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Why is sarcoma more prevalent and common in right heart?
Ewing's sarcoma or Ewing sarcoma is a malignant small, round, blue cell tumor. It is a rare disease in which cancer cells are found in the bone or in soft tissue. It is more common in right heart than left heart? Why? Which one is more dangerous?

Ewing's sarcoma is a bone cancer. As such, it does not arise as a primary tumor in the heart.
Ewing's sarcoma does metastasize. Like any metastatic cancer, it seeds along it's venous return to the heart, "taking root" in suitable tissue.
Cardiac metastases of Ewing's sarcoma are exceedingly rare, with only a few reported cases. Since all blood returns to the right side of the heart first, then the lungs, this is where distant metastases of Ewing's sarcoma are found. The side doesn't matter; it's never good.
Primary heart tumors do occur, about 1/20th as often as metastatic tumors. Of these, myxomas are the most common. Of sarcomatous types, which are very rare, they can occur anywhere.
Ewing's Sarcoma
Metastatic Ewing's Sarcoma to the Right Ventricle
Primary Malignant Sarcomas of the Heart and Great Vessels in Adult Patients — A Single-Center Experience
Echocardiographic and pathologic characteristics of primary cardiac tumors: a study of 149 cases
Primary cardiac sarcomas: an immunohistochemical and grading study with long-term follow-up of 24 cases

About 39.9 percent of reported heart tumor is related to sarcoma tumor and this a dangerous tumor which attacks Pericardial space and block heat valves and vena cava.

@Majid - The most common tumors in the heart are metastatic. They are 20 times more common than primary neoplasms. Of primary neoplasms, at least 50% are myxomas. That leaves a small number. In one study of primary neoplasms the findings were as follows: myxoma (84%), fibroma (4%), lipoma (2%), rhabdomyosarcoma (2%), hemangioma (2%), sarcoma (2%), angiosarcoma (2%), and lymphoma (2%). If you have a reference, I'd be happy to read it.

Can you add references? I'm reporting this from Harrison Internal Medical book.

@Majid - those smaller titles in blue at the bottom of my answer are the references. My guess, if you're reading this in Harrison's, is that you're misunderstanding what you're reading. Harrison's isn't known for being frequently in error (that I know of). I can't check this, as my Harrison's is decades old and I donated it. Same for Cecil's, etc. All pretty much outdated and gone to a new home.


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Whole genome sequence analysis software
Please help to choose Bioconductor R packages and other software for the whole genome sequence data analysis and, in particlular, the goals of false discovery mutation rate, mutations exclusion, mutation contribution and data dimensionality reduction. I could find Expander, MeV, Genesis software for the microarray experiments, however, could not find similar tools for the whole genome sequence analysis of mycobacteria. Sorry, that my question has no code.

What is your question?

This is a good question! why is this getting close votes? it is slightly incoherent and badly written but it definitely merits a response!

Have you searched biostars.org?  That is a bioinformatics board, and I'd say about half the content is about next gen sequencing.

@Bez I voted to close because I think (a) it is broad (b) I am not able to understand what is OP asking for exactly; some kind of all in one package? I retracted the vote but the question needs some clarification.

There are couple of them. First if you want to sequence analysis basic packages are :
http://www.bioconductor.org/help/workflows/high-throughput-sequencing/
Also, Maqweb seems promising.
http://maqweb.sourceforge.net

Add more software, including commercial, please, if you can

source: Stack Exchange

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How is oxygen and carbon dioxide exchange mediated by hemoglobin?
Oxygen is transferred by hemoglobin from the lungs to tissues, while carbon dioxide is transferred by hemoglobin from tissues to lungs. How is this regulated bidirectional transfer mediated?

Under conditions of high CO2 (in tissues such as muscle) and hence high acidity hemoglobin binds preferentially CO2, thereby mediating CO2 removal. Under conditions of low CO2 (high pH) and high O2 (conditions met in the lungs), it preferably binds O2, thereby releasing CO2. Hence, the specific characteristics of hemoglobin allow for CO2 uptake in the body, and O2 uptake and CO2 release in the lungs. Info from wikipedia on hemoglobin

please explain more.and the primary purpose is mechanism of exchanging O2 and CO2.mostly from biochemistry pointview.

@Majid have you done any research on your own? Did you read the Wikipedia article and those linked to it? Your questions are quite broad.

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Why doesn't HDL cause diseases like LDL?
LDL particles pose a risk for cardiovascular disease when they invade the endothelium and become oxidized, since the oxidized forms are more easily retained by the proteoglycans. A complex set of biochemical reactions regulates the oxidation of LDL particles, chiefly stimulated by presence of necrotic cell debries and free radicals in the endothelium.

Why doesn't HDL cause diseases like LDL ? What's the reason?

HDL transports cholesterol and fatty acids away from the periphery toward the liver. So HDL is always good and does not cause any health problem. HDL is protective in coronary heart disease and atherosclerosis

@CRags: we have seen that drugs that increase HDL were not so protective after all. Therefore, blood lipids do not "cause" disease in the straightforward manner Majid asks about and you talk in your answer. It is a fact that some are higher in the progression towards coronary disease, and there is a general feeling that C Rags' answer is right, but more research is needed on the HDL front.

@NickSandor I will read more on that. Thanks for pointing out.

Torcetrapib was an experimental drug that was very good at increasing HDL, but probably did not protect from cardiovascular disease. Dalcetrapib also failed. In a uni exam, I'd give the same answer as C Rags, because it is the accepted wisdom, but there is no clear cut truth.

Thank you for the fascinating question! It was tough to research but very worthwhile.
LDL is actually not such a bad molecule. It is formed from VLDL/IDL after VLDL/IDL distribute triglycerides, phospholipids, cholesterol and cholesterol esters to peripheral cells. With less to give, LDL subsequently tries to be helpful by providing any needy peripheral cell with leftover cholesterol necessary for plasma membrane synthesis and other cellular functions. In fact, even endothelial cells, which line the vasculature, have LDL receptors to welcome any cholesterol packages from LDL. Another function of LDL is to make HDL even ‘healthier’ by removing cholesteryl ester from HDL molecules in the periphery and returning it to the liver.
Remember that LDL does not contain exactly the same components as its precursors. LDL does not have the ApoE & C proteins that VLDL and IDL have. LDL has only ApoB-100 and a concentrated level of cholesterol. LDL-family receptors generally recognize ApoE and ApoB, which are located on VLDL and IDL, thus easily pulling them into the liver out of the bloodstream, via endocytosis. Because LDL contains only the ApoB protein, it is less easily recognized. Thus, more LDL lingers in the blood. This is supported by the lengths of their half-lives--- with VLDL and IDL half-lives being about 6 hours and LDL half-life being about 3 days.

Where disease comes in is with an imbalance of fat in our diet. This is explained in detail by this extensive article on Managing Dyslipidemia: The Triglyceride/High-Density Lipoprotein Axis. The article explains that disease cannot solely be blamed on LDL alone. A high fat diet leads to elevated triglycerides in the blood stream, which increases blood viscosity, interference with endothelial function, stimulation of arterial inflammation, and interference with normal blood coagulation. These conditions can predispose to atherosclerotic lesions. In addition, there is an up-regulation of protein ApoC-III, which subsequently increases the half-lives of VLDL and IDL particles. It even increases the activity of an enzyme called cholesteryl ester transfer protein (CETP), which can exchange cholesteryl ester in HDL and LDL for triglycerides in VLDL and IDL, and vice versa. This leads to change in composition of HDL and LDL, making them more triglyceride-rich, physically smaller, and less interactive with their respective membrane receptors. With HDL even smaller, it is also easily filtered through the kidneys, leading to lower levels. All this means there is more circulating LDL in the blood.
LDL enters the endothelium via breaks in the endothelial wall created naturally (by dying or dividing cells) or through injury (by inflammatory processes including infections, chemical exposures) or it leaks in through junctions between endothelial cells when there is high intraluminal pressure (such as in hypertension). From there, LDL can become oxidized and ingested by macrophages, forming foam cells, which can rupture spewing its contents into the surrounding arterial wall, leading to the beginning of atherosclerotic lesion.
Why can’t HDL cross through endothelial wall, too? Actually, it can! According to the above-mentioned article, “HDL particles [in its native form] appear to have the potential to delipidate cholesterol from foam cells” at the site of a lesion. With HDL being smaller, it can enter the endothelium to interact with foam cells. Its interaction, however, is the opposite of LDL. Cholesterol is transferred back from the foam cell to HDL, reversing the oxidized LDL-induced process. In addition, “HDL protects LDL from oxidation by [using] metal ions” before oxidized LDL can lead to further damage. This mechanism is still unknown.
Why can’t HDL become oxidized, too? Indeed, this can also happen! However, it appears again than oxidized HDL behaves oppositely to oxidized LDL. “Oxidative tyrosylation of high density lipoprotein by peroxidase enhances cholesterol removal from cultured fibroblasts and macrophage foam cells [5].” There is a caveat though. This function seems to depend on how HDL is oxidized. If oxidized by copper or hypochlorous acid, HDL “loses its ability to remove cholesterol from cultured cells [6].”
In short, given the very same conditions including oxidative environment and entry into the endothelial cell, HDL inherently behaves oppositely to LDL. This likely is related to their inherently different composition, but we have yet to understand how this occurs at a molecular level. However, HDL could technically be 'bad' under the right oxidative conditions. In the end, LDL is given a bad reputation because its relatives IDL/VLDL easily escape into other cells via receptors and HDL concentration is lowered partially by renal filtration.
References:

Mera, Steven L. Understanding Disease: Pathology and Prevention.
http://www.ncbi.nlm.nih.gov/pubmed/19592615
http://www.nature.com/nrmicro/journal/v8/n2/fig_tab/nrmicro2269_F1.html
Libby, P (2006). "Inflammation and cardiovascular disease mechanisms". American Journal of Clinical Nutrition. 83(suppl) (2): 456S–460S. 994471841.
http://www.medscape.org/viewarticle/582014
http://atvb.ahajournals.org/content/23/9/1488.full#ref-16


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Why do skin and nail go blue in cyanosis?
I have learned that Cyanosis presents with blue skin and nails. What is the reason for the blue coloration of the skin and nails? Why wont the skin and nails turn another color in the visible spectrum such as green for instance? How is this disease diagnosed?

