text:
Are nutrients absorbed in human esophagus?
Following this question regarding absorption in human oral cavity (sadly not yet fully answered), I'm curious if any nutrient absorption occurs during the descent of food through the esophagus.
And if so, what requirements must a nutrient meet for that.

For several reasons, I seriously doubt that this has been studied extensively.
There is a good reason to study absorption through oral mucosa because a drug or glucose can be held there by people who needing rapid absorption of a drug (e.g. sublingual nitroglycerine) or by people who may be unable to swallow (e.g. a hypoglycemic individual who has lost consciousness). Where there is a reason to know, there is a reason to study something.
The esophagus, on the other hand, is normally an area of rapid transport (a pill, or a fluid, for instance, is in the esophagus less than 10 seconds). While it's assumed that some pregastric absorption through the esophagus occurs and might be beneficial to avoid a "first pass" metabolism of the drug by the liver, there is no good method to keep a drug in the esophagus. With that in mind, absorption from the sublingual mucosa (where a pill might be held) is more valuable than what might get absorbed in as little as 6 seconds in transit to the stomach. From that point, it will spend significant amounts of time in the stomach, the various sections of the small intestine, and the large intestine.
Absorption of drugs from the rectum has been studied, because it can be used, once again, as a method of drug delivery when another route for whatever reason cannot,
Esophageal motility disorders occur, so studies of esophageal function are common. But as the esophagus is never normally the place for absorption of nutrients, there is no reason to study it except for the sake of satisfying pure curiosity. Studies take time, involve volunteers (or paid recipients), risk, and money. Pure curiosity is a reason to study something. But to get the all the previously mentioned factors to come together and fund a study, the reason usually outweighs pure curiosity.
Esophageal scintigraphy: reproducibility and normal ranges
Oesophageal transit of a radionuclide solid bolus in normals
DRUG ABSORPTION BY SUBLINGUAL AND RECTAL ROUTES

an exception to the slow transit time is when there is a diverticulum... here is a case study demonstrating altered absorption of drugs caused by zenker's diverticulum: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2429168/ of coarse the solution is not to take into account the altered absorption in the diverticulum and study the rates of absorption of drugs/nutrients... instead the solution is to just close it up...

yea... achalasia, CREST syndrome, esophageal webs, esophageal spasm, cancer etc... just saying that quick transit time is physiologic, but under pathologic circumstances it might not be the case and the esophagus could potential be a site of absorption into venous circulation and lymphatics... not saying it should be studied because it's probably not important, just saying absorption is possible under freak circumstances... also it's clever that he/she noticed that oral absorption, gastric absorption, intestinal absorption, rectal absorption have all been studied and why not esophagus?

@JasandPruski - actually, you just mentioned an important factoid: some people are trying to treat esophageal cancer with mucosal agents to take advantage of that very fact, as well as it's lack of first pass metabolism. Sorry to seem so picky.

what makes it a "mucosal agent"? different pill design or high 1st pass metabolism?

Prolonged contact with the mucosa. It can't be a pill, though.

then it's a solution, I'm assuming


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Have there been studies done to test Immortality of cancer cells in culture?
This website on cultured cancer cells () says cancer cells may be immortal.
I am wondering if there has been any research done to find if cancer cells are really immortal.

How old is the still maintained living oldest culture of cancer cells?
Has there been any research done on replicative senescence of Cancer Cells invitro?

Edit 1:
If there is some data relating to the number of replications the cells have undergone, it will be very useful

The HeLa cell line is undoubtedly the most used and investigated human  immortal tumor cell line. Extracted from a cervical tumor from Henrietta Lacks in 1951 at Johns Hopkins hospital, Baltimore, MD these cells proved immortal and are still used in many, many labs worldwide today. It is the oldest human cell line in use and, therefore, the oldest human tumor cell line (Callaway, 2013).
In terms of senescence of immortal cells; HeLa cells are immortal, and hence do not grow old as such. However, they are subject to mutations and the genetic profile of HeLa cells does change over time. Hence, although they may not be growing old, they do age in the sense that mutations are accumulating in continuous cell lines.
References
Callaway, Nature (2013); 500: 132-3

Will add refs later, I am mobile. Informative website: http://www.nature.com/news/deal-done-over-hela-cell-line-1.13511

Take your time @ChrisStronks

very interesting read Chris, Thanks for the link

More info: http://www.embl.de/aboutus/communication_outreach/media_relations/2013/130311_Heidelberg/

I am not specifically asking for human cancer cell culture @ChrisStronks. Is HeLa the oldest of cancer cell culture (among all species)?

My answer marked (1) should answer this. In other animals I am unsure.

I wanted to know for sure, as data on animal cell lines seem scarce. All I knew was animal cell lines were established and experimented upon way before human cell lines were started. That's the reason for the post

@ChrisStronks CTVT is not a cell line, it is a natural tumour that has become infectious (thereby making it a pathogenic parasite). A good recent example of a retrograde evolution.

@WYSIWYG I removed CTVT from my answer. Thanks.

@WYSIWYG just wondering, how was it determined that CTVT cells belonged to canids? It seems that chromosomal composition varies vastly

@CRags See this paper. They have done genomic analysis and commented that the mutations seem to have arisen because of UV exposure. I guess there were no major chromosomal aberrations to prevent its identification as a canine derived tumour.

@WYSIWYG Thanks for the link, I think I will post a new question to discuss further on this

Added a reference, finally!

I think, a story about Alexis Carrel and Leonard Hayflick is appropriate here.
In the beginning of 20th century a Nobel prize-winning medicist/biologist Alexis Carrel published a series of papers, claiming that growth of a culture of cells of normal somatic differentiated tissue can be maintained indefinitely without undergoing cellular senescence. This wrong result was held for a fact for many years, before being disproved by Leonard Hayflick, who's shown that normal somatic cells undergo a limited number of divisions before dying and immoratlization happens in cancer cells. It's worth mentioning that the cause of Dr.Carrel's error might be attributed to his personality. For instance (quote from Wikipedia):
Carrel claimed the existence of a "hereditary biological aristocracy" and argued that "deviant" human types should be suppressed using techniques similar to those later employed by the Nazis.

So, the results of his finding might be attributed to a version that he's just scared his laboratory members so much, that they started to secretly replace a deteriorating culture with a new one.
I may be rough on the corners and attribute sins to the man, he's innocent of. For a "fair trial" with evidence etc., you'd better address this paper: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1082700/
See also this popular paper: http://www.theguardian.com/science/2015/feb/18/haruko-obokata-stap-cells-controversy-scientists-lie

Terminology involved makes everything lie a bit.
All the "immortality" and so complicate things a bit. We perceive life as life of our individual bodies. Thus if our body is immortal, that means that it is persistent, without us bothering about our individual cells.
But, there isn't any distinction like that in single cell organisms where cells themselves are taken as "individuals". When cell divide, there isn't usually any distinction of which one is "mother" and which one is "daughter". Both new cells are usually the same. So either it may seem that cells are immortal because they are not dying by old age, or that we define new cells as new individuals and thus the old one died to give birth of two new ones.
But we could take certain aspect of this viewpoint on multicellular organisms as well. Our bodies are defacto created by very old cell-line (or in sexually engaged organism, two cell lines) and then this cell-line created vehicle for itself. From this viewpoint, which is not very different from viewpoint taken when speaking about these laboratory cell-lines, whole life is single cell-line. And from this point of view, life itself is immortal.
So the whole problem is that our point of view, on which we define immortality and individuals, is made only for special types of organism, as has no sense when speaking about single cell organisms. Immortality of cancer cells is thus only buzzword.

You're not even wrong

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What are the differences between a benign tumor and swelling?
What are the differences between a benign tumor and an injury related swelling?
And can swellings due to injury turn into a benign tumor?

Hi @chrisstronks, so what is a swelling?  in another question someone told ne that thats kind of tumor. .. thanks for helping

There is too much confusion of terms here for the question to be answerable.

"Tumor," latin root Tumere is for swelling. If you're looking at a modern definition though, you have to consider the abnormal tissue growth. Yes, injuries may produce a thrombus, embolus, etc. however when you get injured and it swells, that isn't really a tumor. Injury swelling is just a biochemical response, but isn't characterized by cell proliferation.

@Kendall - This would be a fitting answer. I'll edit question and vote for reopening.  Could you turn it into an answer?

@MalicOfSdom - I removed malignancy here, as the step from benign to malignant may make the question too broad. If you are unhappy with the edit roll back. I am just trying to reopen this question. It covers your other closed swelling question as well. Perhaps turn benign vs malignant in a new one?

The term tumor is used in the medical definition of inflammation. However it just denotes a temporary swelling that goes down once the inflammation subsides. This swelling is due to edema (accumulation of fluid). You have to understand that in practice no one uses the term tumor to denote an inflammatory swelling. So the term “tumor” denoting edematous swelling is of historical significance only.
In modern practice the term tumor is used only to indicate abnormal growth of any kind. Either benign or malignant.

In pathology an inflammation is classically described as having the following features:

Tumor : Swelling
Dolor : Pain
Calor : Warmth
Rubor : Redness

Replicated from comment section:
"Tumor," latin root Tumere is for swelling. If you're looking at a modern definition though, you have to consider the abnormal tissue growth. Yes, injuries may produce a thrombus, embolus, etc. however when you get injured and it swells, that isn't really a tumor. Injury swelling is just a biochemical response, but isn't characterized by cell proliferation.

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How was the origin of CTVT parasitic cancer determined?
The wikipedia article on CTVT says that the tumor cell has 57-64 chromosome while a normal dog has 78 chromosomes. Similarly while all chromosomes in dogs except the X and Y chromosomes are acrocentric, many of the CTVT chromosomes are sub-metacentric or metacentric. Reference is given for the data in Wikipedia though a subscription is needed to view the referred articles themselves, so I was unable to confirm the data. (Wikipedia is sufficient for me, though popular opinion seem otherwise)
In addition there seems to be numerous (in the order of thousands) differences in sequences.

Their study showed that the cancer cells all originated from a common ancestor cell, not from the dogs themselves. Comparisons of the cancer DNA with dog DNA from reference samples held by the US Kennel Club and Crufts showed that it most likely originated at least 250 years ago from a wolf or an "old" Asian dog breed such as a husky or Shih Tzu, and spread like wildfire thereafter.

