of the legs are black, so it is not like all the black in the photo is appearing blue.

If you look at the top of the nose, it also appears blue. The black parts that are in full light appear blue: it's just a matter of lighting

Original vs. Adjusted

Adobe Camera Raw Temperature Adjustment +30 / Tint Adjustment +3
The fox has black skin and fur. The blue is just a problem with the White Balance of the photograph. See Adjustments made above.
This is similar to the Blue Dress / White Dress Meme this year.

I find it kind of hard to believe the legs appear blue because of "white balance". The nose and upper part of the legs are black, so it is not like all the black in the photo is appearing blue. – Imprisoned Rhesus

The reason the legs look Bluer than the Nose is that the nose is mostly black with no white and the front part is in shadow. The top part, which is reflecting some of the sky appears blue in the original.
The reason the legs look more blue is

They are not in shadow
There is a good amount of white fur mixed in with the black

The white fur will look far bluer when the white balance is off and will trick your eyes into seeing the black as blue.

Anyone know how to edit to place the photos side-by-side?

How to put images side by side. Nice answer btw +1


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How DNA programs the first cell in womb into a human
Sorry if you see me silly. I am just a programmer happens to be curious about biology...
So far I understand how DNA make protein, how cell divides, how one composed of cells->tissues-> organs.
But, still a piece is missing in my knowledge.. Given the sperm entering the egg creating the first cell, and the nutrients from the mother... how do that very first single  cell diversify , multiply, transform to a human of many different type of cells, tissue and organs ? Is this all the diversification and
specialization of cells directed just by the "child" DNA alone ?
Also, how does DNA (along with living condition ?) decide the course of my life  (making me 1m tall at 6 y.o , have my hair black, my life expectancy etc..)

I think the cyclin proteins ( https://en.wikipedia.org/wiki/Cyclin ) control the cell cycle, of which a part of is cell division. And I think the mothers DNA are used for the "embryogenesis" up until a certain point, and then the child's DNA is used.  ( https://en.wikipedia.org/wiki/Embryogenesis#Formation_of_the_gastrula ). I think this image gives a nice summary. ( https://upload.wikimedia.org/wikipedia/commons/8/8f/Human_embryogenesis.png ) . Sorry for giving a long comment instead of an answer, but i lack confidence in my biology.

Your question is a good one, but is unfortunately too broad for this forum as it encompasses the entire field of Developmental Biology. If you can narrow the focus of your question and ask a more specific question, then it is possible to get a good answer here.

@AMR             curiously, was there anything wrong with my line of thinking for my comment on this question? I feel I have been missing the mark for responses I give either due to my lack of experience or maybe general oversight.

@RoSiv Cyclins control the transitions from G1 through Mitosis/Meiosis, in any eukaryotic cell, throughout the organism's life, not just during dev. Your second sentence, has been shown fly development, though it is maternal mRNAs that are expressed before the embryo's. It has been shown in mouse eggs and it is possible that it occurs in human as well. Unlike fly development though, each duplication is marked with cell division. Flies go through several genomic divisions before they form distinct cells.

@RoSiv The point of my comment wasn't really about your comment, it is that human embryogenesis is extremely complex and no able to be fit in this forum. There are Master Regulators, Body Plan Genes, Signaling from the uterus, Quorum sensing, different stages of cell differentiation from different cell lineages, just to name a few... Timing also plays an extremely important role. Many of our genes are nearly identical to most mammals, but it is when and how much those genes are expressed that is the main reason that we have evolved into Humans and our other cousins are other species.

@RoSiv thanks for the reading materials, they will help me get closer to the answer.

@AMR : I know it is too broad but I don't have enough knowledge to narrow it down, maybe I could after reading articles from Ro Siv's suggestion. Thanks

The short answer is: "Nobody knows yet." The slightly longer answer is that different species use different mechanisms. In amphibians and insect the oocyte, or egg, produced by the mother, has a polarity such that some macromolecules are enriched in different regions of the egg. The best characterized examples are localized RNAs, but there could be other signals as well.  In nematodes the site of sperm entry at fertilization determines the polarity of the cells, which then leads to asymmetry, etc.
In mice, our closest approximation to humans, the early cells after fertilization all seem equivalent, but as the number of cells increases the cells on the inside of the ball and the cells on the outside start to choose different differentiation pathways. There can also be signals from the extraembryonic environment (i.e., the womb).

thanks! I hope it wont take too long for biologists/scientists to figure it out...


text:
Prediction of transmembrane beta barrels?
I studied that prediction of transmembrane alpha helices is more easy and accurate and also good algorithms are available for their prediction. But when we move towards prediction of transmembrane beta barrels (cylindrical structure composed of anti parallel beta-sheets) then for their prediction only a small number of algorithms are present which also don't give reliable results.
My query is that Why it so? Why the prediction of transmembrane beta barrels is difficult and why developers can't develop reliable algorithms for this purpose?