The skin appears blue due to the diffraction of light through the skin. Blood is either bright red (sufficiently oxygenated) or dark red. "The blue appearance of surface veins is caused mostly by the scattering of blue light away from the outside of venous tissue if the vein is at 0.5 mm deep or more. Veins and arteries appear similar when skin is removed and are seen directly" 1. The color of blood is due to the difference in color between deoxyhemoglobin and oxyhemoglobin.
Let's consider the "blue fugates" of Kentucky. The ancestors of this family have different shades of blue skin tones. Dr. Madison Cawein discovered that the family had a high concentration of FE$^{3+}$ brown methemoglobin. This form is useless to the body so the enzyme diaphorase reduces the methemoglobin to FE$^{2+}$ (hemoglobin that can carry oxygen) [2].
Basically the skin color comes down to light diffraction not the blood changing from red to blue.

Cyanosis is the appearance of a blue or purple coloration of the skin or mucous membranes due to the tissues near the skin surface having low oxygen saturation [3]. Cyanosis is a clinical sign diagnosed visually. Cyanosis is an indication for blood gas testing.
References:

http://en.wikipedia.org/wiki/Venous_blood
http://courses.chem.indiana.edu/c122/documents/Experiment10_BloodandHemoglobin.pdf
http://en.wikipedia.org/wiki/Cyanosis
http://www.webmd.com/lung/arterial-blood-gases

When haemoglobin takes on oxygen the colour will shift from blue to red. the reason for this is a change in orientation of the Nitrogen ligans of the haemoglobin molecule.
The red cells pass through the veins in the lung(s) to the aevioli; the blue haem (pH~7.2) exchanges CO2 for O2 (now pH~7.4) 98% saturation and goes from blue to red.
We see the colour(s) because the haemoglobin's Fe in the centre of the ring goes in and out of plane to the ring. The colour comes for this phenomenon due to the 4 Nitrogen atoms and the electron states that exist without and with oxygen. This takes place within about 12milliseconds.
Hope this helps.


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Is there any scientific evidence that a human has ever grown a third set of teeth?
This is about the possibility (or lack thereof) for a person to re-grow a new "permanent tooth" or set of teeth, to replace the teeth that grew after their milk teeth fell out.
I had earlier seen some anecdotal evidence on the internet that this would have happened to some people.
Anyway, what I wanted to ask is if there is any scientific evidence (e.g. properly recorded unusual medical phenomena) that shows that a person has grown a tooth (or a set of teeth) to replace their permanent teeth?

Hello. Can you please link to your sources?

I think this question would be more on-topic on skeptics.SE. Someone who grows a new set of teeth after seing an UFO sounds quite obviously like some kind of a stupid fake story.

My question is not because of the anecdotal evidence (I am not asking anyone to validate the anecdotal evidence). This question could stand on its own without the references to the anecdotal evidence and I have not been able to locate those sources.

I made some edits to this that removed the voodoo to make it more of a stem cell and development based question

@rhill45, it is better without the voodoo. Thank you!

There are legitimate case reports in credited journals of hyperdontia, or the condition of having supernumerary teeth. Such cases are often associated with congenital syndromes-- cleft lip and palate, trichorhinophalangeal syndrome, cleidocranial dysplasia, and Gardner's syndrome. I included a case report and a comprehensive review for you below.
Case Report from American Journal of Orthodontic Dentofacial Orthopedics, 2011.
Comprehensive Review from Journal of Oral Science, 2014.

Googling images of this is always a fun weekday evening past-time...


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If what we eat can be seen in our hair, then to what degree can our food affect the "look and feel" of our hair?
It looks like most things (or everything?) that we consume, whether it is a food, drink, or something we smoke (like e.g. some drug like marijuana) ends up in some amounts in our hair.
If this is the case, is it theoretically possible that there exists some compound that, when ingested, could affect the color of our hair?
Or alternatively, would it be possible for an ingested chemical to weaken or strengthen the disulfide bonds present in hair structure?

It looks like? I'd be fascinated if you give a reference. I thought this is yet unproven theories....

@MARamezani, sorry, I do not have any references. This is just a thought that came to my mind and I was curious about whether it could be possible or not.


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How far can birds see?
I have heard that birds have exceptional eyesight. How far does this mean they can see? What's the resolution like? Are we talking about just vague shapes or something like, at 100 feet, seeing individual hairs on a dog's fur coat?
I've also read that, in general,  primates are the only mammals that have color vision. I know birds are not mammals. Is it common for birds to have color vision as well, like primates?

http://en.m.wikipedia.org/wiki/Bird_vision

This is a massive topic, with so many exceptions any short answer would probably pointless. Is there a specific kind of bird you had in mind? Even simply covering Raptors would fill a chapter of a textbook. Also, where did you get primates being a special case of colour vision? Thats false. Even dogs, famously colourblind, are thought to have two pigments for colour vision (not red, just blue and yellow).

primates are trichromats, many other animals (most mammals) are dichromats (can see color, but less well than primates). Birds, on the contrary, are tetrachromats and can see color better than we do. Hence your 2nd statement is incorrect. The first question needs refinement.


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Could the proteome of E. coli be fluorescently labelled?
What proportion of the total number of proteins in E. coli could be fluorescently labelled for PALM/STORM imaging?

If (G)FP labeling is cumbersome or it changes diffusion co-efficients then you can try quantum dots or click chemistry based probes too. But as pointed out in the answer, you have to do one at a time. If I am not mistaken there are libraries with each protein GFP tagged (at least for yeast afaik there is one)

One at a time, you could potentially label all of them.
If you're asking how many proteins you could label at once, your biggest limitation is probably your microscope. In order to distinguish between different types of proteins you need different color fluorescent labels (dyes, fluorescent proteins, etc). Even the fanciest fluorescent microscopes tend to be set up to excite/record labels in <10 distinct wavelengths.
In practice I've only seen experiments where there were tracking 3 distinct types of proteins at one time.


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What does the gene name "lexA" stand for?
It is an important gene expressed in E. coli that represses the SOS response and also the expression of lambda lytic phase genes. UV light and damage to DNA is responsible for its breakdown and hence the expression of repair genes and, if present, lambda phage genes. However I couldn't find a reference for its original name.

What does gene name X stand for? I think you might be expecting a little bit too much from the standard naming conventions...

What naming conventions?

I think there's some guessing going on here. I've looked pretty extensively and the information is not out there. Nothing conclusive. Lambda is a different depressor, worth noting. I would contact the person who discovered it: Miroslav Radman, Prof. Founder
tel:+385(0)21555601 fax:+385(0)21555605 e-mail:miroslav.radman@medils.hr

@Masih I linked a paper in my edited answer which I believe clears up some of the confusion in "Lambda Excision."

I'd go with Lambda Excision A. Terms like lex or rec often stand for what'd be termed a mnemonic, where for example rec may stand for recombination, or umu for UV mutator. The naming conventions can be difficult.
Edit: A 1981 study by Roger Brent and Mark Ptashne notes some data from initial studies that showed the lexA repressor downregulated a number of genes including himA, which they note to be required for integration of lambda phage.
http://www.pnas.org/content/78/7/4204.full.pdf

According to this website, it is a mnemonic for "lambda excision". I have also found this usage in scientific literature (eg. Harami et al., 2013). However, neither of these sources reference anything and I cannot find any defining paper. Almost all papers simply refer to it as lexA.
As far as I can find (it's difficult to dig up these old papers), this is how the locus (not necessarily gene) was originally described (Howard-Flanders and Boyce, 1966):

There is a ... locus, lex (locus for X-ray sensitivity), in E. coli K-12 ... [A] mutation at this locus increases the extent of UV-induced DNA breakdown. This effect is similar to, but less extreme than, that of the rec locus ...

It's possible that as this locus was better characterised, the name lex was retained for consistency with previous literature but redefined to reflect a better understanding of its function (although I don't think that "lambda excision" does this very well at all).