This was taken from Riddle of Infectious Dog Cancer Solved.

How is the conclusion arrived at in cases like this in general? What percentage / degree of genetic similarity is needed to identify something as belonging to a specific species?
How was the conclusion arrived at in this specific case? (I know I am greedy!)

I don't quite understand what (or maybe better why) you're asking. If Wikipedia is sufficient for you, why do you want more information?

Because what I am asking is not there in Wikipedia

"How is the conclusion arrived at in cases like this in general?" The same way it was in this case, by DNA analysis. It's in your article.

I am asking how DNA was analysed? Especially when there is such gross deviation in chromosome number and structure. Why are you being so antagnostic? Are you fed up with me because I disagreed with you? Lol, it's a free world and a person can disagree with anything!!

I'm not being antagonistic. You stated that you rely on Wiki. That's fine, then did you read about DNA analysis on Wikipedia? DNA analysis doesn't mean comparing chromosomes. It means looking at, for example, histocompatability loci. In the case of your tumor, mitochondrial DNA was very useful. My questions are usually a prompt to improve questions with a bit of research. The answer is in your article. If that's not helpful, you can do a bit of research to let us know what, exactly, you know or don't know, so we don't need to write a chapter on DNA analysis and guess at what you're asking.

@anongoodnurse OK, will read the article again and try to refine my question. Thanks for the pointer

@anongoodnurse after reading different articles I could not find how the genetic matching was done, if you would be kind enough to provide a link I would be grateful.

Your answer to your titular question, How was the origin of CTVT parasitic cancer determined? is that cytogenic studies were done on the tumors. It arose in dogs and was logically assumed to be of dog origin, and was first characterized in 1876. The tumor cells were/are characterized by a rearranged karyotype, which is similar in tumors from in different parts of the world. (1969) Thus it was postulated that that the transmissible agent causing the CTVT is the tumor cell itself and that all worldwide CTVT have a clonal origin. (1985)
Your later question states:

What percentage / degree of genetic similarity is needed to identify something as belonging to a specific species?

When a tumor arises in an animal (say a dog), it is automatically assumed that the cancerous cells, regardless of their ploidy, arose from that animal (in this case, a dog), not a different animal. Not all animals have had their entire genome sequenced, so this question as stated isn't answerable (although the genome of the dog has been completely sequenced). And certainly, not all tumor cell lines have been completely sequenced. The assumption of origin is made by looking at certain genes (e.g. histocompatibility genes) and others known to be species specific.
Since there are relatively few transmissible cancers (that is, where the cancer itself acts as the infectious agent), this is still a safe assumption. While I'm fairly confident more transmissible cancers will be found, I'm also fairly confident that they will be species specific, because in order to escape detection, they will need to be recognized immunologically as "self", as they must survive in the host at least long enough to be transmitted.
This is the case with canine transmissible venereal tumor (CTVT). It is also the case with the contagious tumor Tasmanian Devil face tumor disease (DFTD). Just as with the canine infectious cancer, DFTD cells in different individuals have identical, complex chromosomal rearrangements and are genetically identical to each other but different to the host devil.

Spread of such an infectious cell line between unrelated individuals should be prevented by major histocompatibility complex (MHC) Class I antigens on the surface of the tumour cell, as Class I molecules play a key role in self/non-self-recognition. The recent emergence of the tumor (transmitted by biting) in the endangered marsupial Tasmanian devil (Sarcophilus harrisii) is an unfortunate exception. In the Tasmanian devil, the tumor is very aggressive and kills the host.

In the case of canine transmissible venereal tumor (CTVT), it was shown about five decades ago to be the same dog tumor being spread from dog to dog. The earliest studies were based on histological studies and karyotyping. Paraffin-embedded tumor samples still exist. More recently, with genetic analysis, it is possible to perform much more sophisticated testing on the tumor DNA.

The transmissible agent causing canine transmissible venereal tumor (CTVT) is thought to be the tumor cell itself. To test this hypothesis, we analyzed genetic markers including major histocompatibility (MHC) genes, microsatellites, and mitochondrial DNA (mtDNA) in naturally occurring tumors and matched blood samples. In each case, the tumor is genetically distinct from its host. Moreover, tumors collected from 40 dogs in 5 continents are derived from a single neoplastic clone that has diverged into two subclades. Phylogenetic analyses indicate that CTVT most likely originated from a wolf or an East Asian breed of dog between 200 and 2500 years ago. Although CTVT is highly aneuploid, it has a remarkably stable genotype.

Your quote

likely originated at least 250 years ago from a wolf or an "old" Asian dog breed such as a husky or Shih Tzu...

Has been disputed. Estimates vary widely, from 11,000 years to 250 years.
Canine TVT: Evolution of Somatic Tumour Cell as Transmissible Parasites
MHC gene copy number variation in Tasmanian devils: implications for the spread of a contagious cancer
Clonal Origin and Evolution of a Transmissible Cancer

@CRags - Are you an editor? Perhaps you can update the Wikipedia article to reflect the new information?

ok, will do today later @anongoodnurse


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Conversion and storage of glucose to glycogen
Why is excess glucose, synthesized to glycogen, stored only in limited amounts, as compared with lipids/triglycerides that are stored in our body?
Why is mature glycogen arranged (polymerized) in 12 tiers polymer?

Glycogen storage limitation is due to these additional facts also:

Glycogen is a hydrophilic molecule. This means an increase in glycogen concentration will cause a proportionate increase cell weight due to water accumulation. As cells can contain only limited volume the amount of glycogen stores are limited. Lipids are hydrophobic hence can be accumulated without increasing the volume and weight of cell due to water accumulation.
As a source of energy lipids are approximately 2.5 times more efficient than glucose.

In this presentation from stanford.edu, it's stated that the number of granules is directly dependent on the number of glycogenin molecules available, and the size of the granule is directly dependent on the need for physical association b/t the glycogen synthase, and glycogenin.


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Plural of "dibamus"
Migrated from English site.

Dibamus is a genus of legless lizards in the family Dibamidae, of the infraorder Dibamia.
Genera are usually given in singular, so what is the correct plural of Dibamus?
Families and orders are usually given in plural, so what are the correct singulars of Dibamidae and Dibamia?
Bonus question: What is the etymology of the root dibam-?

There is no plural...Just call them Dibamus species.

@Hav0k Not going to work. In reality, I want to know the plural of an item named Dibamus after the lizard. What are two of those called?

You could use the term "individual". 5 dibamus individuals.

If you try to use Dibami or Dibamuses etc. that will tamper the scientific name, which is an "identifier". i.e. it will indicate to a thing different from Dibamus.  Another fact, the name of a taxon (whatever its rank- species or genus or family etc) is the identifier for a "set", not individual. So the genus name Dibamus indicates a "set" or kind-of organism, and there could not be more-than-one Dibamus sets.

For a casual text (acceptable to public), you could try the term 5 Dibamus lizards; but from strict technical viewpoint, Lizard also indicate to a particular "set".

If you know a vernacular name (Is it Dibam lizard?), then you could use grammatical modifications of it, like 5 dibams or 5 dibam lizards. Since the vernacular-name is not the universal identifier, once in your text you have introduced the readers as your dibam lizards are Dibamus sp; then you can effortlessly continue with that vernacular name

This is advice from a website on plants, but its advice is equally valid for plants or animals.

For example, if you wish to discuss several Pinguicula species, do you
call them Pinguiculae or Pinguiculas? The answer is that you can do
neither! Pinguicula is the name of the genus, a single group of plants
which was very carefully named. If you make up a word like
Pinguiculas, you are either implying that the genus has a letter "s"
at the end (which it does not), or you are saying that there is more
than one genus with the name Pinguicula---a logical absurdity.
So it is just wrong
to fabricate a plural form of a genus name. If you find yourself
writing a sentence where you want to create a plural form of a genus
(suppose you wanted to say, "I saw several Pinguiculas"), reconstruct
the sentence slightly into something like "I saw many Pinguicula
plants" or "I saw many Pinguicula species," whichever you meant. It is
not only correct, but also much clearer.

There is a caveat to this, which is when the genus is borrowed into English as a loanword, for example, a plant of the genus Delphinium has the common English name "delphinium", or an ape of the genus Gorilla has the common English name "gorilla". In this case, the English word is pluralised into "delphiniums" and "gorillas". Note that it is still perfectly correct to say "I saw two apes belonging to the genus Gorilla", but it is just long-winded.
In your case, the lizard does not fall into this category, so you should word your phrase as "several Dibamus lizards" or a similar alternative phrasing.

Nice, but not going to work. My issue is a technical item that has been named Dibamus after the lizard. Now I don't know how to refer to several Dibam...

@NBZ That's a completely different question, but has the exact same answer. The plural of the technical term will differ based on the term itself. For example, the Bittorrent client Azureus is named after the frog Dendrobates azureus, and I would pluralise that as "I am running two Azureus bittorrent clients".

Fine, I guess it will be "Dibamus thruster blocks" or "Dibamus engines" then.

Yup, I would probably do the same in your shoes.


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Is there an organism which has a common English name which overlaps with another organism's scientific name (or vice versa?)
Many organisms have their common names identical to their scientific names. For example, there exist apes of the genus Gorilla known commonly as gorillas, and plants of the genus Delphinium known as delphiniums.
However, are there any examples of the common name of an organism overlapping with the scientific name of another organism, therefore causing ambiguity when the organism's name is spoken aloud? If written with correct formatting, this should not cause a problem in any case, due to the formatting specifically describing a genus/species.