This might just be me being cynical, but isn't it predominantly to do with them being a lot more rare than TMH? Less cynically I would also say that the hydrophobic signal for a TMH is usually very strong. Perhaps TM beta barrel is more nuanced when compared to non-TM beta barrels?

I could tell only from my pretty poor experience.
I had all PDB entries processed with DSSP and then I've tried to find any trends in amino acid preferences. I did not find any except the pretty obvious absence of proline in double (i.e. with two neighbours) strands. Also, negative charged amino acids (I, L, V) were slightly more frequent in parallel strands. After that, I tried a sort of naive Bayes classifier for the amino acid and it's neighbours in two neighbour strands and +/-2 amino acids up/downstream. For single\double parallel\antiparallel strands, the prediction precision was about 60%.


text:
How is protein cavity centre related to binding?
I am confused and I have the following questions:
1. What are (in the context of article below) protein cavity centres?
2. How are they related to binding?
(Automated identification of protein-ligand interaction features using Inductive Logic Programming: a hexose binding case study, Santos et a. 2012)

I don't think this question should be closed. Yet you might want to add a bit more information and references.

no need to get hostile. There is a reason number of votes required for closing/putting on hold question. Regarding question: OP, do you have any reference to the phrase used? Isn't "cavity center" is just central point of given cavity?

As you can find under the table with cavity centers in pdf version of this article:

The table lists the protein’s PDB ID, the ligand considered and the specified cavity center. 22 ligands are similar to hexoses in shape and/or size. The cavity center is the centroid of the reported PDB atom numbers.

And a little later:

The binding-site center is computed as the
  hexose pyranose ring centroid for the positive examples,
  and as the ligand or empty pocket centroid for the negative
  ones. The hexose pyranose-ring atoms are located up to
  2.9
   ̊
  A away from the ring’s centroid. Since some atomic
  interactions can be important up to 7
   ̊
  A [22], we consider
  the binding-site as all protein atoms present within a 10
   ̊
  A radius sphere around the binding center. All other atoms
  are discarded.

So basically @aandreev is right. You can read about centroids here

I could not understand the head or tail of this, can you please tell me if there is any site which clearly explains these calculations?? I am not a biology or chemistry student, I am a computer science student, but my research field is bioinformatics... So i am having a lot of trouble trying to grasp what this thing means....

Could you be more specific, about your problems?

like where would I find information (calculation and explanations) of obtaining centroids of bonding sites of ligands, I want to know about these binding mechanisms and how these calculations are carried out..

https://en.wikipedia.org/wiki/Molecular_binding, https://en.wikipedia.org/wiki/Category:Geometric_centers

no no, I am probably not able to explain what I am having a problem with. Like what I want to know is that how did you obtain this fact "  The hexose pyranose-ring atoms are located up to 2.9 ̊ A away from the ring’s centroid. " . How did you obtain the the ring centroid, from which database and how did you calculate this, I know the general formula for centroid, how did you find it for the ligands

Well, if those guys didn't write it there, they probably thought of it as details - used standard formulas and atomic coordinates.

I did not understand what you meant by thought of it as details, how do one obtain these coordinates and calculate the cavity centres ?? They mentioned about a database, but could not find anything valuable, or probably I did not understand..

Atomic coordinate are in PDB files of proteins.

Sir , I could not find the atomic coordinates in the pdb files, can you tell me how to get the atomic coordinates?