References
Harami GM, Gyimesi M, Kovacs M. 2013. From keys to bulldozers: expanding roles for winged helix domains in nucleic-acid-binding proteins. Trends Biochem Sci 38(7):364-371
Howard-Flanders P, Boyce RP. 1966. DNA Repair and Genetic Recombination: Studies on Mutants of Escherichia coli Defective in These Processes. Radiat Res Supp 6:156-184

Lee Theriot's X-ray sensitive mutant https://thebradentontimes.com/lee-frances-theriot-p24426-154.htm I was a postdoc with Joseph Greenberg working in the same field at the time

This is well documented in Advances in Microbial Physiology, Volume 16, Moseley and Williams, pages 116-117 (searchable via Google Books).
Mattern et al. (1966) designated mutations that made E. coli Bs-1 sensitive to X-ray radiation as exr (X-ray sensitivity) mutations. That same year, Howard-Flanders and Boyce (1966) independently designated equivalent mutations in E. coli K-12 as lex (locus for X-ray sensitivity). In both strains these mutations were close to the malB locus (b4039; lexA is b4043). A year later, Greenberg was using a broader designation with the same causal root (Loci for Radiation Sensitivity) to designate these same mutations.
LexA is also known as umuA (UV-induction of mutations) and tsl (thermosensitive mutations).

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Retinal eccentricity to colour sensitivity
Colour perception goes out to 50 degrees but is the sensitivity to RGB. Question is it the same in the four quadrants of the retinal field? That is if the red colour sensitivity eg is 30 temporal retina 50 degree nasal retina etc. And what are the eccentric limits for each colour [frequency]in the four quadrants.

Not exactly the same question, but a good reference point in the citations.

I think the PO specifically asks about the differences between quadrants here

Simon: could you clarify your question a bit? As of now it is unclear as to what you exactly wish to know. The linked answer by @anongoodnurse is indeed a very good starting point (and a very nice answer :-)


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What is the name of this plant? (found in a rock)
I found it in Western Turkey.It was growing on a rock so what's it?

wow so strange-looking

I have been looking into this for days, but this plant is difficult to identify without its flower. I reached out to a botanist at Dartmouth, who suggests that it is either one of two species-- a nasturtium (Tropaeoleum sp.) or a geranium (pelargonium). The leaves are what are called peltate, meaning shield-like with the stem attached directly underneath.

Source:

Botanist at Dartmouth
http://etc.usf.edu/clipart/48400/48426/48426_peltate_leaf.htm

On further research, specifically of peltate leaves, this plant looks more like Umbilicus rupestris, which is commonly found in southern Europe and grows in damp rock crevices!
Source:

http://en.wikipedia.org/wiki/Umbilicus_rupestris

+1 - Great job! Key here is that the plant is a succulent (neither nasturtiums nor geraniums are). The succulent nature is easier to see in the OP's picture, where the leaves are slightly wilted.


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Why is an allele dominant or recessive?
Alleles refer to duplicate genes, where one allele can be dominant over the other. What makes an allele dominant or recessive, given that both code for a single protein?.

I edited your question a bit for clarity. Feel free to roll back if it is not to your liking!

There are several hypotheses about the evolution of dominance. It is important first of all, to note that empirical observations show that beneficial alleles tend to be more dominant than detrimental alleles. Among the two main hypotheses to explain the evolution of dominance, one has been formulated by Ronald Fisher and one by Sewall Wright.
Fisher's hypothesis
According to Fisher's hypothesis, between two equally beneficial alleles, if one is more dominant than the other than it's heterozygote carrier will have higher fitness. In consequence, beneficial alleles evolve to become more dominant while detrimental alleles evolve to be recessive (so that they can hide from selection in heterozygotes).
Wright's hypothesis
According to Wright's hypothesis, beneficial alleles are more dominant because of the kinetic of biochemical reactions. The rate of a biochemical reaction is a function of the concentration in the substrates of interest. The function is called "Michaelis-Menten function" after the name of the authors. The Michaelis-Menten function looks like this:

Think about a knock-out mutation. Such mutation will decrease by half the concentration of protein the gene in question produce in heterozygotes. Imagine, the concentration of proteins in the wildtype homozygote was 3 (see above graph). The rate of reaction of this homozygote is therefore about 3. The heterozygote would have a concentration of 1.5 and the rate of the reaction is therefore about 2.5-2.75. Assuming that the rate of this biochemical reaction is directly related to fitness, then a the locus of interest, benefical alleles are necessarily dominant and detrimental alleles are necessarily recessive. Selection for dominance is not involved in Wirght's model.
Is Fisher's or Wright's hypothesis correct?
Current state of the art is to consider Wright's model to be correct and Fisher's model to be wrong. In reality, the truth probably lies somewhere in between these two extremes. Note also that some other alternative explanations may exist in the literature but Wright and Fisher original hypotheses are by far the most considered hypotheses for the evolution of dominance. During my undergrad, I remember a speaker (but I forgot his name, sorry!) who showed that some alleles actually have some domain that are directly responsible for decreasing the expression of the other allele on the sister chromosome suggesting that Fisher's hypothesis might sometime be a good explanation as well.


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Chickens roosting, is it sleep or torpor?
At night when they roost, do chickens experience a state of sleep (meaning do they move from NREM1 to NREM2, NREM3 and REM) or are they in a state of torpor (reduced metabolic rate and decreased physiological activity)?

@JamesJenkins sure!

To answer the question, I assume it would require someone to have done polysomnography on a chicken. Assuming chicken EEGs look like humans. Now that is a funny picture!

When birds sleep, they do experience NREM sleep [1]. Furthermore, Kavanau (2002) concluded that NREM has evolved in warm blooded animals [2].

Birds provide a unique opportunity to evaluate current theories for the function of sleep. Like mammalian sleep, avian sleep is composed of two states, slow-wave sleep (SWS) and rapid eye-movement (REM) sleep that apparently evolved independently in mammals and birds. Despite this resemblance, however, it has been unclear whether avian SWS shows a compensatory response to sleep loss (i.e., homeostatic regulation), a fundamental aspect of mammalian sleep potentially linked to the function of SWS. Here, we prevented pigeons (Columba livia) from taking their normal naps during the last 8 h of the day. Although time spent in SWS did not change significantly following short-term sleep deprivation, electroencephalogram (EEG) slow-wave activity (SWA; i.e., 0.78-2.34 Hz power density) during SWS increased significantly during the first 3 h of the recovery night when compared with the undisturbed night, and progressively declined thereafter in a manner comparable to that observed in similarly sleep-deprived mammals. SWA was also elevated during REM sleep on the recovery night, a response that might reflect increased SWS pressure and the concomitant 'spill-over' of SWS-related EEG activity into short episodes of REM sleep. As in rodents, power density during SWS also increased in higher frequencies (9-25 Hz) in response to short-term sleep deprivation. Finally, time spent in REM sleep increased following sleep deprivation. The mammalian-like increase in EEG spectral power density across both low and high frequencies, and the increase in time spent in REM sleep following sleep deprivation suggest that some aspects of avian and mammalian sleep are regulated in a similar manner [3].

From the Abstract and reference [3] above, we see that EEGs have been taking on birds and show that birds enter REM and SWS similarly to mammals.

In response to Chris Stronks, researchers have also studied chickens see Evolution of Sleep: Phylogenetic and Functional Perspective by Patrick McNamara, Robert A. Barton, Charles L. Nunn. In the section for REM sleep in birds, the studies were conducted on pigeons and chickens see pages 204-205.

Although not directly disagreeing, I have to say: but what about chicken? The class of Aves is pretty big, and as the question was on chicken you may be over-generalizing?

@ChrisStronks understood but the other articles establish birds have rem sleep since they are warm blooded and chicken are birds. The last article was to show that researchers have measured EEGs of birds to show it is true.

@ChrisStronks studies were performed on chickens as well. See link.

@ChrisStronks not a problem.

Well done @dustin. My wife wins the bet!

@BenPlont my bad. I bet you wanted to win.


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Is there any disadvantage to having a really low adipocyte count in our times?
The key feature of adipocytes seems to be energy storage. Today humans in Western countries don't have to hunger and have therefore less need to store energy in fat cells.
Do adipocytes have additional functions that still make them valuable?
Wikipedia lists 10–13% and 2-5% for men as essential body fat percentage for woman. What functions don't get fulfilled if the body fat percentage drops below that level?

You mentioned something odd in the tittle "adipocyte count", this was likely a mistake, but I will address it anyway. I recall something about liposuction not being preventative for
   diabetes:
You can have more adipocytes with less lipids in each cell, or fewer
   adipocytes with more lipid in each cell. Hypertrophy vs hyperplasia, just like in the question you asked on muscles elsewhere on this forum. Anyway, when a patient gets liposuction they decrease the number of
   adipocytes. Then if s/he gains the weight back the size of their
   individual adipocytes will be larger than it was before the
   liposuction. Somehow this was bad, and it increased insulin resistance. in a way, decreased "adipocyte count" is dangerous.

here is the other, obvious stuff on endocrine function of adipose tissue that you surely already know since your profile is very endocrine based, but anyway, here goes:
Adipose tissue has hormonal functions, secreting horomones (leptin, adiponectin, and resisting... these modify appetite as well as insulin resistance) and modifying them (converting testosterone to estrogen vi the enzyme aromatase).
The adipose-derived hormones are quite mysterious to me, I don't know much about them. The effects of the aromatase in adipose tissue are more obvious:

men will have increased estrogen levels (for example leading to gynecomastia aka man boobs, as a chubby guy I know this all to well)
women will have higher estrogen which will stimulate LH secretion from the pituitary stimulating theca intern cells in the ovary which will increase testosterone levels. The condition in women is known as PCOS.