For extra points, "boa constrictor" is both the common English name and the scientific genus+species name. Whereas "gorilla" is the genus and also the species, but they're not commonly referred to as "gorilla gorillas" ;-)

One great example I know of is the duck-billed platypus (Ornithorhynchus anatinus),  often simply called a platypus, which shares its name with the Platypus genus of ambrosia beetle.
Wikipedia gives a brief history of the taxonomy of the duck-billed platypus:

The common name "platypus" is the latinisation of the Greek word πλατύπους (platupous), "flat-footed", from πλατύς (platus), "broad, wide, flat" and πούς (pous), "foot". Shaw assigned it as a Linnaean genus name when he initially described it, but the term was quickly discovered to belong already to the wood-boring ambrosia beetle genus Platypus. It was independently described as Ornithorhynchus paradoxus by Johann Blumenbach in 1800 (from a specimen given to him by Sir Joseph Banks) and following the rules of priority of nomenclature, it was later officially recognised as Ornithorhynchus anatinus. The scientific name Ornithorhynchus anatinus is derived from ορνιθόρυνχος (ornithorhynkhos), which literally means "bird snout" in Greek; and anatinus, which means "duck-like" in Latin.

Plants known commonly as geraniums belong to the genus Pelargonium.
Similarly, plants known commonly as cranesbills belong to the genus Geranium.

"Armadillidium" is the name of a genus of isopods (woodlice, also called armadillo bug). The armadillo familiar to residents of the southwestern US is a mammal belong to the genus Dasypus.There are related genera going all the way through South America.

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Can an upper forearm amputee correctly control the Median and Ulnar nerves
I'm an engineer who is looking to build a robotic hand for people without their upper forearm(from center of forearm in direction of hand), controlled by the Thalmic Myo(an EMG sensor). I am first checking for the idea's viability.
I was wondering if one who does not have their upper forearm can still send the correct nerve impulses for a desired hand movement through their Median and Ulnar nerves?

Yes, severed nerves still convey neural responses from the brain.
In fact, nerve potential recordings in the ulnar and median nerves of the stumps of arm amputees have already been successfully applied to control arm prosthetics (Jia et al. 2007; Kuiken et al., 2007.

I will work on formatting the refs later. I am mobile. Kuiken et al.: http://www.ncbi.nlm.nih.gov/pubmed/17276777. Jia et.al: http://www.ncbi.nlm.nih.gov/pubmed/17482005

Will such patients have phantom arm syndrome? @ChrisStronks?

@CRags - likely. Many amputees have phantom sensations, but I am not an expert on that. I am only familiar with Ramachandran's work and that suggests it is very common in upper arm amputees. The severity differs.

I am asking particularly about people with prosthesis as they need ulnar, radial and median nerves in functional order. If you find anything incidentally anytime please add it with a comment to me! Thanks!

@CRags - For now I can say that active use of (conventional) prosthetics reduces phantom pain. I will update if I find out more.


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More general usage of the term 'congener'
In taxonomy the term 'congener' refers to two species within the same genus. In more colloquial usage, it can refer to any two objects within the same category. Is there a way to refer to related species that is not specific to a particular taxonomic rank--as in, in the same order or family but not necessarily the same genus?
Update: I guess the term 'relative' works, but I still wonder if there's a better term.

Confamiliar is used sometimes (just google it). At lower taxonomic levels, such a term somehow loses its meaning, doesn't it?

Can you give us an example sentence where you'd like to use this term? I'm finding it hard to understand why you wouldn't just use the family or order name itself (i.e., "Tigers, like other big cats, ..." instead of "tigers, like their confamiliars, ...")


text:
How much total RNA can be extracted from Drosophila brain
I am wondering how much total RNA could be extracted from a single D. melanogaster brain.
I could not find this information from the literature.
The closest hit was this paper, that claims that 16-21.9µg of total RNA can be extracted from 100 brains, which translates to at least 160ng for a single brain.
I also found in the supplementary material of this paper that 1µg of total RNA was extracted from 5-10 fly brains, which would also make > 100ng for a single brain.
I am asking the question because I am envisioning to perform RNA-seq of single Drosophila brains. The standard Illumina TruSeq library preparation protocol works with 100ng of total RNA. Thus I am wondering if this is realistic, or if I should rather target low input library preparation protocols.

In my opinion you should try low input library prep protocols because in my experience even with a decent quantity of RNA, standardizing the sequencing is not an easy job. The manual says that this kit works with 10-20ng of RNA; always assume the higher limit to be true. There is a higher chance of loss (relative) during extraction also. Try doing precipitation with 5M LiCl and a little glycogen along with alcohol; but assuming your yield is 80ng you can still run replicates for statistical comparisons.


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Non-harmful bacterial invasion of cells
There are bacteria that can enter body cells as parasites.
Could it be that some of these are benign, such that the guest will not kill the host cell it lives in (especially in human)?

I think lactobacillus might be a good answer here

@ChrisStronks, thanks for the edition. Yes I tried to google it, didn't find good answer. And yes, it's really the direction of mitochondria, if there is something like that, at least not harmful to human.

@Barbos, no worries. Interesting thoughts. +1

@rhill45 Lactobacillus don't enter cells IIRC. I think some Wolbachia infections of insects may be possible, not very sure though.

@MarchHo he did say that sorry missed that. Driving and iPhone and SE prob bad idea

@MarchHo, according to wiki and few others, Wolbachia don't lives in human, only insects, and I am asking more about humans. But still, very interesting, thanks.

@Barbos Hmm, I didn't see the "in human" part, so apologies for the irrelevant example.

@MarchHo, it is relevant, helpful and interesting! Thank you. Also I added "in human" a little bit after posting the question - so I need to say sorry.  Just already heard before, that in some spices there are some symbiotic relationships with microbes (inside cells), but it's good to see real example. So again, thank you!

You wish to limit the examples to bacteria?

@canadianer, what else possible? (not talking about viruses of course)

Isn't this how mitochondria came to be a part of our cells?

Why just humans??

@WYSIWYG because I already know that there is such thing in other spices.

@Anne What you are referring to is called endosymbiontic theory.

Plasmodium vivax was historically used to induce fever as a treatment for syphilis (malariotherapy).  Not exactly benign, but it had a therapeutic benefit nonetheless.

Survival of the host cell is in many cases dependent on the egress strategy of the pathogen. There are many examples documented in various species. The only case I found that's somewhat relevant to human cells was were mutant Legionella pneumophila, defective in the lytic pore complex, did not produce necrosis of the host cell. However, the cells did release the bacteria after a while, probably apoptosis due to accumulation.
EDIT: I found an article documenting Cryptococcus neoformans infection.

Cryptococcus neoformans causes disease in people with immune deficiencies such as AIDS. Upon infection, C. neoformans cells are ingested by macrophage immune cells, which provide a niche for survival and replication. After ingestion, macrophages can expel the fungi without causing harm to either cell type, a process named nonlytic exocytosis.

I couldn't find any examples in humans (aside from mitochondria, if those count), but there are examples of varying degrees of intracellular endosymbiosis in insects, plants, and single-celled organisms.
An example is Ca. Carsonella ruddii, an endosymbiontic bacterium of psyllids (a family of plant-feeding insects).  The bacterium lives within specialized host cells called bacteriocytes.

Many insects harbor intracellular bacteria that produce and excrete essential amino acids into the host cytosol. Although, in some cases, ‘dead-end’ bacterial cells with incomplete genomes are replaced by new endosymbionts, this is not the case for the bacteriocyte Carsonella ruddii. The genome of Carsonella is reduced to a mere 160 kb (within the range for organelles), has lost all genes for many essential functions, and no other bacterial endosymbionts are present to offer potential compensation. Thus, Carsonella seems to be at the end of an endosymbiotic continuum in sap-feeding psyllid insects and represents the recent acquisition of a new type of organelle for biosynthesis of amino acids.

Source: The intracellular cyanobacteria of Paulinella chromatophora: endosymbionts or organelles?
Wikipedia's article on endosymbionts has some other interesting examples.

there is a word symbiosis which means interaction between two different organisms living in close physical association, typically to the advantage of both.Often, especially with microbes, one organism lives inside another — the host.
symbiotic microbesWhen both organisms benefit from the relationship, it is called mutualism. When only one organism benefits, but the other one is not harmed, it is called commensalism.
and yes,bacteria can have symbiotic relationship with human.bugs inside
One example is the bacteria that live inside the human digestive system. These microbes break down food and produce vitamins that humans need. In return, the bacteria benefit from the stable environment inside the intestines. Bacteria also colonize human skin. The bacteria obtain nutrients from the surface of the skin, while providing people with protection against more dangerous microbes.
moreover Your body is made up of around ten trillion cells, but you harbour a hundred trillion bacteria. For every gene in your genome, there are 100 bacterial ones. This is your ‘microbiome’ and it has a huge impact on your health, your ability to digest food and more. microbiome


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How do tea, coffee, and beer dehydrate you?
For the long time I am trying to find out if the following is truth: They say that some beverages dehydrates. I heard that about tea (sometimes green, sometimes black, sometimes both), coffee, beer and more (for example coke).
How does hydration from these sorts of drinks compare to others (e.g. water)? Why do these drinks less efficiently hydrate?

Diuretics
These drinks contain minor diuretics. Caffeine is the diuretic found in tea and coffee. Alcohol is the diuretic in beer. Diuretic substances increase the amount of urine produced i.e causes dehydration. This is often offset by the water content of mild diuretics like tea, coffee, and alcoholic drinks.
Tea, coffee, and coke
Caffeine belongs to the xanthines, and inhibits re-absorption of Na+ by cells, and increases flow rate of filtered fluid through the kidneys. This reduces water content in your body. In other words diuretics do dehydrate you, specifically caffeine will. Coffee, coke, and tea (very low doses of caffeine) are mild diuretics.
Beer
On the other hand alcohol is an anti-diuretic hormone inhibitor that inhibits arginine vasopressin.

OK, thanks. I wonder if the benefit from amount of fluid we get from them is bigger or smaller then the handicap of dehydration.In other words it is worth to dink them if we want to have a good drinking regime?

@TedGar That's a great separate question I guess!

As a quick guess: there isn't enough caffeine in a mug of tea to dehydrate you in any noticeable way, you would have heart complications if all you drank was coffee, and the alcohol would wipe out your liver. But I imagine there is still enough liquid retained to hydrate you, but you would be drinking much more than the equivalent water.

Thank you, it seems logically. And I'll try open a new question, who knows…

There's some data to show moderate caffeine intake doesn't necessarily dehydrate you, but the parameters are undoubtedly obscured by what you're doing, and what you're drinking. In terms of alcohol, i believe it was approx 10mL urinated for every 1g ethanol, though i cant substantiate that claim with a source.

