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Aerobic vs anaerobic respiration comparison
The following graphs compare glucose decomposition in yeasts (in anaerobic vs aerobic conditions respectively)
My question is, why doesn't the first one look like a straight line as the second one does? Don't they actually follow similar processes?

Sorry, my German's (i think) a bit lacking.  What are the axis?  Also, they are similar but not identical processes.

y: Glucose concentration, x: time

@ZaferCesur you might want to expand on why you think this question has not yet been answered by the existing answer (clearly you think so because it has a bounty) and is this also from some kind of homework assignment etc?

I think the reason as to why glucose concentration is faster in the aerobic case than the anaerobic one, is perfectly explained by Chris. To summarize:-

The energy requirement of the organism in both the condition remains more or less
  constant. Since aerobic respiration generates more energy per glucose,(38ATP)
  it takes more time for the same concentration of the glucose to be
  depleted, than it takes in the case of anaerobic respiration where
  less energy is released.(2ATP)

The non-linearity in case of anaerobic respiration can probably be explained thus:-
In the aerobic case, glucose is oxidised to water and carbon dioxide, both of which do not influence the respiratory process. The first step of glycolysis, the phosphorylation of glucose has a very negative free energy change, i.e. is practically irreversible. Therefore a dip in glucose concentration will not affect the rate of energy release and therefore the rate of energy released will stay constant resulting in a linear graph. But in the anaerobic case, the final product is un-metabolised ethyl alcohol. The conversion of pyruvic acid formed as a result of glycolysis to ethyl alcohol is not so strongly irreversible(smaller free energy change), and at high product concentrations, becomes considerably reversible. This means that the ethyl alcohol produced will affect the rate of glucose metabolism, and will retard it by negative feedback (Le chatelier's principle). This will lower the speed of glucose utilisation at low concentrations of glucose, i.e. high concentrations of ethyl alcohol. This reduce the value of slope at lower concentrations of glucose in the graph, and hence produces the non-linearity.

Your graphs show two things: Starting at the same concentration (150mM/l) the metabolization of glucose is not linear under anaerobic conditions. The other observation is that under aerobic conditions the glucose is metabolized much slower.
This is because under anaerobic conditions on 2 molecules of ATP are generated from the metabolization of one molecule of glucose (for all the details on the biochemical pathways look into the "Ethanol Fermentation" article in the Wikipedia) while for the complete respiration of one molecule of glucose under aerobic condition generates 32 molecules of ATP (2 from the Glycolysis 2 from the [Citric acid cycle], aswell as 26-28 in Oxidative Phosphorylation (Electron Transport Chain and Chemiosmosis) 3).
So to generate enough energy the yeast has to metabolize the glucose much faster when the conditions are anaerobic which explain the form of the graph, while under aerobic conditions the graph stays linear. The metabolization starts in both cases with the glycolysis, but afterwards is different. Aerobic conditions produce water and CO₂, while the anaerobic conditions produce ethanol and CO₂.

I think in anaerobic conditions they are fermenting, what is different from respiration. Respiration produces much more ATP from single molecule of glucose, because the biochemical path is different, involves more steps, each one producing a little energy.
Also note that, on the graph on the right, the X-axis goes up to 6. Which means glucose is being processed much faster on the left. Maybe that's because mitochondria are numerous and can process the sugar faster?
As for the curve, I can only think that fermentation is so slow that the ATP produced is being consumed by the cell in the same rate. With respiration, the ATP is produced in big amounts and thus begins to accumulate, what regulates the process to slow down. But I may be missing something important here.


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What is the depression between bridge of nose and brow called?
In a human being, what is the depression often found between the bridge of the nose and the brow called?

Nasion [New Latin nāsion : nas(o)- + Greek -ion, diminutive suff.] is the region below glabella , also known as the bridge of the nose.

The nasion is the midline bony depression between eyes where the frontal and two nasal bones meet, just below the glabella.It is one of the skull landmarks, craniometric points for radiological or anthropological skull measurement.