In a person with little adipose tissues, there will be less conversion of testosterone to estrogen, so men will have less estrogen. Women will also have less estrogen, and less testosterone, aka they will not have PCOS in those women that already have PCOS, but thats not saying much :)

I may be wrong on some of this information, anyone please correct me.


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Double stranded nucleic acids are more 'durable' than single stranded nucleic acids?
I'm struggling with a question I've been asked.
"Why is double stranded genetic material more 'durable' than single stranded one?"
I know that double stranded genetic material is more stable due to multople strands. The single stranded isn't as stable as the double stranded since it lacks the second strand and therefore the bases are open.
Stable isn't the same as durable, and I've never heard in class that one is more durable than the other one. Did I miss something or is this just a mistake?

I'm having trouble understanding the question right now, but I do know that single stranded RNAs are more likely to be digested by RNAse enzymes than double stranded RNAs. From an error correction viewpoint, the second strand provides a template for fixing the first strand, so single stranded genomes would be more likely to mutate, or just get cut in 2.

A similar question has been asked in the past: http://biology.stackexchange.com/questions/23851/importance-of-double-helix-dna-structure

I don't know what one means by durable. For example it could be a simple question of stability as you mention, or is this in reference to DNA data storage where the double stranded nature can be used to identify or recover areas that are damaged over time.

I'm having troubles as you. I don't know what is meant. I asked my teacher today, and she said that the sentence is totally correct. She meant it like that. Furthermore, she added that it has nothing to do with stability. I don't find anything valueable in my book, nor in the internet. Any help is appreciated.

Do you mean durability against physical stress (shearing etc)?

This sounds pretty close. I would be happy to see an answer according to this idea.

I'm interpreting "durability" as the DNA's resistance to physical stress, such as shearing. The Bustamante lab at UC Berkeley does a lot of very cool single-molecule biophysics looking at forces involved in protein-protein interactions and protein-DNA interactions. This Bustamante et al. review paper, Single-molecule studies of DNA mechanics includes a look at the force required to break ssDNA and dsDNA:

Single molecules of dsDNA were broken
  with a receding water meniscus [26] at forces estimated
  to be 960 pN (correcting Young’s modulus doubles the
  published scission force of 480 pN). Short dsDNA molecules  pulled  with  an  AFM  tip  [27]  sustained  forces
  over 1700 pN.

pN = picoNewton
AFM = atomic force microscopy
dsDNA is more resistant to stretching/shearing forces because the double helix arrangement is "springy". I recommend giving the paper a read for more info. Very cool stuff.


text:
Is this description of etiology of celiac disease correct?
There is a detailed and, to my inexpert eyes, plausible description of the etiology of celiac disease and other autoimmune disorders posted here: http://no-gluten.org/CeliacDisease.htm
Is it is at all accurate? If any of it is speculative or incorrect, which parts are those? Red flags to me are that it cites no sources and is much more detailed than any other description of celiac that I've seen. But, again, it does coincide with what little I do know of human immune biology.


text:
Why do we have more male infants born?
For every 104 male babies, we have 100 female babies and there are statistics which are more reliable. (Those tell us that we have 997 female infants born per 1000 male infants born.) What is the reason for that? Why do we have more male babies than female babies?

Hello. I didn't know that. Can you please link your reference? Quick thoughts: There might have more miscarriage for males than for females babies. Also, there might actually have some environmental determinism of sex in humans but current studies had horrible stats for what I read. Might be worth to have a look to this post about sex determination system

Why the down vote on this post? This phenomenon has been documented but the articles are scarce so they are hard to locate especially for humans. I believe this a good question.

Where is this datum coming from (104:100 F:M)? from what time periods was this taken? does this take into consideration entire world population from all countries? is this population representative of all socioeconomic backgrounds? Before we can answer the question, we need to know this is a valid comparison.

I'm really sorry about this mistake which was corrected.

A great mistake

Before we get lost in the why, I think a reference is important as presumably it comes with statistical analysis attached. I'm curious to find if the seemingly small difference even statistically significant?

Are you asking for the evolutionary reasons for a difference (the evolutionary why), or the developmental/embryological reasons for a difference in sex ratio (the developmental why)?

It could be female infanticide that reduce the number of female babies or could be abortion when a poor family gets to know that the child is female. Basically, nobody likes paying a dowry when u r poor. Without any scientific evidence to back up this ratio, I can't take it at face value.

To explain my vote to close; it is based on my comment above, which the poster has not addressed. As the answers show, the question can be interpreted in two different ways. Either way, the question is good and should be kept, but I think it must be clarified.

@TheLastWord There exists quite alot of studies that show this pattern, from many different countries, also ones where dowries are not an issue. As I mention in my answer below, infanticide might a partial explanation, but probably not the only (or main?) cause.

Note: This is based on literature searches I've done a while ago out of general curiosity. I'm in no way an expert on human reproduction.

First, I'm not sure if you are asking about evolutionary reasons or the  developmental causes for for a difference in sex ratio. Here, I will focus on the developmental causes.
There is much evidence for a male bias in human sex ratio at birth (secondary sex ratio), and the ratio have been shown to change over time, e.g. as in 20th centrury Europe after WWI and WWII (see data in Gellatly, 2009),in relation to environmental or parental factors (see e.g. Jacobsen et al, 1999), or between ethnic groups.
A bias in sex ratio can be due to (at least) three different mechanisms (Irving et al (1999)):

deviations in X/Y-ratio of sperm
selection of sperm within the female reproductive tract
biases in implantation success and/or survival for embryos of different sex

I guess that success of fertilization/zygote formation could maybe be considered a separate step (between 2-3). From what I've seen, there is little evidence for explanation one, see tests in e.g. Irving et al (1999) and Graffelman et al (1999). Graffelman et al (1999) also tests for an effect of male age, but do not find support for this idea.
A problem is that it is extremely difficult to study these factors under natural conditions (practically and ethically). Interestingely, there is also evidence for an excess loss of male fetuses in recognized pregnancies (Ingmarsson, 2003, Boklage, 2005), and this would indicate that the sex ratio close to conception is even more skewed towards males than the sex ratio at birth. This is even more curious with the background of an unbiased sex ratio in sperm (explanation 1 above). However, it is very problematic to study what happens in the first part of pregnancies, since a number of weeks have usually passed before the pregnancy is even recognized. I haven't found any papers reporting the human primary sex ratio (sex ratio at conception), which could be affected by factor 1 & 2 above.
Even so, the most likely explanation seems to be a strong bias during embryogenesis, as mentioned in Boklage (2005):

The usual excess of males is present through pregnancy beyond clinical recognition, but not present at fertilization. The difference, therefore, must arise between fertilization and clinical recognition, through a preferential loss of females during embryogenesis.

The same paper also points out that fewer than 25% of natural human fertilizations go full term (probably even less), and 2/3 of these fail before the pregnancies have been clinically recognized. By back-calculating from the secondary sex ratio and the excess of failed male pregnancies, the sex ratio close to conception has been estimated to 125-135 male:100 female (Pergament et al, 2002))
The exact causes for such a bias during is not entirely known from what I've seen. However, Boklage (2005) mentions a couple of different explanations. For instance, among mammals in general, the earliest stages of embryogenesis proceeds more rapidly in male embryos:

Since some of the products of these earliest stages are signals from one part of the embryo to another, or from the embryo to the maternal physiology, signals which are required for continuation and maintenance of the pregnancy, the establishment of viable, clinically recognizable pregnancy is correspondingly more efficient in general for male embryos (Krackow, 1995; Kochhar et al., 2003).

The same issue is also mentioned in Ingvarsson (2003):

Studies in recent years indicate that sex differentiation begins at conception. The SRY gene on the Y-chromosome is already transcribed at the 2-cell stage and triggers growth acceleration in the XY embryos. This accelerated growth is believed to be important for the male embryo as it allows complete testicular differentiation before the levels of oestrogenic hormones become too high as pregnancy progresses.

Boklage (2005) also mentions genomic imprinting and chromosome X–Y segregation as possible explanations for a bias (see references in paper for more).
So, in summary; there is evidence for an male bias in secondary sex ratio (sex ratio at birth), even though there is usually a excess of failed male fetuses in recognized pregnancies, which means that the male bias must be even higher very early in pregnancies. There is some evidence that this might be due to a higher success of embryogenesis of male fetuses, but the evidence isn't strong and the issue is difficult to study.