New question: http://biology.stackexchange.com/questions/28098/dehydration-from-caffeine-alcohol-and-other


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How does menstruation proceed during one period?
I'm simplifying things here:

A. Does a woman bleed constantly, like a drop every 10 minutes? Two hours without pad or tampon and your underwear is dirty?

or

B. Does a woman bleed suddenly a bigger amount of menstruation fluid? Then hours might pass before it happens again?

or

C. Both.

Might be a stupid question. I'm sorry. I read all the other information on the internet but no one answers this one for some reason. I read girls should change the pads and tampons a few times a day (like every 6 hours). Does that mean A is correct?
Thanks for any helpful information!
(Well, I guess I'm male.)
Edit:
What I want to know: If I was a woman, how would I experience the days of period bleedings? From what I read in the comments and answer(s), one should expect A (constant bleeding) and should wear pads/tampons all the time (for 2 to 7 days) and sometimes one could also experience an exceptional heavier bleeding (B)? Are there (healthy) women who would experience B most of the time? I visited Wikipedia and other random sites but they all have the other important information without answering my question. (Also I will be glad to accept an answer, which satisfies my need for knowledge.)

It would help the quality of your question if you cite the websites that you read that weren't helpful.

This isn't much of an answer but here goes... Two things; it depends on which day of the period it is. There can be rather brief, heavy bleeding on the later part of the first day or sometime during the second. On most others days, the bleeding will be lighter with drop every now and again. I think most women would agree with me on the fact that when there is a rather heavy flow it can be felt. So, to boil things down, the correct answer is C :) If you want me to make this an answer I'd be happy to! :)

@L.B. Sure make an answer. See the edit in the Q first.

@Donkey, to find out, you really have to go through one yourself and find out how your own cycles are like. It's kind of like printer ink--> there is some adjustment/irregularity in the beginning, then it should be predictable/regular.

This isn't much of an answer but here goes... Two things; it depends on which day of the period it is. There can be rather brief, heavy bleeding on the later part of the first day or sometime during the second. On most others days, the bleeding will be lighter with drop every now and again. I think most women would agree with me on the fact that when there is a rather heavy flow it can be felt. So, to boil things down, the correct answer is C.
Here are a couple of links to sites that will back me up on this: Advice From AnnaMarie and Center for Young Women's Health.

I don't know, I can't vote (yet). So it's just like comments and answers suggest, you put the answer in actual words. Speaking of additional questions: How would one notice the bleeding has started? Except going to bathroom or checking, can one feel not being clean, even if it is a simple light bleeding on the first day?

I would say you have downvotes because you are providing anecdotal evidence or experience which isnt based on research. Sure you could be right but your answer is based on a small subset either you if you are a woman or women you know. It comes down to what is your proof that this is how it works? Now compare your answer with the one with the most up votes. Do you see a difference?

The answer is both. Different women experience menstruation differently depending on the levels of different hormones in their body, personal medical conditions, medications, on their age, and the activities they do in their lives. Bleeding is due to the sloughing off of the highly vascularized endometrial lining of uterus which is no longer receiving the appropriate levels of progesterone for its maintenance from the corpus luteum, in the absence of an implanted embryo in the uterus. You can imagine how different this common event would be if a woman was taking warfarin, had a bleeding or coagulation disorder, had polycystic ovarian syndrome, was a runner, or was a 13-year-old vs a 41-year-old. It varies!
Source:

Welt et al. Physiology of the Normal Menstrual Cycle. Last updated Feb 28, 2014. http://www.uptodate.com/contents/physiology-of-the-normal-menstrual-cycle.
http://www.womenshealth.gov/publications/our-publications/fact-sheet/menstruation.html

Are sudden bleeds common?

@CRags, they can be, and it could or could not be "normal." It really depends on how it affects the quality of life of the woman. Possible causes of sudden heavy menstrual bleeding may be due to leiomyomas, thick endometrial lining, hormonal imbalances, blood thinning medications, etc. For other causes, see mayoclinic. Sudden is also a subjective descriptor, because some women are more atuned to their bodies than others and can tell when they might menstruate, preparing ahead of time.

Thanks for the answer. I knew about menorrhagia. My idea was that consistent heavy bleeding would be present. The phrase “sudden bleeding” sounded like bleeding heavily but inconsistently. I wanted to know if such cases existed.

@CRags, yes I believe such cases exist, but I know this only from peers. I am in the medical field, but am not an OB-GYN, who would be the best person to give credit to my answer.

Which alternative is more common? Can a woman experience both due to changed life style, hormones, medication, etc.? (like I said: "simplifying things here", let's say a normal, healthy woman 20+, no extreme cases)

Heavy menstrual bleeding affects anywhere between 20-40% of women in countries such as the US and Britain but elsewhere is unknown. See BMJ. It is very common for women to experience changes in their menstruation in terms of quantity of blood loss and even frequency of menstruation depending on change in lifestyle, hormones, medication but it depends on what exactly she changed. A range of variation is very common even in the same woman.

Basically there is every variation under the sun possibly but I have structured my answer so that the more common variations are earlier.
On average a woman loses around 30-40 ml of fluid, this is a combination of mucous, secretions, endometrial tissue and around 50% blood. Because of this it is a slightly darker colour than just regular old blood. This of course varies with women with blood disorders or taking medication to "thin" the blood bleeding a lot more. The second day is typically the worst. On the worst day a woman may use 3-6 pads but this can be substantially more and changing every 2-3 hours is not uncommon. It is most typically more or less constant with some worse moments in the day, but there is a huge variation.
Clots are quite common but not all women get them. They're typically more common in older females and may look just like tissue. The size of these clots can very from the size of peas to grapes and even larger than 6-7cm in some women. This is a little more worrying as this may cause anaemia or iron deficiency unlike the regular bleeding above which typically doesn't. Women affected with blood clots are much more likely to have pain.
Pain itself is more common in younger women. However usually this settles down and usually it is not painful enough to affect daily activities. In some women however they get dysmennorrhea which basically means painful uterine cramps. This is because the blood flow to the uterus is restricted due to the hormone balance and the muscle is contracting really powerfully. The lack of blood flow causes the muscle to get starved of oxygen and the pain is said to be similar to angina or like a heart attack (both being caused by a similar mechanism).
Menorrhagia is the medical term for heavy periods. This is characterised by more than 80 ml of fluid each month and affects 1 in 10 women. Usually this is diagnosed by the number of pads and tampons used. Women affected by this may require to double protect, use both a tampon and pad. They may also take a number of extra underwear or trousers to work. The symptom affecting these women is termed flooding. Unexpectedly they get a "flood" which just basically goes everywhere and is uncontrollable and is usually quite a lot of volume. This is sometimes due to an underlying disease, of which, is most commonly fibroids but may also be contraceptive devices that go into the womb/uterus, blood thinners or polycystic ovary syndrome.
There is however much variation. Some women will have only 10ml or so of blood (light periods) and that's normal for them. Some women may have irregular bleeding lasting all month. Other women may have longer periods such as 10 or even 20 days per cycle. And then cycles themselves can vary from short (20 or so days) to very long with only a few cycles per year. Basically there is every variation possible under the sun.


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mRNA Transcription from Nuclear DNA
How does a cell "know" the coding strand vs. the non-coding strand of DNA during transcription of mRNA?

This is determined by the promoter -- the DNA sequence to which RNA polymerase binds. It's assymetric, and the polymerase binds in a specific orientation, that determines the strand and the direction it will go once elongation begins.

Strands in DNA double helix (and other nucleic acids) are anti-parallel: one strand in the helix is in 5'->3' direction while another is in 3'->5' direction. RNA polymerase can only synthesize RNA in 5'->3' direction, and so it uses the 3'->5' strand as the template (the second DNA strand is, I think, completely ignored by the polymerase during synthesis).
From one promoter transcription of both forward and reverse genomic strands can theoretically happen. However, the two possible nascent RNA strands are synthesized outward from the promoter and away from each other (i.e. they are not overlapping).
During evolution position of some promoters (but definitely not all of the promoters in the genome) have evolved to be in the place were at least one of the two theoretically possible RNA products can be translated. Transcription in the opposite direction (i.e. away from the gene) actually frequently happens in eukaryotes. These RNAs belong to a class of promoter associated RNA, but but they were not shown to be translated (their function is largely unknown).
UPDATE (2015/02/19): New publication in Molecular Cell by Duttke et al. is demonstrating that genic promoters are "intrinsically directional" and, just as @Leon Avery commented here before, the divergent (i.e. bidirectional) promoters are actually two unidirectional promoters side-by-side, in reverse orientation relative to each other. So my above statement "From one promoter transcription of both forward and reverse genomic strand can theoretically happen" is incorrect. However, the authors also say that approximately half of gene promoter regions in HeLa possess this bidirectional initiation property, so it is still an important feature to keep in mind when thinking of transcription of eukaryotic genes.

In short for me: You say that transcription runs into both directions and both strands are produced as mRNA? If not, please edit your question, at the moment this can be read into it.

Sorry for not emphasizing this importnat point: a gene promoter typically leads to syntesis of mRNA transcripts in one direction from one strand only. However, other RNA transcripts, generally referred to as promoter associated RNA, were show to be syntesized at promoters in both directions. Promoter associated RNA was shown to be up to a few hunderd bases long, most frequently just about 18 bases long (I think the 2008 Science paper from Lis lab was one of the first papers on this phenomenon, but there was other important research into it since).


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Transfect Mammalian Cells with Single Stranded DNA?
Agrobacteria can deliver parts of their DNA to plant cells as T-DNA, transfer DNA. This DNA is delivered as a single strand and can be integrated into the plant genome or can be converted to a double stranded molecule by priming the T-DNA to make it a substrate for a DNA polymerase. This article describes the process, but Nature makes getting to the article hard, sorry.
What I'm interested in is delivery of DNA to mammalian cells. I tried to find articles that used single stranded DNA in mammalian cells, but couldn't find much. Maybe I didn't spend enough time searching. I saw some suggestions that single stranded DNA could trigger apoptosis, or that single stranded DNA could be used to manipulate DNA repair mechanisms to cause integration into the genome.
However, is there any way to deliver a single stranded DNA, and have it converted to a double stranded plasmid in situ? Would probably need an RNA or DNA primer, but I don't see why you couldn't pre-bind the primer and deliver the whole complex.

http://www.pnas.org/content/96/7/3729.full.pdf
Let me know if that's anything like you're looking for and I'll keep looking into it.