Source:https://radiopaedia.org/articles/nasion

source: Stack Exchange

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

sort: votes


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Why is 450 nm monochromatic light perceived as blue or violet depending on its intensity?
Trying to do some color matching I purchased a 450 nm laser. I expected monochromatic light of this laser to have similar properties to those of all others I've already played with — 808, 640, 520, 405 nm — in that they all cause an unambiguous color sensation.
But when I shined it onto my wall (having removed the lens), I was surprised to see something unusual. In the center, where the intensity is high, it looks as "very blue" — much like those 465 nm blue indicator LEDs we can see everywhere today, only more saturated. But on the sides, where the intensity falls off, the color looks like violet! When I shine this laser on a ceiling obscured by a wall, I see its reflected light as violet. When I move the spot so that the reflected light becomes more intense, I begin to see it as blue again in the intense areas, and still violet in dimmer ones.
I've checked with a spectrometer, and there doesn't appear to be any fluorescence in the light spot to confuse me.
Interestingly, if I increase amount of ambient lighting (white LED lamps + CCFL ones), sensation of blue once again transforms to violet. Also, the "very blue" intense spot looks violet in bright sunlight, although I can make it blue again by focusing into a smaller spot to make it brighter. In a fully dark (apart from the laser) room I still do notice the violet areas on the sides of the spot.
405 nm light also seems a bit silvery-whitish when its intensity is high, unlike at low intensity. Maybe it's the same phenomenon, which I simply didn't notice before because the tint is not that blue in this case.
In both cases of 450 nm and 405 nm the additional color on high intensities is still "shiny" due to the speckles specific to high monochromaticity, so this indeed doesn't look like the result of fluorescence of the objects I shine the light to.
I've asked several people whether they see it the same, and they answered affirmative.
I suppose it's not related to color balance, because I only changed the intensity of ambient light, not the tint to observe the changes in color. Especially it shouldn't be due to color balance since I can simultaneously see different colors in the areas with different intensities.
Interestingly, while I thought the "very blue" color to be the main color of 450 nm, CIE 1931 XYZ value for it, converted to sRGB, appears to be (if we desaturate and normalize to fit in sRGB range) (0.43,0,1), which is purple, not blue.
So, what is going on here? Is it a well-known phenomenon? Could it be due to some fluorescence of the retina itself rather than the objects lit by the laser?

This is a general feature of human perception of blue-white mixtures. It's known as Abney effect. It's not limited to highly monochromatic blue colors (not even to blue colors). We can observe this blue-related phenomenon even with longer wavelength light than 450 nm – e.g. sRGB blue, whose dominant wavelength is about 464 nm. Here's what most people would undoubtedly call blue – in HTML notation #0000ff:

And here's a mixture of 60%† white with 40% blue (in HTML notation #cacaff):

To me, if I haven't stared at shades of truly violet a few moments ago, this mixture seems to have a considerable amount of violet — more than I'd expect looking at the primary blue. Naturally, shorter wavelength light should give even more violet perception, until it becomes violet even in its pure form.

† Percentage is given in linear scale, actual color presented is gamma-corrected to be displayed on sRGB monitors.

Your examples are useless: the first square is not monochromatic if produced by a computer display. It is not laser light.

@Anixx it's not required to be monochromatic. It's good enough to be indistinguishable from monochromatic+{a bit of white}. This perceptual feature is not limited to monochromatic light — I just don't have access to 450 nmD LEDs, but do have 450 nm lasers.

This merely corroborates the experience but is in no way a bioengineering or biology explanation.
If you stare, at arm's length, at any discrete colour 5mm LED of high brightness, it's colour will appear to shift after a few minutes. This is not the (scotopic/photic) night vision effects from Cones to Rods towards blueshift but rather the cone's protective response to the high-density stationary colour indicators and makes that spot less-sensitive.
Also if one often stares at the bright ceiling or street lights for several minutes, then look away, they will see a remanent ghost image with that previously dominant spectrum now suppressed so it will appear in the inverse pastel colour.
It appears as the spectrum has been diminished in that spot,  because it has, by a reduced sensitivity of the cones in the eye for detecting that spot of light. The recovery time is about the same time or a bit more as it takes to react.  The human retina contains about 120 million rod cells and 6 million cones .
This may be safe as long as the light is not held too close to the eye and certainly not looking into a direct laser beam, rather a diffused image.
Even some 5mm LEDs at 20mA can be so intense as to be painful quickly at arm's length with >20,000 millicandella luminous intensity measure by std methods. But it only needs to be as bright as an auditorium ceiling light intensity for this example of color-shift to occur.
 Added
Each depends on the spectrum of dominant and sub dominant peaks in the spectrum that results in the apparent shift in appearance. The 450nmD must  have this sub dominant spectrum in an otherwise monochromatic spectrum for this affect to occur.  Because our eyes are logarithmic yet spectral densities of monochromatic light sources are displayed on linear scale, it is often not reported.  I.e. there must be some red 6xx nmD spectrum for this blue to appear to become purple when our eyes attenuate the blue after a period of intense viewing for several minutes.

I don't think this mechanism is the same as that observed in the OP: the one you're describing relies on an afterimage to distort colors. It'll make a "wrong-color" point or line in the visual field. But the OP is about the light which is not intense enough to make a prominent afterimage. It's easy to look away from the blue part of the 450 nm light spot and see violet in the same part of the visual field (i.e. same part of the retina), without any ghost color spots. So I think that color shift mechanism is different.