The evidence provided by these results is indirect. That is unlikely to change. Ethical, technical and financial considerations argue against the destruction for karyotyping of statistically sufficient numbers of products of natural human fertilizations. Granted, any bias of the sort we seek to discover and understand might, after all, operate differently, or not at all, in sham fertilizations of hamster oocytes, versus oocytes from artificially induced human ovulations, versus naturally fertilized human oocytes. The best evidence we have, or are likely to have in the foreseeable future, indicates that the consistent excess of males observed in human births does not originate in a consistent bias in spermatogenesis or in fertilization.
  (Boklage, 2005)

Finally, it should also be mentioned that the bias in sex ratio at birth can be partially due to sex-selective abortion and infanticide, but to what extent is not entirely known (see Wikipedia: Sex-selective abortion).
You might also find this related question on the heritability of sex ratio interesting: The gender of offspring of Twins?.

This is just a conjecture, I can't find support for it in this moment, but: the 125:100 m:f ratio close to conception could be due to the Y chromosome "behaving" like a selfish element.  It could confer some sort of advantage to spermatozoa carrying it (they can swim faster or penetrate the oocyte better etc). The skewed ratio is then corrected by the maternal system favoring the female zygotes  (easier implant in the uterus etc). I'd like to know @Remi.b 's opinion on this.

There is an article in the Journal of Popular Science from 1885. However, I do know there is at least one more recent article floating around some where since I read it. At the moment, I can't find it but will update if or when I do.
The article goes on to state that during times of scarcity the number of male births outweighs the number of females whereas in times of plenty, the number of female birth outweighs the number of males. I will let you read linked article but give you the information I recall from the more recent article I can't locate at the moment.
The reason for the differences in births has to do with the lifestyles men and women lead. Men tend to do more dangerous activities at younger ages which causes unnatural deaths early on. Due to these unnatural deaths, in times of scarcity, the reproducing population converges to 1:1 (not exactly) male to females due to the lifestyle choices of men. It was also hypothesized that women are almost guaranteed to find a mate so having less females during rough times wont hurt the population since they should all find a mate.
Additionally, the phenomenon of environmental factors influencing male and female births is well documented in alligators. The first linked article also goes on to examine this occurring with other species as well.

Thanks to @Anne, who sent me a discover article, we have the name of two sets of researchers on this topic. Here is an exert from the article Famine Can Tilt the Sex Ratio of Future Generations. But Why? (Discover, Nov. 2013). Additionally, we can look up the articles by the respected researchers now. I believe the research by Robert Trivers and mathematician Dan Willard will be the most applicable.

While demographers were struggling to understand sex ratio anomalies in the context of culture, evolutionary biologists had largely embraced an idea put forth in 1973 by biologist Robert Trivers and mathematician Dan Willard. The Harvard-based pair theorized that as the physical condition of a female declines — if she’s nutritionally deprived, for example — she’ll tend to produce a lower ratio of male to female offspring. Evidence of the theory came from red deer and humans; in both species, adverse conditions in the mother’s environment during pregnancy are correlated with a shift toward female births.
Although natural selection ideally favors a 50/50, or .500, sex ratio in a population, mammals typically produce slightly more males than females. Because sex ratio is biased toward males, the figure is expressed by dividing male births by total births. It’s estimated that women give birth to 3 percent more boys, for a standard .515 sex ratio (with 48.5 percent female births). When fewer boys and more girls are born than that, it’s described as a sex ratio decline.
Evolutionary biologists say male mortality, which is overall higher than that of females, explains the male bias in sex ratio: A slightly skewed sex ratio at birth that favors males ensures that there are roughly an equal number of males and females of reproductive age. (Theoretically, a .500 sex ratio at birth may be possible if the gender difference in mortality is eliminated.)

Again thanks to @Anne, who provide this link as well, we see that men do outpace female births. We can see the world data here.

@Remi.b I don't think it is survival probability. In all species, females hold the cards when selecting mates. We easily see males in all species have to impress the female via either strength, feather color, etc.

actually.It is not my primary purpose.It is not a reason ,It gust describes the advantages.

@Majid what is not your primary purpose?

I imagine this answer is along the right lines; men die more (war for example), so more men are born and in times of stability their population is a little higher. I would like to see the more modern example text. The 1885 one is unreferenced, and draws conclusions from unreferenced anecdotal evidence and scientific studies from completely different species; bees. To me, using an outdated, and arguably unscientific article and using it to comment on modern population seems like it could be purely conjecture.

@dustin So your answer says, but without that article I can't really get a good grasp on what you're trying to conclude. I'm also dubious about there even being a real difference in the questions population data.

Aaaahhh reading your edited answer I got something I missundertood! Ha ha Sorry about that. That seemed so silly to me. The explanation still relies on kin selection/group selection theory but it is not as non-sense as I thought it was before. Also the mechanism by which in a XY system, selection can influence the gender would still need some explanation but your answer makes sense. I apologize for my comments. Hoping this is fine for you, I deleted my above comments to clean things up! +1

@Remi.b that is fine. I couldn't find the information I needed. It is thanks to Anne we have the Discover article and researchers names so we look up there actually papers.

@Remi.b this is good question but the material is extremely hard to find. You should have seen all the different searches I attempted and failed at.

Yes, and many references on the subject are old. In addition to that, I remember one article on the subjects that had really bad data analysis. Finally the underlying mechanisms by which selection operates seem to be largely unknown. So it is definitely a question that is to handle with kid gloves.


text:
How does most of lymph get back into the blood stream? (I don't mean the lymphatic system)
I once read that it was because of osmotic pressure that it returns to the blood stream, by entering the venules. But why? If lymph originated as plasma how come that the solute concentration is higher in the venule? Doesn't plasma contain solutes such as salts, nutrients, oxygen, etc. ?

Could you please define what you mean by lymph? Are you just talking about the non-cellular material that lymphocytes are transported in, or what?

@MattDMo With lymph I mean a fluid which originated as plasma; most of this lymph returns to the blood stream simply by defusing back inot the venule.

I think you have confused oncotic pressure with osmotic pressure

Technically 'lymph' is used to refer to the fluid found within the lymphatic system. If it's not in the lymphatic system, it is not lymph fluid. Thus, your question is really asking about interstitial fluid or the plasma that was filtered out of blood capillaries.
The answer to your question is based on the Starling equation. Normally fluid leaves a capillary due to a net pressure that favors the interstitium. This net pressure is based on the hydrostatic pressure within the capillary being greater than the interstitial pressure of the surrounding tissues, and the oncotic pressure of the capillary (that draws fluid in) being weaker than the hydrostatic pressure of the capillary (that pushes fluid out). At the venule end of this system, the capillary oncotic pressure is stronger than the capillary hydrostatic pressure, drawing fluid back into the circulatory system.

Remember that albumin is the most important component which establishes the oncotic pressure within a vessel, and that this protein is normally NOT released out of a vessel during filtration. Thus, it passes from the capillary into its corresponding venule directly.

Yes, plasma that enters the interstitium contains many of the same components as when it is in the blood, but the main difference is the protein content, losing the majority of proteins as it enters the interstitium.
Now, if you are asking how the majority of LYMPH fluid re-enters the blood stream, the answer is through the R lymphatic and L lymphatic (aka thoracic) ducts, at the location of the R subclavian or R internal jugular, and L subclavian veins, respectively. Once fluid enters lymphatic capillaries, it goes through a system of lymphatic vessels, trunks, and finally, the above mentioned ducts to rejoin blood.
References:

http://www.biog1445.org/demo/06/lymphaticsys.html
http://intranet.tdmu.edu.ua/data/kafedra/internal/in_mow/classes_stud/uk/med/medprof/ptn/англійська%20мова%20за%20професійним%20спрямуванням/2/№%2003.%20Heart...htm

Nice elaborated answer!


text:
What are the requirements for a spectrometer to be used in biological research?
Suppose one would do spectrophotometry on biological materials. What would be the minimum requirements for the measuring device so that the results could be published in a reputable journal? I suppose that two important properties are

resolution of the spectrum (would e.g. 25 nm be enough? 15 nm? 5 nm?)
measurement error (10%, 5%, 1%, ..?)

What else (if anything) should be taken into consideration?

This is very contextual. Can you give any specifics about your experiment (what is in the solution for example)?

I am in the process of buying such a device, so I was hoping to hear about general principles. User Mad Scientist gave a good answer.

For all the common uses of a spectrophotometer in biology, any commercial one should be sufficient. For all the routine stuff, the quality of the spectrophotometer is usually of negligible importance.
There are no general rules on what errors and resolution are acceptable, that always depends on what you're measuring. The error should be significantly smaller than size of the effect you're looking at, otherwise you get no useable data.
There are many sources of error with biological systems, the spectrophotometer is really one of the last ones you would think of. Simply the error of pipetting is likely far larger than the error of the spectrophotometer, and differences in the preparation of your biological samples might introduce an even larger error. Unless you're doing something beyond the routine uses of UV/Vis spectrometry, you probably don't need to worry about this.


text:
Is there any knowledge of physics can be applied in to evolution?
I have asked a similar question in Biology.SE (What physics knowledge can be applied to biology of organisms and ecosystems?), but it just about organisms and ecosystems, not evolution. After watching a clip that Richard Dawkin talks about applying Darwinian evolution to physics, I would like to ask a vice versa question: is there any knowledge of physics can be applied in to evolution?