@Kendall Thanks for that paper. While it's interesting, it seems to focus on nuclear entry of single stranded DNA with agrobacteria proteins, and does not test if the delivered DNA can produce protein.

Not sure any of them are what you want, but have you gone through all the references from https://en.wikipedia.org/wiki/Transfection#Methods ? :-)


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Can genetic engineering be performed without a laboratory setting?
I'm becoming more interested in genetic engineering as I learn more about it, and it's becoming more and more apparent that there's very few resources on genetic engineering at home. A similar question was asked here, but the best answer linked to a failed indiegogo campaign. Is it feasible to genetically modify an organism without a laboratory setting? If so, what materials could be used to do this?

You could probably do very simple genetic engineering in a home lab. Getting the competent bacteria and plasmids to put them in might be hard, as suppliers will be reluctant to sell to you. You'll need some equipment like an incubator to grow the bacteria, and maybe a centrifuge to purify the DNA. Chemicals might be hard to get too. Isopropyl alcohol and ethanol are often used to isolate DNA, and can be obtained pretty easily. SDS, NaOH, and bacterial media might be hard to get. Also, don't expect to sequence DNA at home.

Your best bet at genes you could use at home would be green or red fluorescent proteins, you can get UV LEDs at radio shack, with a little soldering you can make a small UV lamp to observe the fluorescent colonies.

You'll have to be careful about the local laws, in some countries you need a laboratory with permission for handling GMOs, doing such work outside it would be illegal.

At the molecular level, you wont observe the requisite aseptic technique, pH monitoring, water purity or chemicals at home. The best bet at experimenting with genetics at home would be to cross plants to observe change ala Mendel. At least, in my opinion.

Just out of curiosity, why has this been downvoted? It's a valid question, I believe it follows community rules, regardless of how misinformed it was.

I downvoted as I strongly discourage promoting freewheeling with genetically modified organisms, especially by folks who don't even know how to do it. Why would he want to do it? What are the safety measures? Does he know about ethics?  Emergency plans? Infection dangers? Good Laboratory Practice? This question should be closed

The only reason I answered this was to try and demonstrate how hard it would be to do the simplest type of genetic modification, hoping it would discourage people. I've seen this type of question before, thought someone should at least explain how hard it would be.

Discouraging people from home experimentation and discouraging people from asking about home experimentation are two different things.

I wasn't aware that downvoting based upon opinion was encouraged.

@DylanKatz - it is not 'encouraged' as far as I know. It is my personal reason for downvoting, which I provided kindly on your request. We can continue this discussion on meta.

Thought I'd attempt to expand this into an answer, THOUGH THIS IS IN NO WAY MEANT TO SUGGEST YOU SHOULD ACTUALLY TRY THIS. THERE MAY BE LEGAL ISSUES INVOLVED IN CREATING A GENETICALLY MODIFIED ORGANISM, EVEN A HARMLESS ONE, DEPENDING ON YOUR LOCATION. SOME OF THE CHEMICALS REQUIRED TO HANDLE DNA ARE DANGEROUS, AND SHOULD ONLY BE HANDLED IN A FUME HOOD AND WITH PROPER PROTECTIVE EQUIPMENT. I HIGHLY RECOMMEND THAT YOU DO NOT ATTEMPT THIS.
First, you cannot do genetic engineering outside of a lab. You might be able to set up a lab at home, but don't expect to do this using standard household chemicals. Lets assume you're only interested in adding DNA to bacteria, because that's relatively simple.
The first step you need to add DNA to bacteria is to get the DNA. Your major plasmid suppliers probably won't like selling to a non-lab, but if you're lucky you might get some from Invitrogen, Aldevron, or another supplier. If you know someone who works in a molecular biology lab, you might be able to get some from them, but that might violate rules with their university or employer. If possible, I'd get a green or red fluorescent protein gene, as those proteins are easy to detect using a UV lamp you might be able to build with UV LEDs, you might also be able to use a black light. Note that I do not know what promoter would be best to use on your gene. The lac operon is often used to express proteins in BL21 E. coli using the molecule IPTG as an inducer, but that requires you to have IPTG and BL21 bacteria.
Speaking of bacteria, you need competent bacteria. E. coli is the most often used species, but several strains are available. DH5a E. coli is most often used to grow up DNA plasmids, which is something you'll want to do because you probably won't be able to get much plasmid, so you have to make more or you'll run out. But DH5a usually isn't used to produce protein. BL21 E. coli is most often used to produce protein, but you'll probably need IPTG to induce the bacteria to make the protein. You might be able to get IPTG from Sigma Aldrich, but good luck getting them to sell anything to you.
Once you have the bacteria, you'll need to grow them. You need bacterial media, which might be obtainable because it's relatively safe. LB media is a mixture of yeast extract, tryptone, and salt. If you want solid plates you'll need agar too. You can probably get the media sterile enough by boiling it. You'll need some ampicillin or kanamycin to make sure only bacteria with your desired gene is allowed to grow, again Sigma Aldrich might sell it to you.
Of course you can't just put DNA into bacteria, the bacteria must be competent. You can make chemically competent cells by carefully treating them with calcium chloride and magnesium chloride. You'll also need dry ice, these need to be kept very cold. So now you can add your plasmid your competent cells, heat shock them in water at precisely 37°C for precisely 60 seconds, and plate them on your agar media. Then you need to incubate them at 37°C overnight.
If you need to purify the DNA plasmid back from the bacteria, you need to pick a colony off that plate and put it in liquid LB media, also at 37°C overnight with antibiotic. Here you'll need a centrifuge to spin down the cells and remove the left over media. Then you'll need to lyse the cells to release the DNA. You might be able to do this with soap, but you'll probably need NaOH and SDS. Once the cells are lysed you need neutralize them with an acetic acid solution, vinegar might be good enough. Then you have to centrifuge the cell debris to pull the insoluble crap out and leave the plasmid DNA and RNA in the supernatent. At this point you can extract the DNA and RNA with a phenol:chloroform:isoamyl alcohol mix. Good luck getting that, as the vapors from that solution are harmful to inhale, and really bad if you spill it on you, and should not be used outside a hood. But if you manage to get the extraction to work, take the top layer and add an equal amount of isopropyl alcohol and put it in your freezer for a couple hours. Then spin it down, carefully remove the supernatent and you should have a pellet of DNA in the bottom. You might have to clean the pellet with a 70% ethanol solution (140 proof) and another centrifugation. Quantifying your DNA at home will be almost impossible.
Also, this all assumes you just want to put a ready-made plasmid into bacteria. Trying to change the plasmid will require restriction enzymes, PCR, etc.
So yes, you can do genetic engineering at home if your home has an incubator (preferably with shaking), a centrifuge, a water bath, a -80°C freezer, a fume hood, a variety of chemicals, and a decent set of pipettes. But if you have $10,000 you don't really need you might be ok.

I'd make the warning about phenol/chloroform more explicit, doing that extraction outside of a fume hood is a pretty bad idea. Phenol is pretty toxic and not something I'd use in home experiments.

I think you're overestimating the difficulty of buying cells and chemicals, I'd guess that registering a business might be enough to fool suppliers. But the other arguments are valid, you're likely to run into significant walls trying to do anything useful at home. Even with second hand equipment, a basic lab would still be a considerable expense.

@MadScientist Tried to emphasize the phenol chloroform risk a little better. Another thing to worry about is that setting up any lab in your home is a good way to get the cops to start bothering you, since 90+% of home labs are probably meth labs.

@user137 Amateur drug labs are often found by the local fire department for a reason.

@Chris Molecular biology usually avoids the worst chemicals, but isopropyl and ethyl alcohols and phenol chloroform are all flammable, so the fire department might still find your molecular biology lab when your house burns down. These experiments have some danger, and they should not be done without proper equipment, but it's probably a little safer (legally and health-wise) than meth cooking.

Ah okay, I wasn't aware that this was such a dangerous/illegal process. Thank you for your answer.

This answer strikes me as too pessimistic. For instance, we rarely use phenol/CHCl3 extraction to purify plasmids -- we use Qiagen kits or spin columns. You don't need dry ice to make competent cells, if you use them immediately, and anyway, the Krogers where I shop for groceries sells dry ice. And I think most of the companies involved will sell non-hazardous reagents to anyone with a credit card. The biggest problem is that it would be expensive. You'd definitely need a centrifuge of some sort. And of course the big barrier is that you need to have some idea what you're doing.

@LeonAvery The expense is why I mentioned phenol and chloroform, if you have the money for qiagen kits you probably don't need to worry about at home molecular biology. And I suspect the hard part about at home competent cell production is maintaining a culture of E. coli all the time, having a -80 freezer is nice for long term storage.

To put the hazards in perspective: my father has a home woodworking shop. There are half a dozen big power tools that could take off a finger in a fraction of a second of carelessness, and some mildly hazardous glues, finishes, solvents, and lubricants. Indisputably, Dad's shop is a more hazardous environment than my lab, yet I've never heard anyone suggest this is too dangerous a hobby. DIY mol biol would be expensive. We usually expect a full-time worker to spend about $1000/month on supplies, and the minimal equipment, even from eBay, would set you back thousands.


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Can drinking caffeine, alcohol and other diuretics be part of a good drinking regime?
Tea, Coffee, Beer, Coke etc…
I wonder if the benefit from amount of fluid we get from them is bigger or smaller then the handicap of dehydration. In other words it is worth to drink them if we want to have a good drinking regime?
Opening on the recommendation from this question.

A PlOS One study notes drinking moderate amounts of coffee (aka moderate caffeine intake) doesn't necessarily lead to dehydration. They note coffee has hydrating qualities akin to water. Further empirical studies found no substantial fluid loss in caffeinated beverages.
EDIT: Make note we're talking normal doses and moderate intake, though source 2 goes into diminishing effect of caffeine-mediated fluid loss in heavy/prolonged uptake.
The issue therein is with alcohol, which tends to inhibit vasopressin and the kidneys are constantly permeable to fluids.