@rishika https://www.cgl.ucsf.edu/chimera/docs/UsersGuide/tutorials/pdbintro.html


text:
Protein Structure Parameters
I'm wondering about the minimal set of parameters necessary to define a protein's structure.  My understanding is that the backbone geometry is defined by the phi and psi angles (torsion angles), and then from this template the side-chain rotamers are defined.  Is this sufficient to yield a geometric structure, or are there other factors involved?
On a related note, how exactly are two protein structures compared? I often see references to percent similarity, but what does this really mean?  In the Protein Data Bank, atomic coordinates are given, but my intuition is that coordinates are only important relative to all the other amino acids in the chain.  In other words, absolute coordinate comparison would seem to be uninformative.

If you're going for bare minimum data length, you'd also have to consider commonly occuring structures - think Huffman coding. Alpha helices and beta pleated sheets, for example, are a lot of data that can probably be compressed quite readily. It also occurs to me that one could define very rough parameters which give many possible configurations, but only one stable one, amongst other shortcuts.

Ah, interesting point I hadn't considered (encoding).  I think I'm going more for geometric parameters.  Perhaps another way of saying it - are torsion angles and side chain rotamers sufficient to completely determine a protein's structure?

By "protein structure" do you mean the position of the atoms in a protein at a particular point in time?

@LuboAntonov Yes, exactly - specifically the folded state.

Your percent similarity is sequence identity.

Comparing Protein Structures
There are a number of things you can look at such as root mean square deviation. This method compares the co-ordinates of two structures by superposing them on top of each other.

RMSD: This is implemented in the modelling Modeller or can be used in USCF Chimera

RMSD will provide a number in angstroms squared, with higher values indicating structural differences. A RMSD of 0.0 would indicate the structures are identical. There are different types of RMSD calculations such C-alpha, backbone and all-atom. C-alpha RMSD will only look at the C-alpha atoms to calculate the RMSD. Backbone RMSD will look at the backbone only and all-atom will take into account all the atoms to calculate the RMSD.

Other Things to Look at

Assuming the structure was created yourself, was the structure minimised? To remove clashes?
In addition phi, psi angles and mentioned above have you checked for clashes in your structure? Clashes can be checked in USCF chimera which checks for clashes with a default value of 0.6 Angstrom van der Wall radii overlap.

It depends on how accurate you want the description to be. Ideal bond lengths are normally assumed, so the structure can be described using φ, ψ, ω (for the backbone) and χ1-χ5 (for the sidechain) angles. This is what is used in most cases. However, the positions of the hydrogens in the sidechains are not uniquely defined by this description. This also does not describe hydrogen bonds and disulfide bridges, but those could be deduced from the relative positions.
You can get more information here: http://kinemage.biochem.duke.edu/teaching/anatax/html/anatax.1b.html
This description should be enough for most applications, though.


text:
SNPs and locations
I am new to reading raw DNA. When comparing two people's raw data, why does one person have a different SNP than the other, at the same location, on specific chromosome? But on a different chromosome there will be the same SNP, at the same location, for both people.

Genetic variation, my friend. People are bound to share similarities and have differences in their DNA, as influenced by errors in transcription, the environment, inheritance, etc. SNPs can be functionally significant or insignificant.

I think it is important to point out that "on a different chromosome [..] at the same location" is not the same location, and that there is not necessarily any relation between similar positions on different chromosomes. I presume you mean something like 'at basepair #74 501 on Chr1 and then also basepair #74 501 on Chr6'. These are totally unrelated positions in the genome, these chromosomes are independent. 2 genomes may vary at one position and not at the other, it's unsurprising.
Is this what you mean? We should be clear about this.

Because that's how genetic variation works. SNPs are called single nucleotide polymorphisms for a reason: they are polymorphisms. This means that they are loci where different individuals will have a different nucleotide. This is precisely why they are studied and why we have databases of SNPs and the various genotypes they can manifest.
Remember that mutations can occur spontaneously in a single individual. In fact, they can appear spontaneously in a single cell. This means that if you sequence the genome of two different cells of the same individual it is actually possible that you will find small differences.
Finding small differences between different individuals is certain. Our genomes are not identical and while most differences will be in non-coding regions, you will also have SNPs within genes. How much of our phenotypic variation depends on such small differences is an active topic of research but it is safe to assume that small, single nucleotide changes cause at least some of the variation you see in the people around you.
In any case, what would be surprising is if two individuals were to share the exact same SNP forms for all SNPs in their genomes (I'm sure this happens, but I would expect it to be the case only for close relatives and probably not even then). This variation is the whole point of SNP and the only reason we analyze them.