Are you wanting to know about the biophysical interactions of nucleic acids driving evolution, or applying brownian motion to evolving population models?

@GoodGravy I want to know both to have a good start to google better

Related question on Physics.

@HDE226868 I agree that it's a related question, but it's not a duplicate one.

@Ooker No, I didn't mean that! I just put it here because it's relevant to the question, just as you linked the other question in your question here. I didn't think it was a duplicate.

Meteors an such are part of astrophysics. Meteors can cause extinction, which is related to evolution. So I would say yes.

There's some. The basic idea is that entropy, as rigorously defined in statistical physics, can be equated to complexity. This is an idea that has been around since at least the 1957 paper by Jaynes. In a fairly hand-wavey way, one can then say that a system that is being fed a large quantity of free energy (as the earth is by the sun) tends to become more complex over time (i.e. evolve).
Thinking this through a bit, the above argument applies as easily to weather patterns as it does to living creatures. Recently, with the rise of computers and modeling there have been attempts to apply these kinds of general ideas (increasing free energy leading to increasing complexity) to living creatures in a more systematic way. Jeremy England is one researcher working on this problem, and this link goes to a pretty good pop-science-style writeup of his work on the topic.

your answer is indeed what I'm looking for. Thank you so much.


text:
Is a Ginkgo tree a conifer?
I know Ginkgo is a gymnosperm, but I was wondering whether Ginkgo is also technically a conifer. I did a Google search, and found several confident authoritative-sounding answers. Unfortunately, those answers were divided between "is" and "is not". So which is it? Is a Ginkgo a conifer?

The scientific answers are pretty clear: Gingkos are not closely related to the conifers, they are closer related to the cycads. See this phylogenetic tree based on the 18S RNA from paper 2:

It shows that conifers and Ginkgos are relative close related, but not on the same sub-branch of the tree. The last common ancestor between Ginkgos and Conifers is older than the one between Ginkgo and Cycadales. This classification has been made on the basis of genome comparisions and also based on an analysis of the chloroplasts.
References:

Chloroplast Phylogenomics Indicates that Ginkgo biloba Is Sister to
Cycads
Molecular Phylogeny of Ginkgo biloba: Close Relationship Between
Ginkgo biloba and Cycads
Advances in Ginkgo biloba research: Genomics and metabolomics pe
rspectives

I see. Now I understand that Ginkgo, cycads, conifers, and gnetophytes constitute (extant) Gymnosperms. Gymnosperms and Angiosperms constitute seeded plants. Filicopsida is a category of fern, used as a convenient outgroup, outside of seeded plants, for this phylogenetic analysis.


text:
negatively charged albumin as major carrier of acidic/negative charged drugs in blood
I reading that orsomucoid (alpha-1-acid glycoprotein) is the major carrier of positively charged (basic) drugs in the blood, while albumin carries negatively charged (acidic) and drugs with neutral charge.
On the other hand I've read that albumin is excluded by the basement membrane in the glomeruli, and in general by negatively charged glycosaminoglycans in the interstitial space, because albumin is negatively charged.
I did a quick search online and I couldn't find the information explaining this contradiction. Does anyone have an explaination?

Running the sequence for human albumin through expasy protparam confirms albumin is negative at neutral pH. This paper provides experimental evidence that albumin is negative because it reverses the charge on positively charged DNA-peptide particles. However, simply because albumin is overall negatively charged doesn't mean it has a uniform charge. There are probably pockets with positively charged or hydrophobic character.


text:
What is this plant ...?
I would like to know what is this plant ? Does anybody have an idea ? Somebody offered it to me but there is no explanation about how to care about it...
Some purple flowers appeared, during 2-3 days. And now it seems it lacks something, but I don't really know what to do :(

Any idea ?
Thank you very much !

What other information can you add about the plant? But also see this meta post.

As we can see on the picture, there are green small and thin leaves, and a big pink part in the middle. When I give water to the plant, this pink part seems to "drink" and fill up with water, as when we touch it, it is wet, like a sponge...
A few days after I got the plant, purple flowers appeared (as on the picture), and wilted 2-3 days after.
Now, the pink part is fading, and turning grey/green...
I have no idea about where this plant is from. But it seems that it is an indoor plant.

That is a beautiful Pink Quill, or Tillandsia cyanea. I have included two websites below about this plant, both of which include care tips.

http://home-and-gardening.info/2009/09/18/a-guide-on-growing-tillandsia/
http://houseplants.about.com/od/bromeliads/a/Bromeliads.htm

My pleasure! Enjoy!


text:
Why does human hair grow and behave differently depending on its location?
Why does human hair behave differently depending on its location? For instance, head hair grows to an indefinite length, but eyebrows maintain a particular length and appearance. Head hair and eyebrows may exhibit balding, but not ear, arm, nose, and facial hair (etc). Why is this so?

The answer for why is in this post: basically because of differences in follicle cycling. Are you asking how exactly is this controlled?

Thank you for the link. And, yes, I am asking how this is controlled.


text:
Why can't we call dog breeds different species?
I understand this question might fall into opinion based, but I'm trying to write it so that it meets the "Many good questions generate some degree of opinion based on expert experience" part and not get closed.
A closed creationist question about directly observing the evolution of new species made me think about just declaring dog breeds as new species just to provide an answer to that question. Turns out I'm not the first one to think of it, and to be honest I probably read that article and forgot about it.
That article quotes geneticist Jerry Coyne as saying:

“If somehow the recognized [dog] breeds existed only as fossils,
  paleontologists would consider them not one species but
  many—certainly more than the thirty-six species of wild dogs that live
  in nature today.”

There is also this question about breeds of dogs being different enough they can't breed. The answer posted to that question discusses attempts to breed beagles with irish setters, and having great difficulty.
I'm aware that the commonly used definition of different species is individuals who can't interbreed and make a fertile offspring. However the Scientific American article I referred to above mentions that animals are often classified as separate species because they are separated by a geographical barrier, and if they could mingle they would make fertile hybrid offspring. The same articles mentions fruit fly research that bred two different species of fruit fly and made fertile offspring, even though they would never interbreed in the wild.
This is speculation, but let's imagine taking an island and putting several breeds of dogs on that island. Many of those breeds would easily interbreed and create mutts. But I'm pretty sure there would some sorting, the large dogs like st. bernards and great danes aren't going to easily interbreed with tiny dogs like chihuahuas. If we came back to this island after 50 or 100 years, we'd probably see small dogs and large dogs (assuming the island had decent ecological niches for both sizes of dogs to survive in)
Creationists like to ask why we haven't observed the evolution of a new species and don't want to listen to arguments about the fossil record or DNA sequences. If we just define some dog breeds as different species, we'd have an easy answer. I think some dogs would at least come close to meeting that definition for these reasons:

Dog breeds with large size differences would have great difficulty breeding.
Some pairs of breeds seem to have trouble interbreeding (Beagles + Irish Setter).
Some animals recognized as different species can create fertile hybrid offspring.

So why don't we recognize some dog breeds as different species?

Your island thought experiment is very interesting.  One thing to consider: how would natural selection act on these breeds?  Would large or small breeds be selected against?  What breeds have genetic issues the reduce fitness (eg, hip problems are common in large breeds).  I suspect that the size differences most likely to result in "species" would not be stable in a more natural environment.

@NBrouwer It would have to be a very special island. This points out that wild dog populations don't include the more extreme breeds like bulldogs, and tend to be more like their wolf and coyote relatives.

Interesting island experiment, but with intermediate sizes they may eventually all interbreed to produce a single population of mutts. What about introducing only two breeds of dogs - one very large and one very small.  If the island has sufficient resources that both can survive, would they effectively develop into different species?  Might they evolve in ways that pushed them further apart?

A side note: if you're looking for an example of observable speciation to use in arguments with creationists (and are willing to consider non-mammalian examples), it is worth noting that a substantial proportion of plant speciation events are 'ploidy events. 'Ploidy events generate new species essentially instantaneously by producing an offspring that is self-fertile, but not capable of back-crossing to close relatives.
http://www.pnas.org/content/106/33/13875.full

I don't enjoy the idea of comparing people to dogs, but this is a bit akin (please note the bit) to asking if people who are genetically short (or "little people", both proportionate and disproportionate dwarfism), pygmies, short people, normal sized people, tall people, very tall people, and people with acromegaly (gigantism) can be called different species. I compare because it's fairly clear to most individuals that we are all the same species: homo sapiens. About breeding, it is very likely that a reproductive specialist would be quite concerned (I certainly would be) about a woman with drarfism carrying the child of a very tall person (who had very tall parents), but not the opposite pairing.
Below is a photograph of the wedding of Tom Thumb and Lavinia Warren. That union produced no children. Her bridesmaid Minnie, (her sister), who was only 27 inches tall, also married a little person (Edward Newell). She became pregnant with a normal-sized child, but died during the birthing of a 6 pound baby (her baby died as well).

Are they a different species? No. A paleontologist (a good one) would be able to tell that the bones of a little person was actually of the same species based on certain conformations, just as I believe paleontologists today could distinguish prehistoric small cats from very large cats. Size matters, but not nearly as much as the type and distribution of teeth, the shape of the jaw, etc.  In other words, I strongly disagree with the following:

If somehow the recognized [dog] breeds existed only as fossils, paleontologists would consider them not one species but many—certainly more than the thirty-six species of wild dogs that live in nature today.