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What is the most complex biological organism (or precursors) that we have been able to synthesize from raw materials?
In the Miller–Urey experiment they produced several amino acids.  I'm not sure if there were other similar experiments that got further.
http://www.jcvi.org/cms/press/press-releases/full-text/article/first-self-replicating-synthetic-bacterial-cell-constructed-by-j-craig-venter-institute-researcher/ is a reference to making a cell, but they really injected an engineered genome into an existing cell (which is pretty amazing!)
But I'm interested in work to make completely synthetic life with no preexisting biological components.

Since you're discussing the boundary between living and non-living matter, can you provide a concrete definition for what you consider life for the purpose of this question?

a self replicating cell - but I'm open to other definitions if they exist.  And I'm also not looking only for creation of complete life - just the furthest we've gotten.  Lets imagine is the goal to make (even in lab conditions) a single self-replicating bacteria from raw materials, how far along are we?  1%, 5% 70%, etc.  I'm interested in what we've made until now and where the next steps are to go further.

This might interest you: http://biology.stackexchange.com/questions/19316/first-rna-polymerase-mrna/19737#19737

Modern bacteria are extremely complex (they've been evolving for about 4 billion years) and probably look very little like the first organisms on earth. We're not even sure if early life used DNA. Whatever we can produce in a lab from no pre-existing components, is bound to be hard to recognize as life as if it had evolved on an entirely different planet.

I think the simple answer is that no one has come anywhere close to doing what you ask for, under any commonly accepted definition of "life". Jack Szostak's work  (http://molbio.mgh.harvard.edu/szostakweb/) is a good place to start researching this.

@LeonAvery - if you want to post your comment as an answer, I can select it as no one else has offered anything better.


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Are codons that map to the same amino acids interchangeable?
From wikipedia, in the section on the RNA codon table, I see a mapping between codons and amino acids. There, Valine is related to GUU, GUA, GUG, GUC.
Does it mean in the same context that these four codons are interchangeable? Could one replace GUU with GUG?

Yes, those codons can be exchanged to get the same amino acid, but it might affect how much protein is made, see codon usage bias

There are some subtle nuances, as well: http://www.ncbi.nlm.nih.gov/pubmed/11943474

You seem to have read the table a little wrong: T doesn't appear in RNA. Probably you meant GUG, not GUT.

@LeonAvery - yes - I read it wrong.  thanks for the correction.  Corrected in question.

In Spinal Muscular Atrophy (SMA) a single nucleotide C to T transition mutation occurs in SMN2 gene sequence at 840 that produces the same phenylalanine but it gives rise to some translational enhancer/silencer interactions, so intended final protein lacks exon7, gets unstable and shortlived and patients suffer from lack of motor-neuron functions which lead to paralysis.

I think given that you're just getting started with genetics, you can say that the codons are interchangeable. This is generally true, though not technically correct. Here are a few reasons for why this is the case, though there's probably more:

Specific organisms use specific codons with different frequencies. This is usually related to the tRNA abundance in the cell. Using a codon for which there is relatively less tRNA available would be expected to lead to a decreased protein synthesis rate.
Using different codons can affect mRNA secondary structure, which could affect expression.
Some codons, especially stop codons, can influence translation contextually through a process called recoding. This can include frame-shifting, read-throughs, cleavage or, perhaps most famously, coding for the amino acid selenocysteine and much more. See here.
Different codons can also influence translation contextually through pausing. This affects the rate of protein synthesis as well as its folding. See here.
Changing codons can affect regulatory sequences such as miRNA binding sites. Though these are usually present in the UTRs, they can also occur in the CDS.

Nice answer - I was considering posting another but it would be better if you just added this as another bullet point, as it is not mutually exclusive to your suggestions; this paper describes translational pausing of different lengths for different codons, even for the same amino acid, which affects protein 3D structure as well - so it would appear that codons in the DNA have another layer of information beyond that of simply saying which amino acid to add to the protein next!

In addition, changing the codons could affect silencing or modifications by siRNA, miRNA etc.

A good answer is already provided by @canadianer, but as with many things in biology it is important to keep in mind what organism and/or cell type we are talking about. Because the nuances of the answer to a question about a seemingly universal process sometimes actually depend on whether we want to know about bacteria, or fungi, or mammalian stem cells, etc.
So I think the answer to your question is that synonymous codons are not always interchangeable because of what @canadianer described, but regulation of codon usage is probably more relevant in context of prokaryotes.
For example, for sure availability of a particular synonymous tRNA can be rate limiting in protein synthesis in prokaryotes, but I actually haven't heard of this happening in a eukaryotic system. If there are demonstrated examples, please paste it in the comment..
Also, the secondary structure of the coding part of mRNA is probably less important in eukaryotes, since they have a multitude of ubiquitous RNA-binding proteins that practically coat mRNA (e.g. hnRNP in the nucleus, and probably something similar in the cytoplasm, too)

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


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How does Haloxyfop control young grassy weeds in fields of broadleaved crops?
Haloxyfop (haloxyfop-P-methyl) is a selective herbicide used to control grassy weeds in young stages. The mode of action (iirc) is basically inhibition of acetyl CoA carboxylase (ACCase). Why does this affect the monocots, while not harming the dicots?

On the Botany department website of Purdue University (http://www.btny.purdue.edu/weedscience/moa/ACCase_Inhibitors/text.html) I found the following information on Acetyl-CoA carboxylase (ACCase) inhibitors:

[...] (ACCase inhibitors) inhibit the enzyme carboxyltransferase, an [...] Acetyl-CoAesterase which speeds the formation of malonyl-CoA from acetyl-CoA and CO2.
  Malonyl-CoA and acetyl-CoA are the building blocks of phospholipids and triacylglycerols [...] (that) combine to form lipid bilayers that serve as the cellular membranes. Affected plants cannot produce new cell membranes. This takes place in the grass’s meristematic tissue, which explains the mushy and disintegrated growing point. [...]
Selectivity [...] Monocots (grasses) [and] dicots (broadleaves) [...] both possess ACCase enzymes in their cytoplasm and chloroplasts. Dicots have a prokaryotic form of the enzyme in the chloroplast and the eukaryotic form in the cytoplasm. Monocots have the eukaryotic form in both their cytoplasm and chloroplasts. Only production of the eukaryotic form is inhibited.

So to sum up, ACCase inhibitors act on eukaryotic ACCase, not the prokaryotic type. ACCase is essential for cell membrane formation. Blocking ACCase results in a depletion of its product, namely malonyl-CoA. Malonyl-CoA is essential for the synthesis of long fatty acids used in the cell membrane. Without cell membranes, cells lose integrity and turn to mush. Tissue growth is impossible without ACCase activity. Since monocots only have the eukaryotic ACC in both cytoplasm and chloroplasts, they die. Dicots, on the other hand, express prokaryotic ACC in their chloroplasts, making them resistant to ACCase inhibitors.
After some literature search I also found that blocking (knocking out) acetyl-CoA carboxylase in Arabidopsis (a dicotyledon) results in dead plant embryos and, hence, non-viable seeds (Baud et al., 2003).

I am mobile, but here is my source: https://www.google.com.au/url?sa=t&source=web&rct=j&ei=nFnIVILZDoiU8QW72IGACA&url=http://onlinelibrary.wiley.com/doi/10.1046/j.1365-313X.2003.016010.x/pdf&ved=0CBsQFjAA&usg=AFQjCNGqIyW0fggl5kulKagsSzN29hjlAg&sig2=q7Q1EGkJvmGTvjO2xYBmuA

@J.Musser I am working on the others! Very I interesting material!


text:
What kinds of cells does human saliva contain?
I have heard that our saliva contains cells. What cell types can be found in human saliva?

I clarified the question and vote for reopening.

It contains white blood cells (leukocytes) and cells from the inner lining of the mouth (buccal epithelial cells). The DNA obtained from these cells is the basis of DNA profiling based on saliva samples.
Source: Salimetrics


text:
What does units/mg mean for Streptavidin
I got streptavidin for surface reaction. The label says "biotin binding: 16 units/mg". What does units/mg mean?
Does it mean "1 mg biotin can bind to 16 units SA"?
How much is the unit here?

From which company do you have this product?

@Chris from invitrogen

16 units/mg means 16 units per milligram of protein.
Many companies, including Invitrogen, define 1 unit streptavidin as the amount of streptavidin necessary to bind 1 microgram of biotin.

Thank you for your answer. Then 16 units/mg actually means 1 gram of SA could bind to 16 gram of biotin? How come this happen? The molecular weight of SA is hundred times larger than of biotin, is it possible to have thousands of binding position?

"Milli" means one-thousandth, "micro" one-millionth :)

@leetom The units are not same. The label says 16 units/mg. You must find out how much 1 unit of biotin weigh to make a comparison. For example if one unit of biotin weighs 1/16 milligram then 1 mg SA will bind to 1 mg biotin.

@CRags ChrisStronks,  Ah sorry, I made the mistake ;)

Just to add to Chris Stronk's answer:
1 U SAV can bind 1 ug biotin
This tells you that in a 16 U/mg SAV sample, every mg of SAV will bind 16 ug of biotin. You can figure out the molar ratio from this:
$16\mu g\ BIO\cdot\frac{1mol\ BIO}{244310000ug\ BIO}\cdot\frac{52800000mg\ SAV}{mol\ SAV}$
Which equals:
$\frac{3.46mol\ BIO}{mol\ SAV}$
Theoretically, each SAV tetramer can bind 4 biotins. This tells you that there is some heterogeneity in the sample and that, on average, each SAV tetramer can bind 3.46 biotins.

it does not reflect protein heterogeneity, but sample impurity (some 14%). Probably mostly water or salts. +1 for the clear calculation.

@ChrisStronks Yes it may be true that some amount of the sample is be salt, depending on if a buffer was used prior to lyophilisation. However, reduced binding capacity may certainly be due to protein heterogeneity. One, biotin is essential to all organisms and, during production of SAV, it is expected that some amount will bind to endogenous biotin, using up a binding pocket. This cannot be accounted for in the common binding assays. Two, depending on the method, purification of SAV can require harsh elution conditions which can deform some of the binding pockets.

that's interesting. Thanks for the explanation.