I reported both examples which are similar electrochemical responses yet different.  Staring at a  right Yellow LED with some orange red spectrum will shift towards that spectrum because the 592nmD wavelength is attenuated. Or the 420 nmD wavelength is attenuated and the lower level broad spectrum  6xx nmD reddish spectrum becomes purple in the net mix. Each depends on the spectrum of dominant and sub dominant peaks in the spectrum that results in the apparent shift in appearance.

nmD is the dominant wavelength of CIE eye corrected nmP peak wavelength of emitted light. This due to our sensoral bandpass filter slopes spectral response of our eyes is centred around 525nm green and the slope shifts the peak towards green and our brain equalizes these RGB sensors to become a flat white response.

Well, the OP is about a laser, not a LED. The laser I'm testing has FWHM about 2 nm (or less, I'm limited by resolution of my spectrometer). There can't be much difference between nmD and nmP there.

There is ALWAYS a difference nmD vs nmP if it is not green 525nm . Any expert EE in filter analysis understands the effect of spectral peak shift due to bandpass filters. (in this case our eyes)  Also the same effect occurs in yellow (AlInGaAs) LEDs so it is a valid analogy.

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


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Are MacAdam ellipses theoretically predictable?
MacAdam ellipses were found as a fit to experimental results on color matching by human observers. Multiple color spaces attempting to make euclidean distances more perceptually uniform, like CIELAB and CIELUV, are based on these experimental data too.
But what about theoretical side of the color distance question? Is current color vision theory able to predict sizes and orientations of these ellipses? If not, what are the obstacles?

So, are you basically asking if there is a biological explanation (supported by a mathematical model) for the size and position of these ellipses and reason for their occurrence? There is a formula for the ellipses. See here (section 3.4).

@WYSIWYG yes, I'm interested in a biological explanation and calculation — something like, starting from biochemistry (for phototransduction), through neuroscience (or whatever branch of biology studies this), to a prediction of whether a pair of spectral distributions of irradiance of the cones would be distinguishable. The formulas given in your link are from the empirically-based color spaces like CIELAB, which is not what I'm looking for.

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


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Looking for raw cell videos from a light microscope
First off, I'm not looking for online lectures.
I am trying to find creative commons licensed videos of live cells moving around without annotation or anything extra. I would prefer a few minutes of video of tumorous somatic cultures of eukaryotes in vitro and at a few different magnifications but it doesn't really matter. I don't have a microscope or I'd just get some pond water and look at multicellular organisms. The license must be creative commons or public domain, the author must be citable, and the subject organism should be known.
Any ideas where to find such video? Thanks!

The website you want is The Cell: An Image Library. They also have movies. A quick search of 'Homo sapiens tumor' revealed several Creative Commons videos of tumor cells moving around in vitro with attribution and no annotation or anything else. Sometimes the site can be a bit buggy, but it's a pretty awesome resource when it works.

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


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Autoimmunity and central tolerance
Where in the body are self antigens important? In terms of central tolerance and autoimmunity, but also in terms of T cell activation?

Could you clarify a bit? What do you mean by important? Most problematic? Most relevant? I assume the body you refer to is the human one?

This was a question in a PhD defense so I can only add my own interpretation. It's in the mouse and by important I mean anything really, relevant for proper development, where defects may lead to autoimmunity, and/or poor activation...I'm not entirely sure.

There can be many responses. They are important for alloimmunity (so by transfusion, transplantation, etc...), for recognizing pathogens, cancer, virus, etc... By T cell activation, the regulator T cells recognize these antigens as self, and prevent the autoimmune reaction.
I guess they were thinking on MHC1 and MHC2. MHC1 shows the inside of the cells, so e.g. by viral infection or cancer non-self oligopeptides (from degraded proteins) bind to MHC1. These non-self antigens are recognized by CD8+ T cells, which destroy the affected cells. MHC2 is used by APCs to present possible pathogens to CD4+ T cells in a similar way.

Self-antigens are not recognized by the body. This is due to self-antigens being presented to the immune system of the body during the embryological development. Any immune cell which recognize the pattern are destroyed during the intrauterine period, preventing the emergence of Auto-immunity in the Life-time.
Self-antigens become important in the following situations:

There are self-antigens, called cryptic antigen, which are not presented to the immune system during embryologic development. These antigens generally are not present on the cell surface or they are present behind a barrier which is usually not penetrated by the immune cells. Eg.: The sperm antigens are not usually exposed to immune system as the sperms are behind the blood-testis barrier. Other such barriers are blood brain barrier, blood retina barrier, etc...