That statement is based on a fairly profound error in thinking: a cognitive bias that is mistrustful of science in general due to a lack of familiarity with the rigors involved in the scientific methods of paleontologists in particular. I say this without rancor or animus of any kind; where I settled down (in the deeply religious region), the vast majority of my children's friends' parents are creationists, and the vast majority of our friends are fundamentalists. We argue about science all the time; I know the basic arguments. I'm familiar with their websites. I personally find myself in the camp of Christian thinkers like geneticist Francis Collins, M.D., Ph.D., the director of the Human Genome Project, who understand genetics and find no threat to their faith in evolution or science. (E.g. Creationists reject all science which indicates the age of the Earth is >~6000 years.)
The truth is that the definition of a species is not that easy, even for prokariotes. Difficult as well is a pure definition of life.
Finally, about size. The domestic dog exhibits greater diversity in body size than any other terrestrial vertebrate. This is due to a small number of (or perhaps even a single) alleles: the IGF1 Allele. It's hard to argue difference of species on the basis of a small number of alleles: we allow much more variability for other alleles without wanting to classify as different species: eye color, hair color, hair length, straight vs. curly coat, degree of tail curl, ear morphology, etc.
A Single IGF1 Allele Is a Major Determinant of Small Size in Dogs
Lessons learned from the dog genome
A species definition for the modern synthesis
Single-Nucleotide-Polymorphism-Based Association Mapping of Dog Stereotypes
Canine Genetics Facilitates Understanding of Human Biology
How many species of prokaryotes are there? (PNAS)
Ernst Mayr and the modern concept of species (PNAS)
Hybridization, ecological races and the nature of species: empirical evidence for the ease of speciation
Is it Useful to Have a Clear-cut Definition of Life? On the Use of Fuzzy Logic in Prebiotic Chemistry

I think the size diversity would throw paleontologists off though. Dog diversity is a result of selective breeding, not natural selection, so you can get a much greater diversity in less time. If you didn't know what a dog was, much less that it had been artificially produced by humans, you might not realize that dobermans and chihuahuas are the same, especially when so many different species are separated by subtle differences.

Have you ever read any paleontology papers? Size doesn't matter. Elephants belong to the family Elephantidae, the sole remaining family within the order Proboscidea. Their closest extant relatives are the sirenians - dugongs and manatees- and the hyraxes, with which they share the clade Paenungulata. Have you ever seen a manatee or a dugong, or, incredibly, a hyrax? Please, give paleontologists credit where credit is due. I have opinion supported by sources. Where are your sources? I think you're wrong isn't an effective argument.

I'm not saying they wouldn't recognize the dogs as related, just as different species instead of different breeds. If the current breeds of dog had developed naturally instead of artificially, I think we would have classified them as different species. And dog breeds are different by more than size, a chihuahua is not a scaled down doberman, dogs have differently shaped skulls and different proportions for limb length.

Any sources to support that opinion? Did you compare the hydrax to the elephant to the dugong? Why do you think they'd be different species? Please support.

The wikpedia page on the hyrax explains why the hyrax is similar to elephants, and the page on paenungulata describes other features of the group. Both pages mention information about the placement of soft tissue such as the testes and DNA evidence, information that usually is not available from fossils and had to be obtained from living members of the group. Furthermore, these diverse species are members of 3 orders. Dogs would members of 1 genus.

@anongoodnurse: Since you mention elephants, consider the recent 'discovery' (or IMHO redefinition) that there are three existing elephant species, rather than the two (African and Asian) that've been accepted throughout history.

I don't think taxonomy works as precisely as one would hope...NOT that they don't have standard approaches but they are often working with inadequate information.  Rightfully, if a population of chuahuahuas and St Bernards lived side by side in the wild, they would, from a biological standpoint be considered a different species because they could not interbreed.  IT would be physically impossible.  And, in short time, behaviors of both would tend them to start staying away from each other.  NOT that evolution works preemptively, but as behaviors vary...those tiny dogs that simply stayed away from the massive males would tend to survive (NOT die in child birth) while those that inadvertently got pregnant by the massive male DID die in childbirth...any inherited tendency toward the safer behavior would be selected for.  The "example" of dwarfism...when it is known, does not apply to finding fossils in rock strata.  Through testing and actually experience we know very small people can interbreed with very tall people.  Often the pregnancy doesn't end well.  But for now and for reasons other than pure science, no one is considering re-naming human taxonomic groups...and they shouldn't IMHO.   But with dogs, with sometimes completely different structures and sizes of skulls and other body parts and the recognition that the massive dog's fetus would not life and be birthed from the tiny dogs womb would incline them to be described as different species.  Size AND VARIATION in structure does matter in taxonomy.

I don't think this really answers the original question.

I don't hink this either. Can you please edit your question accordingly, add some references and also remove the personal part against anongoodnurse?

Don't under estimate @anongoodnurse's answers :-) -1 If you think you can do better, do better. Don't try to be better by downgrading others. Instead, try to build on previous answers and use them to provide superior material.


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Does antibody staining / immunolabeling block or inhibit protein function?
In dissociated live cells, does staining them with an antibody block the protein's function?
I am sorting cells based on their expression of a few marker genes, and culturing them post-sort for several days.
How can one assess if the protein is still functional?

That depends on a number of factors: The actual place where the antibody binds, the protein itself and also the number of available protein molecules. About which protein are you thinking?

Also, the assay for functionality completely depends on the protein you're testing. Assuming you have an in vitro assay for your protein's function, you could try performing the assay at a given protein concentration with varying concentration of antibody to see if there is a significant effect on activity in vitro. It might not correlate well in vivo, but it is a start.

Thanks for your input, @Chris. I do not have a specific protein in mind; rather I have a panel of proteins which I want to use to sort cells based on their expression, and I am worried that these antibodies will mess with the cell's behavior, as I will continue to observe them after selecting for them.

Thanks, @A.Kennard. That makes sense, although I don't have an in vitro assay for my proteins' functions. Do you know of any examples where people have verified the activity of proteins for which they added antibodies in vivo?


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Can concentration of a protein be determined from a gel quantitatively (rough estimation)?
I've got a His-tagged protein in 6M urea, 500 mM imidazole buffer that needs to be quantified before dialysis to ensure there's enough protein worth dialysing. I ran out of my elution buffer which should be used for blanking. I made a fresh buffer with the same contents, it started giving me false results. I could interpret that problem is with the buffer (probably because of change in chemical batch) from the readings I got in BCA and Bradford assays. Hence, I ran a gel to get an idea of presence of protein. Are there ways to estimate protein concentration quantitatively from the gel?

I suppose you could get an estimate if you made a calibration curve with known concentrations of protein, then try to match the intensity of your unknown with the calibration curve. Probably wouldn't be very accurate. I recommend fixing your buffer and using the BCA assay.

Yup, I am doing that with a BSA standards. BCA assay gave me negative values for all the dilutions. I've tried fixing the buffer, it couldn't help me in any way. Thanks!

Yes, you can use SDS-PAGE as a semiquantitative estimate of protein concentration. You need to create a standard curve with a protein of known concentration to compare against. Quantification is done by densitometry. It's a quick and easy process, but keep in mind some limitations:

Band intensity depends not only on the amount of protein but also on the amino acid composition of the proteins and the dye used
The unknown protein and standard should be run on the same gel to remove variations in gels, electrophoresis, staining, destaining and imaging
Densitometry can be quite qualitative depending on how it's done

I'm not sure if you're looking for a protocol, but it's relatively straight forward. I usually load 2, 4, 6, 8 and 10 uL of 100 ng/uL BSA as a standard and 2, 4 and 6 uL of the protein of interest (based on past experience with my proteins and their purification). The gel is stained with Coomassie and the band intensity estimated with a program called ImageJ. A standard curve is created by plotting intensity as a function of mass, from which the concentration of the unknown can be found.

Wow! This is new to me. Thanks a lot!! Does a scanned image of gel work on ImageJ?

@piscean_1993 Yes, but you'll introduce artifacts into the image during printing and scanning. It's probably best to keep it digital if possible.


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How is the reflectance spectrum of solids measured?
I was reading this question about autumn leaf colors. One of the answers refers to an article by Archetti et al. In the article, box 4 (page 5) shows the reflectance spectra of leaves of different color. How is the reflectance spectrum of such solid materials measured? There was a recent question about spectrophotometers but it appears to assume the sample is in a liquid form.

As the name implies, reflectance spectra are measured from light reflected off an object. Any object with reflects light, such as any opaque object) will work for this technique; to me this seems like solids are ideally suited for reflectance spectrphotometry. You might be used to transmission or absorbance spectrophotometry, which measures the amount of light transmitted or lost after passing through a sample. These methods are typically used for liquids which allow passage of light to some extent.
The paper (1) cited by the review you mention says that they used a "RAMSES-ARC hyperspectral radiance sensor," which is probably just as awesome as it sounds. In principle reflection spectrophotometry works very similarly to transmission-based spectrophotometry: generate monochromatic light, shine it at the sample, and measure the intensity of light that comes back at that wavelength (or over a range of wavelengths)$^†$. If you do this for many different wavelengths of light, you have a reflectance spectrum. This link might have some useful information.
$^†$ Edit: Modern-day spectrophotometers use a more efficient method in which broad-band light is passed onto the sample and the response at a single wavelength can later be mathematically reconstructed. If you're interested in these types of details, refer to Fourier Transform spectroscopy.