@canadianer Thank you for the explanation! :)


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How to retrieve full gene names list and Entrez gene IDs and other annotation information from HUGO gene name list (in R or any)?
How to retrieve full gene names and Entrez gene IDs and other annotation information from HUGO gene name list (in R or any other software or language)?
Is it possible vice versa: having full gene names or IDs get HUGO names or the other annotation data?

Try DAVID. It has a gene ID converter option. There are many other Gene ID converters.

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

I would recommend just downloading the database, which HUGO allows you to do free of charge.
The HUGO website has a "downloads" tab at the top that takes you to the following page
http://www.genenames.org/cgi-bin/statistics
You will see a table of statistics relating to how many protein- or non-protein-coding genes there are catalogued, etc.
Under the tables is a section called Complete dataset download links -- this is the section you want (unless you only want a subset of the data - but why not get it all!)
This plain text file (once uncompressed) can be loaded into R (or any other language) to be parsed and analysed as per your requirements.
It is worth updating the version you download quite regularly, as they update the HUGO database with new/updated info quite regularly.

Install bioconductor and use this library: http://www.bioconductor.org/packages/release/bioc/html/biomaRt.html
You can access BioMart which lets you translate between different ID types


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Gene expression for mouse feeder cells (inactivated MEFs)
I'm looking for a paper with gene expression data for mouse feeder cells, inactivated by gamma radiation or mitomycin C. Ideally I'd like RNA-seq data but I'll use microarray data if that's all there is.
I've spent quite a while looking (in GEO, Google Scholar, PubMed, etc) with no luck. Any leads would be appreciated.


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Crossing white eyed Drosophila with sepia eye
So, I'm doing some drosophila experiments with my high schoolers and I had really poor production of wild type individuals for doing the experiment resulting in not enough to cross with everyone... I am trying the following crosses and hoping the kids can still learn from it, but wanted input from any fly-herders on what I can expect with the first two  crosses....
Sepia males x White Eye females
Sepia females x White Eye males
Dumpy males x Wild-type females
Dumpy females x Wild-type males
I don't think the gender separation will make any difference except in the white x sepia crosses since it is X-linked.
What should I get in the sepia x white crosses? Since they both control eye color and are both recessive I'm not sure. Am I correct that w is epistatic, thus should block sepia in an x-linked manner (same as if I had used wild-type instead of sepia)?
I assume the Dumpy x Wild-type will go by the books (F1 all wild-type with F2 3:1 ratio). Fingers crossed.

I posted this on Reddit as well, so credit to km1116 for working this out. Here is his response which follows my original logic (though I'm not sure if he is right):

female x male:
w x se
F1: wild-type females and white males
F2: 1/4 white-eyed males, 3/16 wild-type males, 1/16 sepia males, 1/4
  white-eyed females, 3/16 wild-type females, 1/16 sepia females
se x w
F1: all wild-type offspring
F2: 1/4 white-eyed males, 3/16 wild-type males, 1/16 sepia males; 3/8
  wild-type females, 1/8 sepia females
wt x dp (either direction)
F1: all wild-type
F2: 3/4 wild-type, 1/4 dumpy

My rationale for his answer is the genotype of the cross looks like this:
XwYNN with XWXW nn , where "W" is normal eyes, "w" is white", N is Wildtype and n is sepia.


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Length of sleep time
Why do we wake up after 6-8 hours of sleep ? Why don't we sleep for lets say 20-30 hours ? What mechanism is it that controls when to wake us up and how does it determine the moment that we should wake up ?

Related question.

It's considered a requisite on biology.se that at least some reading/research is carried out and presented with your question. Otherwise it will be closed as homework. [For example, have you read about circadian rhythms?] The site tour and the help center  provide guidance on how to use this site. Please take a few minutes to read about the kind of questions which are on topic here.

Think this review from Nature can answer your question. A brief summary  ( with slight simplification):
The ascending activating system (that is responsible for wakefulness) has two branches:
The first one ascends to the thalamus and activates the thalamic relay neurons - these transmit information to the cortex. They get their main input form two acetylcholine producing group of cells:  the pedunculo-
pontine and laterodorsal tegmental nuclei (PPT/LDT). These two group of cells are also the source of main input for reticular nucleus of the thalamus.

The neurons in the PPT/LDT fire most rapidly during wakefulness and rapid eye movement (REM) sleep, which is the stage accompanied by cortical
  activation, loss of muscle tone in the body and active dreams

The second branch, directly activates neurons in the hypothalamus, basal forebrain (BF) and cortex, bypassing the thalamus. This pathway has origins in monoaminergic neurons in the upper brainstem, caudal hypothalamus, as well as the noradrenergic locus coeruleus (LC), serotoninergic dorsal (DR) and median raphe nuclei, dopaminergic ventral periaqueductal grey matter and histaminergic tuberomammillary neurons. Input from this pathway to the cortex is extended /augmented by the lateral hypothalamic peptidergic neurons (that contain melanin-concentrating hormone (MCH) or orexin/hypocretin), and BF neurons(that produce acetylcholine or GABA).
Sleep is promoted by the so called VLPO (ventrolateral preoptic nucleus).
The VLPO send outputs to major group of cells of the arousal system in the hypothalamus and brainstem.

The VLPO neurons are primarily active during sleep, and contain the inhibitory neurotransmitters, galanin and GABA.
  The VLPO also receives afferents from each of the major
  monoaminergic systems. Both noradrenaline and serotonin inhibit
  VLPO neurons. The latter do not have histamine receptors, but the
  tuberomammillary neurons also contain GABA, which is inhibitory
  to VLPO neurons, as well as several other potentially inhibitory pep
  tides, such as galanin and endomorphin. Therefore, the VLPO can
  be inhibited by the very arousal systems that it inhibits during sleep.

As you can see in the quote from the paper these two systems can mutually inhibit each other and basically work as a seesaw or 'flip-flop switch'. In this system activity in one  subsystem shuts down the inhibition from the other subsystem and disinhibits its own action (selfreinforcing loop). The transition from one state to the other is relatively fast. Orexin plays important role in stabilizing the switch in one position or the other.

Regulation pf sleep:
Homeostatic:
It is unclear how homeaostatic regulation of sleep work, yet it has been proposed, that adenosine accumulation in the brain may signal for 'need for sleep'. The extended wakefulness causes the exhaustion of brain glycogen reserves and depletion of ATP levels. As ATP is degraded to ADP, AMP and eventually adenosine, extracellular adenosine levels rise in some parts of the brain including the BF.

In addition, adenosine might disinhibit the  VLPO via presynaptic A1 receptors by reducing inhibitory GABAergic inputs.

This implies that during sleep ATP and energy sources are regenerated and free adenosine levels drop, thus inhibition of VLPO might take place again.
Also it is important to note that the amount of sleep we need is proportional to the time we spend awake.
Circadian regulation:
It is known that humans have quite precise :circadian rhythm:

The suprachiasmatic nucleus (SCN) serves as the brain’s ‘master
  clock’. Neurons in the SCN fire in a 24-hour cycle that is driven by a
  transcriptional–translational loop, which persists even when the neurons are dissociated in cell culture.

The SCN has moderate output to the VLPO or orexin neurons, but it has more important projections to the adjacent subparaventricular zone (SPZ) and the dorsomedial nucleus of the hypothalamus (DMH).

The SPZ also has relatively limited projections to the VLPO, orexin
  neurons and other components of the wake-sleep-regulatory system. However, a major target is the DMH. This region receives inputs from many more neurons in the SPZ than the SCN, so the SPZ is in a position to amplify the output of the SCN. (...) The DMH is one of the largest sources of input to the VLPO and orexin neurons and is crucial for conveying SCN influence to the wake–sleep-regulatory system. The DMH projection to the VLPO comes largely from GABA-containing neurons (that is, those that promote wakefulness by inhibiting sleep), and the projection to the LHA originates from neurons containing glutamate and thyrotropin-releasing hormone (which should presumably be excitatory and promote wakefulness).

So as you can see our circadian rhythm as direct control over our sleep-wake cycle, and that the SCN can heavily promote awakening through SPZ and DMH.
Thorough review and details can be found in the article I linked at the beginning, I only tried to select key information to provide a (not so ) brief summary. We only sleep about 7-8 hours normally because this is enough for homeostatic regeneration and our circadian rhythm promotes wakefulness in the morning (this is quite simplified).
Based on their abstract these limited access papers might also be useful (unfortunately I do not have full access to them right now):

http://www.eurekaselect.com/87813/article
http://www.sciencedirect.com/science/article/pii/S0074774210930018
http://www.sciencedirect.com/science/article/pii/S0896627315001312

I think what the OP is getting at is less about the mechanism of sleep -> wake transition and more about how the length of sleep time is regulated...
In that regard, it's an interesting question without a definitive answer. In a sense, it is a question of homeostasis and the time when your sleep need/pressure is satisfied determines when you wake up (without an alarm clock).
It is hypothesised that sleep drive is a function of the previous wake period plus any sleep debt you carried from the previous days.  One molecule, adenosine, is thought to represent that and the accumulation of that in the brain makes you want to sleep [Ref. 1].  Thus, the clearance of external adenosine in the brain to a certain level may be part of the homeostatic mechanism signalling enough sleep.
Another hypothesis is that sleep is required to encode memories long term [Ref. 2] and to calibrate emotion/mood [Ref. 3] which themselves can add to the sleep need and those processes would need to be completed to a certain level to release that sleep need.
As for the specific moment for awakening, if there isn't some external arousal stimulus like daylight/alarm or the rush of cortisol cycle driven by your circadian mechanism, then it will likely correlate to the end of the current 90min sleep cycle when your brain is close to the wake state coming out of REM [Ref. 4]. In fact, it's thought you wake a little every 90min through the night, it's just you don't remember it.
[Ref. 1]: Link to adenosine and sleep review
[Ref .2]: Link to sleep and memory review
[Ref. 3]: Link to sleep and mood review
[Ref. 4]: Link to brief summary of sleep staging


text:
Are boat-tailed grackles efficient flyers?
The boat-tailed grackle's deep-V tail would seem to cause a great deal of drag or even downward deflection (like an airplane's elevators). How much does this actually affect the bird's flight?