It sounds to me as though you have misunderstood something about the chromosomes that make up a human genome.

on a different chromosome [..] at the same location

is not the same location at all. There is no surprise in finding 2 genomes to differ in one place, and not at another unrelated place.
edit If this is a mis-reading of your question, and you meant that the 2 persons' SNP was "at the same location" as the other person, then the rest of the answer is irrelevant. 'A SNP' refers to a location, given a name/identifier for the purpose of measuring variation with SNP-chips; necessarily the same location in any person, which may vary, but needn't always differ between everyone (come on, there are only 4 possible values). You should re-phrase your question "why do they differ at SNP 1 and not at SNP2?".
Background
SNP means nothing more than 'a single basepair in the genome, that might vary in a population', so let's just talk of 'difference at a position'.
A single haploid set of the human genome consists of 23 chromosomes, 22 of these are quite 'ordinary', while 1 is involved in sex determination. Of course, most of our cells are diploid and so we have 2 of these sets, with pairs of Chr1, Chr2, ...Chr22 and X/Y.
What I think your problem isn't, that you perhaps thought it was
I haven't analysed large bits of genomic data but I believe heterozygous positions (positions at which one individual's paired chromosomes differ) are represented in that individual's sequence data. For this reason, I do not think your question is asking 'how can 2 persons have a difference at basepair x on one copy of Chr1, and no difference on the other copy of Chr1' - because both copies of Chr1 are merged as one person's dataset.
In fact it's impossible to assign (meaning to group in to haplotypes) heterozygous sequence to either one copy or the other without more information, i.e. sequences from parents & grandparents, to see which variants are inherited together (are linked).
What I think your problem really is
I think you are asking 'how can 2 persons have a difference at basepair x on Chr1, and no difference at basepair x on Chr6 (say)?'
This is easily answered. Basepair 100 of Chr1 is a completely different and unrelated position in the genome to basepair 100 of Chr6. There is no reason to expect that these positions should be related.
A helpful thought experiment
We can concatenate the chromosomes rather than re-setting our count at the beginning of each, then bp 100 of Chr6 will instead be denoted (approximately) bp 1,080,000,100 of the genome - this makes the difference in these positions crystal clear.


text:
How is the "global pLDDT" score in the Protein Data Bank calculated?
Consider this list of entries for the Tobacco Mosaic Virus (TMV). I selected to sort by 'Global pLDDT' from best to worst. It is my understanding that pLDDT is usually calculated per residue for a given prediction of a protein structure by comparing it to some 'true protein structure' (taken from PDB for example?).
I assume the 'Global pLDDT' is some form of aggregate of these per residue values? But what is the 'true protein structure' it is compared to? Other entries in the PDB?

pLDDT is a measure of confidence that ML models like AlphaFold provide for predictions of protein structures. The entries you are sorting here are not predictions, they are all experimental structures. As such, none of them have any pLDDT assigned. Notice that the order of your list does not change if you switch from 'Best to Worst' to 'Worst to Best' while sorting on Global pLDDT.
In the query builder for your link, notice the 'Include Computed Structure Models (CSM)' switch. It is set to not include predicted structures, although it appears the CSM providers RCSB integrates don't have any for TMV anyway. Here's RCSB's documentation for CSMs.
For experimental structures you probably want to sort by resolution, but the most important thing is to make sure the structure is exactly the molecule you think it is, e.g. not a mutant or a cleaved fragment, etc.

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


text:
Trying to differentiate between the three muscle tissues with small pictures
For an assignment I have to differentiate the three types of muscle tissues in these three pictures
.
I'm having difficulty seeing the striations and branches etc. because the pictures are so small. Am I missing something?

The first one is cardiac muscle(it has branches and anastomoses(where they join), the second one is smooth muscle(no striations, single nucleus), and the third one is skeletal muscle(striations, circular fiber structure with membranes).

Without answering the problem for you, because you have not shown work yet to try to figure out which is which, let me tell you that you have three options.

Skeletal Muscle- striated, peripherally located nuclei, same thickness along length, non-branching
Cardiac Muscle- striated, few centrally located nuclei, branches and anastamosis
Smooth Muscle- non-striated, centrally located single nucleus per cell, tapering ends

Now, hopefully, based on your pictures, which are indeed sufficient for you to figure out which is which, you can answer your own question. Good luck!


text:
The human organism knows what we have to eat?
My mother has told that if your organism needs a vitamin, you want fruits include that vitamin. For example you have lack of C-vitamin you would like to eat lemon. Is there any explanation for it, or just it is a myth? The human organism knows that what we have to eat?