(1): Doring TF, Anchetti M, Hardie J. (2009). Autumn leaves seen through herbivore eyes. Proc. R. Soc. B 282(1801): 121-127.

is it really a matter of serially sampling different wavelengths? Or can you perform some kind of FFT-like procedure and analyze it all at once? (+1 nonetheless :-)

@ChrisStronks fair point. I wasn't really aware how spectrophotometers are actually built/implemented, more just the conceptual idea behind them. I can edit the answer to reflect this.

I would have given you another +1 but alas I can't. Very interesting addition (I am interested in computer vision applications but pretty newbie on the topic :-)


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How to do a whole genome analysis of Multidrug-resistant Mycobacterium tuberculosis
I'm looking for tutorials and software that can help me study whole genome sequence data is and genome wide associations. I have Matlab and Bioconductor R so anything involving those packages would be preferable.

I have made some major edits to to your question to stop it being closed for HWK. Feel free to roll back :)

You've picked a fascinating and very important organism to study. Unfortunately there are many many steps with many software packages that you'll need and each next step will depend on what you find making any particular tutorial nigh on pointless. I'm sorry to say that I don't think anyone will dump an entire project proposal or workflow as an answer. I'll give you an answer to get you started on your research.
Example
An excellent example of such a study is Fellay et al., 2007 and you can find their materials and methods supplement here.
An introduction to this kind of research
First you need to find the sequences of proteins that you think are significant. There are a bunch of ways of doing this, but I suggest standing on the shoulders of giants and scouring the literature (regardless, find an example where this has been done elsewhere). If there isn't much out there or for an entirely new viewpoint on something, this answer might help for finding proteins in the DNA sequence.
Sequence alignments against other strains is your best bet of identifying mutations (and possibly an indicator of resistance, which is what I guess you're after). There are plenty to choose from, but BLAST is a good tool to start with. You should compare your resistant strain with non resistant strains. Be very careful when analysing the data, not every mutation will be significant.

Thanks for trying to help me. Nice photos you take, you are a talented photographer. I have 1000 books on bioinformatics and years of software engineering and computations experience. I need  a rational way and the best software for mutation analysis. I don`t like microbes at all.

biostars.org are a community with a focus on the software/programatic side of biology. Perhaps you could reframe your question there?


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Typical in-vivo protein concentration
I am studying RNA-binding proteins involved in RNA granules. I am searching the literature for an order of magnitude of the absolute global concentration in the cytoplasm. Although I am aware this quantity can vary greatly from proteins to proteins, I would be happy if I find some papers having estimated it for some given proteins.

I guess you would want to exclude cytoskeletal proteins

Hard to find data for eukaryotes. For E coli some of these things have been measured and rough numbers have been made. I recommend the BioNumbers database as a great starting place: http://bionumbers.hms.harvard.edu/default.aspx . In particular, look up the (famous) table linked to by Bio Number ID 102990. It lists that at exponential phase E coli has about $2.35\times10^6$ protein molecules of 1850 types, so about 1270 copies of each protein. E coli is about 1 $\mu$m$^3$, so that's a concentration of about 20$\mu$M per protein if my math is right. But that's bacteria which are very different.


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Plant dependence on CO₂ levels
I was wondering which kind of plants would survive longest without CO2 : plants with fatty, thick leaves or plants with thinner, less fatty leaves?
And can we conclude that the plant species that are more dependent on CO2 levels, would benefit from the greenhouse effect?

Plants do not need CO2 for survival. They need it just for photosynthesis; if you supply them with alternate carbon source such as glucose then they would survive (See here for non-CO2 Carbon-source utilization). There are non-photosynthetic plants which are totally dependent on carbon sources other than CO2; some are carnivorous like venus fly-trap.
I am not sure what you intend when you correlate leaf thickness to CO2-dependence. Leaf morphology can affect photosynthesis rates but afaik there is no relationship between leaf morphology and CO2-dependence.

can we conclude that the plant species that are more dependent on
  CO2 levels, would benefit from the greenhouse effect

Greenhouse effect is not equivalent to increase in CO2; increased CO2 levels can cause greenhouse effect which is a physical phenomenon of entrapment of IR radiation.
CO2 is fixed by an enzyme called Rubisco; like most enzyme catalyzed reactions this will reach a saturation limit i.e. addition of more CO2 will not increase the rate of photosynthesis. However the rate of photosynthesis is limited at the Rubisco step because of low levels of CO2 (See here) and it can be expected that most photosynthetic plants will be benefited by increase in CO2. However, not all plants would be resistant to increased temperatures and moreover the rate of enzyme catalysis would also change with temperature. So it is not that easy to predict.


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Which sex of trees bears fruit?
Which sex of trees bears fruit? The males or females? And what specifically cause that one to bear fruit. Is it the same as it is with blossoms in trees?

The distinction between male and female is not that clear in plants, at least at the level of individuals. Actually the details may be rather complicated (see [1]), but in general we can distinguish between plants that have:

male and female individuals (dioecy)
male and female flowers on the same individual (monoecy)
flowers that have both male and female structures (bisexuality)

In the first case, only female individuals produce flowers that -- when fertilized by the pollen from the flowers of a male individual -- develop into a fruit. Examples are Hazelnut, common nettle and a few other species [2]. However, dioecy is rather rare among extant flowering plants [3].
Monoecious plant species are somewhat different. A good example is maize. The male flowers of a maize plant are located in the tassels at the apex of the stem, wheres the female flowers are are in the leaf axils. Note that each corn developed from a single flower and that the cob is actually the infructescense.
Then there are bisexual plants. In these, every flower has the potential to be fertilized and develop into a fruit, which is why they are also called perfect flowers. Plants have developed several strategies to prevent self-fertilization, e.g. the temporally delayed expression of female/male structures within the same flower.
Resources:
[3]: Bawa, K. S. (1980). Evolution of dioecy in flowering plants. Annual review of ecology and systematics, 15-39.


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Why do dog's eyes glow green on a photo?
Taking my current profile picture as a prominent example:

This photo has been taken with flash. As I gather, this is the same effect that makes a human's eyes glow red on photos, namely the reflection of the flash at the choroid and then passing back through the retina.
The retina is full of bloodvessels and the blood inside them gives the reflected light it's reddish color.
If it's the same effect, why is the color different?

Come on that's photoshopped

Nope. Not at all

Then it's a star wars dog or you got some weird camera thing going on. Try  post another with a person looking at the camera and that will rule out the camera thing. User 137 is right below but I've never seen something like this.

Dogs, cats, and many other mammals have a Tapetum lucidum which reflects light back through the retina to help with night vision. Humans don't have this layer. The tapetum is probably reflecting green light that would have normally been absorbed.

The rod cells - cells used for night vision - are the most sensitive in the green region of spectrum. It does make sense for tapetum lucidum to reflect these preferentially

It's also interesting that different dogs can reflect different colors.  My Border Collie mix reflects greenish, but my (probably) Plott Hound reflects blue.  (This is with an LED headlamp at night, not camera flash.)

@jamesqf Sometimes 1 animal can do two colors at once.


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Are there ways to speed up the growth of plants?
I'm interested in what humans can do to speed up the rate of growth in a plant. I'm interested in both the context of home gardening and large-scale, institution-backed projects.
Obviously, optimal growing conditions are one factor that can be modified. I imagine that there are also genetic mutations that can be done (possibly even at home!). Botany is not my field so what I'm looking for here is are the basics and some good resources for further reading.

Yes.

The research team, led by the Durham Centre for Crop Improvement Technology, and including experts at the University of Nottingham, Rothamsted Research and the University of Warwick, have discovered that plants have the natural ability to regulate their growth independently of Gibberellin, particularly during times of environmental stress.
They found that plants produce a modifier protein, called SUMO that interacts with the growth repressing proteins.
The researchers believe that by modifying the interaction between the modifier protein and the repressor proteins they can remove the brakes from plant growth, leading to higher yields, even when plants are experiencing stress.[1]

Bacterization is the process by which bacteria applied to the soil and plant parts. Under certain conditions yields were able to increase 10 to 13 percent. However, not all results were able to be reproduced so this is something you can look into more as well. [2]
Another option is to artificial increase the amount of CO$_2$:

Over the years there have been numerous laboratory experiments which conclude that increases levels of CO2 result in increased plant growth no matter how that plant growth is quantified. Sylvan Wittwer in Food, Climate and Carbon Dioxide tabulates the results. [3]

Lastly, you can look into genetically modified organisms (GMOs) which is a hotly debated topic.
With a Google search, you will see that that there are numerous articles on methods to increase plant growth, to numerous for me to give a blurb about them all. Therefore, I linked a few that seems promising as well as interesting.