It's considered a requisite on biology.se that at least some reading/research is carried out and presented with your question. [For example, do you have any evidence that boat-tailed grackles fly less efficiently than other birds? What criteria would you use to measure that?] Otherwise it will be closed as homework. The site tour and the help center  provide guidance on how to use this site. Please take a few minutes to read about the kind of questions which are on topic here.

@anongoodnurse: A Google search for this information turned up no satisfactory information. Now, 50 minutes after posting, this question turns up as the number one result and a duplicate of this very question on a copy-cat site shows up a few entries lower. I have no evidence other than my intuition and curiosity. You can be sure that I'm quite familiar with how StackExchange works.

I don't know... perhaps Physics.se would be a better site for your question. Yeah, copying happens. If you think it's iffy, flag a mod with the info.

Aside from a detailed study of the flight envelope of many bird species(which might not exist), the answer might have to be 'They're efficient enough, according to the  boat-tailed grackle at least'. Lots of birds have ridiculous plumage or other things that impede their flight. See: peacocks, birds of paradise, etc. Birds, weirdly enough, aren't designed to fly very well. Some are designed to look good or hide efficiently or whatever it is birds do.

@Resonating: Of the birds with unusual plumage shapes that I'm aware of, the only ones I've had the opportunity to observe with any frequency are the grackle which fly a lot and (with much less observation) peacocks which don't seem to fly nearly as much. I don't imagine lyrebirds, for an example which I haven't had the opportunity to observe, fly very well - the same (observation or flight ability) probably goes for many of the birds of paradise that you mentioned. As for a general statement of whether birds are designed to fly very well - I can think of many counter examples.

I added an image of the boat-tailed grackle for the unfamiliar.

I should have been more accurate. Not all birds are designed to fly very well. Albatrosses, swallows, all birds of prey, etc clearly are. From kmm's excellent answer, I'd conclude a soft 'not very much' given the lack of sexual dimorphism, which implies it's not for sexual selection. Does it flatten while in flight?

@Resonating - I completely agree with you, but, having raised peacocks, you'd be astonished on what those large and showy birds can actually do in the air. It took my breath away.

@Resonating: The female is quite different. So I would say that it's all about sexual dimorphism.

Are they? I have only pictures to go by, so I'll take your word for it.

@Resonating: The Wikipedia article has pictures for comparison. (I could take my own pictures and post them. I could choose from among many thousand specimens.) The male is iridescent black and the female is dull brown and lacks the tail V.

They seem to have roughly similar length tails but if the female is missing the V shape that's significant. If the females don't have the boat tail then it doesn't have an adaptive purpose, and we can conclude it's for sexual selection reasons and probably at least a little bit of a hindrance.

I don't know of studies specifically of boat-tailed grackle flight, so I'll focus on elongated tails in general and come back to grackles at the end.
Long tails in birds are obviously interesting from the standpoint of sexual selection. Going all the way back to Darwin, one hypothesis has been that females prefer males with long tails. There seems to be evidence for this, although experimental reduction or elongation of tail feathers is perhaps of questionable success. See this back and forth in Behavioral Ecology.
Those interested in the study of flight have also studied elongate tail feathers to get at the questions you ask: are long tail feathers aerodynamically costly?
Balmford (1993) compared the aerodynamic properties of different tail shapes. He found that:

A forked tail that has a triangular planform when spread to just over 120° gives the best aerodynamic performance and this may be close to a universal optimum, in terms of aerodynamic efficiency, for a means to control pitch and yaw.

But the results were more complicated. Forked tails are only used in extreme maneuvers, they are more unstable, and suffer from greater loss of performance when damaged. He leaves open the possibility that natural selection, rather than or in addition to sexual selection, has played a role in shaping bird tails, possibly for increased aerodynamic performance.
More relevant here, Balmford et al. (1993) studied pairs of species, one with a long tail and one without, to assess the aerodynamic cost of long tail feathers. They studied ~600 specimens and used aerodynamic modeling to predict cost. Their results are summarized in this figure:

Graduated (rounded) tails are costliest over all lengths. Forked tails are notably less costly over all lengths, and shallow forks more efficient than deep forks (but there the difference is not great).
They conclude:

Our model suggests that as long forked tails deepen, it becomes more likely that they are aerodynamically costly..., and therefore increasingly probable that sexual rather than natural selection explains their evolution.

And of the species pairs:

... then among species with long forked tails, sexual dimorphism in tail length should increase with fork depth. Pairwise comparisons of closely related species support this prediction.

What of boat-tail grackles then?
From what images I could find, it looks like boat-tailed grackles appear to have graduated tails when spread. If so, then these tails would be very inefficient and males with longer tails would incur a proportionately higher cost of flight than males with shorter tails.
Balmford, A., A. L. R. Thomas, and I. Jones. 1993. Aerodynamics and the evolution of long tails in birds. Nature 361:628–631.
Thomas, A. L. R. 1993. On the Aerodynamics of Birds' Tails. Philosophical Transactions of the Royal Society of London B: Biological Sciences 340:361–380.

Instead of a fork or a simple graduated shape, boat-tailed grackles have a deep V (you might say in the vertical direction as opposed to a fork in the horizontal direction. They don't flatten that V in flight.


text:
why male penis not considered as cartilage?
Penis don't have bone like ears & nose, then why why male penis not considered as cartilage?
en.wikipedia.org/wiki/Cartilage

Because it's not cartilaginous…

Welcome to BiologyBeta. Everything is not either cartilage or bone. We have many other tissues. Have a look to this wiki article. The penis contain neither bones nor cartilage.

Btw, Are you sure the Botany tag was a good choice? The tag human-biology or anatomy would be better choices.

@Remi.b Also see baculum: http://www.mapoflife.org/topics/topic_203_Baculum-%28penile-bone%29-in-mammals/

If it doesn't have fur like a cow it must be a chicken? ....

feel the tip of your nose. Mush it around, It's got a certain stale gummy bear feeling to it. Now feel your ears, all over. The outer edge, the back, the hard part in the front where the ear meets the face. Feel your adam's apple. This is cartilege.
When you feel your penis, does anything even feel close? Nope. It's just soft. Soft tissue, to be precise.
When stimulated, there are comparmemts within the penis which engorge with blood.

When they fill up with blood, the penis gets hard. That's all there is to it. No bones, no cartelidge.
If you have any questions, noe's the time to ask.

+1. And you are telling me I am nice? Answering this question is the nicest thing one could ever do. I deleted two nasty comments to this question.. and left the third :) respect


text:
What is a positive epitope fragment
What is a positive epitope fragment? I found one paper on the subject:

COBEpro: a novel system for predicting continuous B-cell epitopes by
Michael J. Sweredoski and Pierre Baldi

The group tries to predict possible epitope sequences for the generation of antibodies. This includes also non-linear epitopes where not all amino acids of the epitope are line up behind each other, but come in close contact due to a 3D-structure. To train their algorithm, they use data, where the boundaries of the epitopes and the non-epitopes are known and clearly mapped.
The "Dataset and Preparation" section in this paper contains the following:

In this article, we used several different datasets to train and
  benchmark COBEpro. These datasets were derived from several different
  previously published sources: BciPep (Saha et al., 2005), Pellequer
  (Pellequer et al., 1993) and HIV (Korber et al., 2003). The BciPep
  datasets consist of epitope/non-epitope sequence fragments. The
  Pellequer and HIV datasets consist of whole antigen proteins annotated
  with precise epitope boundaries.

The "positive epitope fragments" are known and verified ("positive") epitopes from these datasets in the training database. The fragment refers to restriction of length to 20 amino acids which they choose to apply. Shorter epitopes got amino acids added so they get 20 aa long, longer got truncated.

so basically what this means is that epitope fragments which has been verified as epitopes are called positive epitopes??

For this paper: Yes. I haven't seen this term anywhere else, though.


text:
What software/approach to use to build a graph based on microarray gene expression correlation?
What software to use to build a graph based on microarray gene expression mutual correlation?
I have tried Cytoscape`s Reactome FI and a recipe from R bioinformatics cookbook, however, need a more reliable robust software or R/Python tutorial on how to make a graph with gene-nodes and edges built on the rule of significant (p<0,05) positive and negative Pearson/Spearman correlations.

do you have any examples of similar graphs - perhaps an illustrative example could help (draw one in powerpoint and save it as an image) plus some idea of the data, and what you are trying to show

I'm voting to close this question as off-topic because this is not related to biology but is basically about how to visualize a graph/network. How to build gene networks from expression data is still a valid question but that is not what is asked.

Hi @VassiaAlk - Cytoscape is pretty well designed for constructing a "network" of genes that are connected by their degree of correlation in expression; check out the online resources (e.g. http://apps.cytoscape.org/apps/expressioncorrelation). This site is aimed at biological questions, therefore this is off topic. Best


text:
What Websites Have Image Libraries for Bacteria and other Microorganisms
What Websites Have Image Libraries for Bacteria and other Microorganisms?
With age of cell phone microscopes and hand held spectrometers it would be interesting and valuable to be able to compare in-home/at-work microbiology with data-banks. To be able to test for health or enjoy the visuals of tree of life seem relevant. What websites are out there?

Sites for microscope blood analysis would be a nice compliment to this.

While I doubt that this might be possible in all cases (and I would be careful about classifications), there are indeed some great ressources, which contain a lot of images. Since there is a vast number of bacteria present on this planet, there is of course a limitation to bacteria available in photos, representing only the most common or important.
These are:

Bacteria in Photos
American Society of Microbiologies Microbelibrary
Microbiology in Photos

Then there is an information page available from the CDC, which informs about parasitic diseases. These are non-bacterial, but probably also interesting. It can be found here:

Laboratory Identification of Parasitic Diseases of Public Health
Concern


text:
Is recombination suppressed in the males of all Drosophila species? Any other species?
Following up from this question, I am wondering if the phenomenon of genome-wide suppressed male recombination is limited to Drosophila melanogaster or is common to all Drosophila? The answer to the aforementioned question hints that this may be the case but has no reference on that, and doesn't directly state it.
For an added bonus, is this recorded in any other species?