Probably organism not organisation

@ChrisStronks Please don't recommend Skeptics unless you explain the requirements of the site. Especially the notability rules, which otherwise tend to get most questions by new users closed.

@MadScientist - I have removed my comments. What are notability rules? And which requirements do you mean? those from Bio.SE or Skeptics.SE?

Assuming you mean organism, not organisation, it's not entirely false that cravings can be driven by deficiencies. In the case of the eating disorder pica, where a person eats non-food items like dirt and clay, can be caused by iron deficiency (Source). However, that article also suggests the possibility that pica causes iron deficiency by causing the person to eat items that lower iron absorption. So, my answer to your question is, maybe.


text:
What will happen if a scorpion pierces itself?
If a scorpion pierces itself, will it die or immune to its poison? If it produces the venom its blood should be immune to itself poison.

Not necessarily. If the venom is produced and stored in an isolated venom sac or other container, the rest of the scorpion might not be exposed, and wouldn't need to be immune. Not familiar enough with scorpion physiology to really know, but I do know that a common component of scorpion venom is phospholipase, an enzyme that can disrupt membranes. These enzymes are usually produced in an inactive form that must be activated by removing part of the enzyme. Other venom components may be stored in inactive forms as well.

Cross-posted on Skeptics.

I am sorry. I have deleted it on Skeptics.

If scorpions evolve by fighting each other, perhaps there is a kind of 'arms race' where the anti-venom of one scorpion is stronger than the other's sting, it will survive it...but if the sting of one is stronger than the others antivenom, it will win the fight , kill or stun it? Is this how scorpons have become more toxic over time?
https://www.youtube.com/watch?v=zB5xiog7jk8

Scorpions are immune to their own venom (reference) as has been said in some studies as well (reference) But some other studies and eye witness accounts have referred to the contrary.

in an experiment a scorpion, Bulteus australis, was killed by an
  injection of the same venom as its own (reference).

So, it should be safe to say that there is a very low chance for a scorpion to be affected by its own venom. It is said that

Mutations in the scorpion’s own membrane protein genes make the
  arachnid immune to its own venom (reference).

A scorpion could die quickly if venom is injected into its brain (nerve ganglion). Larger species inject a higher amount of venom to overcome the smaller ones and should have specific neurotoxins if smaller scorpions are their prey to disable them (reference).

Didn't know this one was answered +1. I tried, and failed :-) Haven't seen you around for a while!

@AliceD Busy with some paper writing and PhD applications.. hard to get into a decent funded PhD project these days so the effort continues.. :)

authors: Μαρίνα Ξανθή


text:
Why I have to pee more often in low temperature?
I realised that I have to pee more often in winter or simply the temperature is low. Is there any scientific explanation, or just simply psychology?

This question, and its answer, are surprisingly fascinating.

@blackcornall when you notice this are you experiencing symptoms of hypothermia?

@rob No, I am not. Just simply feel the cold.

This phenomenon has been demonstrated in studies [1][2] which show a significant increase in urine output in the cold. The latter study shows the biggest increase is when a person is initially exposed to the cold rather than when they continue to be exposed or rewarmed up. In the study, the average urine out was 157 mL/hour when a person was initially exposed to the cold, 103 mL/hour when they were being maintained at that cold temperature and 70 mL/hour when they were being rewarmed.
The mechanism however is unclear. This study showed that the mean arterial pressure increases. It is well known that the cold causes our blood vessels to constrict (in order to keep the blood and therefore heat inside our core body). The thought was therefore that our kidneys try to lower our blood pressure by taking more fluid out and emptying it into the bladder. This is called cold-induced diuresis.
Other thoughts include that we lose the water we ingest by sweating (perspiring), pooping (defaecation) and peeing (micturition/urination). In the winter, we don't typically sweat as much, which ISN'T counterbalanced with a lower water intake, so we need to pee more.
Another possibility is that aquaporins (the pores that water comes out from our kidneys) are inhibited by the cold. This means more fluid would be filtered out. However there isn't really much research in this area that I am able to find.

Interesting possibilities, but some references would be awesome.  It would also be interesting to know whether the premise posed in the question is actually true or if it just seems true (perhaps because it's less pleasant to use the bathroom when it's cold, or for some other reason).

The last paragraph would be especially nice to have a reference for. In warm-blooded animals, it’s not obvious how a cold environment affects the temperature sensed at the level of the aquaporins. I guess you’re positing some more elaborate mechanism via CNS thermoregulation/ADH? (And minor point: aquaporins don’t affect filtering (glomerulus) but reabsorption more distally (collecting duct).)

@rob, as requested I have added two references which demonstrate this effect.

Cold-induced diuresis, where kidneys relieve blood pressure by increasing urine production.
http://en.wikipedia.org/wiki/Cold-induced_diuresis
The blood pressure is thought to be increased by vasoconstriction due to the cold. One source that supports that theory: Sun, Z. American Journal of Physiology -- Regulatory, Integrative, and Comparative Physiology, February 2005; vol 288: pp R433-R439. American Heart Association: "High Blood Pressure."

Could you elaborate this answer a bit more (e.g., why is blood pressure higher in the cold?). As of now it is more of a comment and comments should not be posted as an answer.

@ChrisStronks the poster doesn't have comment privileges yet.

@dustin - I know, that is why I ask for a little bit of elaboration.

This is the reference @rob was asking for. +1


text:
Alternative plant taxonomies to Linneaus
In addition to Linneaus-inspired taxonomies of the botanical world, I suppose there are some other proposals for different kinds of taxonomic accounts, perhaps for specific sub-domains of botany or perhaps historical. I'd be keen to learn about those.
Additionally, if any of you know there are some other alternative non-taxonomic approaches to botanic classification that are widely-used in sub-domains or in the early days of science, I'd be keen. I guess there are still some "common sense" classification to be made between use (ornamental/non-ornamental; medicinal/edible/poisonous), but perhaps there's more.

The most common alternative to taxonomic classifications are functional classifications. Emphasizing ecological similarities rather than similarities in relatedness, they can be regarded as complementary approach to, but not as a replacement of taxonomy. Why do we need this? Because species often perform very similar tasks, exhibit very similar characteristics and, most importantly, are very, very numerous (there are ~ 300,000 vascular plants). Reducing this redundant complexity is crucial for decision-making in conservation politics or the projection of vegetation change under future climatic conditions (Woodward & Cramer, 1996).
The idea behind this is to use functional traits, such as seed size, height, photosynthetic pathway, root density, etc., as a surrogate of a species' ecological 'role' -- its response to environmental factors and its impact on ecosystems. Seed mass for example (functional trait), is a proxy for the dispersal ability of a plant (function, performance). You should have a look at Lavorel et al. (2007), there is a nice table (too big to include here) that links specific traits to the actual ecological functions they describe. But look at this figure from the same paper:

By applying multivariate statistics like cluster analyses or ordination methods, species can then be classified into functional types. To make up one example, a functional type that might emerge from species with the following traits

height: > 20 m
seed size: > 0.5 cm
woody: yes
Specific leaf area: low

would certainly represent climax forest trees. This classification does not distinguish between individual species, because, from an ecosystem perspective, they all are functionally roughly equivalent.
For further research google 'Functional trait', 'Plant functional type' or have a look at refs 3 and 4.

Citations:

Woodward, F. I. and Cramer, W. (1996): Plant functional types and
climatic change: introduction. Journal of vegetation science, 7(3):
306–308.
Lavorel, S., Díaz, S., Cornelissen, J. H. C., Garnier, E., Harrison, S. P., McIntyre, S., Pausas, J. G., Pérez-Harguindeguy, N., Roumet, C., and Urcelay, C. (2007): Plant
Functional Types: Are We Getting Any Closer to the Holy Grail? In: Canadell,
J. G., Pataki, D. E., and Pitelka, L. F. (editors): Terrestrial Ecosystems in a Changing
World, Global Change—The IGBP Series, pages 149–164. Springer Berlin Heidelberg.
Halloy, S. (1990): A morphological classification of plants, with
special reference to the New Zealand alpine flora. Journal of
vegetation science, 1(3): 291–304.
Leishman, M. R. and Westoby, M. (1992): Classifying plants into groups on the basis
of associations of individual traits–evidence from Australian semi-arid woodlands.
Journal of Ecology, 80: 417–424.