This is important because if for some reason (infection, trauma, etc...) such antigens get into the general circulation they will cause an immune reaction leading to autoimmunity

Self antigens play a role in graft rejection and transfusion reactions. This is mediated specially by the T-cells. This is the reason why transplant patients receive life-long immune supressants and cross-match is done before transfusion
Self-antigen non-recognition also means non-self antigen recognition. This is the basis of cells infected with viruses or tumor cells getting destroyed. As the new protein peptides (viral or mutated regular proteins) presented by the MHC 1 are not recognised as self, such cells are destroyed protecting the body
The corollary of 3 is that any pathogen which resembles the self-antigen are tolerated and active immunity does not come into play i.e. the epitopes that are recognized as self do not cause any immune response
Some pathogens have antigens that closely resemble human antigens. When T-cells mount response against such antigens, a specific sub-clone of T-cell or B-cell (which are activated by the T-cell) may gain the ability to act against the body cells (due to mutations in the hotspots of the anti-topes) that have antigEns resembling the pathogens. This is called molecular mimicry. A well established disease that is due to this mechanism is the Rheumatic Heart Disease. Post-streptococcal Glomerulonephritis is also another example.

That is the old model of the immune system. There are many other models, which are closer to the reality. E.g. many self recognizing cells become regulating cells instead of dying, and a lot of non self cells (microbes) can be tolerated by the immune system until they don't cause cell death and other messy things... By auto immunity, not just the molecular mimicry is the problem, e.g. a single T cell can have different receptors, so one of the receptors can be self recognizing, while the others can recognize a pathogen, and so on... Immunology is very complicated...

I see, I think I have to read on the newer models then. Can you suggest a good source?

http://scholar.google.hu/ :-) I have the same problem, I read mostly reviews and scientific articles, probably dissertations if have more time. I don't know of a book which is up to date. E.g. none of the ones I checked, mention gasotransmitters, which is a relatively new topic in immunology. Wikipedia is often incomplete, or sometimes even completely wrong. I'll try to make an own wiki, but I have too many tasks: developing programming framework, learning stock exchange indicators, learning data mining, learning immunology, making training plans, etc... 24h in a day is simply not enough. :S

Please let me know if you've found a book worth to read!

http://en.wikipedia.org/wiki/Danger_model Be aware that wikipedia is not a reliable scientific resource, so if you want to learn this in depth, you have to find scientific articles and reviews in the topic.

I think there are no set models (completely proven models). I can't read Hungarian though! Thanks for reference. Will post a book if I find one

Ohh sorry :D http://scholar.google.com (was redirected automatically by google)


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What is a phospho-protein binding domain?
Is this just a domain that binds proteins that have been phosphorylated? And it mediates signalling between an activated/phosphorylated protein? How is this significant with BRCA1?

Do you have some reference that you're reading, or some more context?

A phospho-protein binding domain binds phosphorylated proteins. For which purpose it does this, depends on the protein. To tell more about it, more background would be nice.

This is a very large topic but I will try to partially provide an answer. Now your question has three parts as far as I understand it.

Do phospho-protein binding domains only bind to phosphorylated proteins i.e. is that their sole (observed) function.
What roles do phospho-protein binding domains mediate.
Function of BRCA1 phosphorylation/phospho-protein binding

Just to get some basics out of the way, there are three amino-acid residues in a protein that can become post-translationally modified by phosphorylation, including serine, threonine and tyrosine. Now the purpose of protein phosphorylation ranges from activation/deactivation signals to binding and changing cellular localisation i.e. recruiting a protein to different part of a cell. Now tyrosine phosphorylation, which I know by far the most about is capable of all the above. So if you think about a receptor tyrosine kinase (RTK) such as epidermal growth factor receptor (EGFR), once a ligand such as EGF binds to it, it becomes tyrosine phosphorylated (activated) through its intrinsic tyrosine kinase activity. Once tyrosine phosphorylated, many proteins are capable of binding to tyrosine-phosphorylated RTKs such as Grb2 to induce a signal downstream of RTKs. So as you can see, phosphorylation of RTK affected cellular localisation of GRB2. Excellent Ras signalling review by Karnoub & Weinberg, 2008 Nature reviews (Fig 5). Grb2 binds to phospho-RTKs through a specific domain called Src-homology 2 (SH2) domain, which provides a platform for other proteins such as Son of sevenless (SOS) which is a GEF to bind to it and induce RTK signalling through Ras. So in the above case the role of phospho-protein binding domain (SH2) is to change cellular localisation of multiple proteins and mediate signalling.
Now I'm no expert in BRCA1 but just had a quick look and it seems serine phosphorylation of BRCA1 may be responsible for its recruitment to the DNA site of damage and if serine residues in BRCA1 are mutated, the protein will no longer get phosphorylated, which may effect its recruitment to the DNA sites of damage, which may affect its DNA damage response function (Clark et al 2012 Comput Struct Biotechnol J). Now BRCA has a phospho-protein binding domain called BRCT, and that is also thought to mediate DNA binding and binds to phosphorylated and non-phosphorylated proteins. So BRCA1 phosphorylation and phospho-protein binding is though to be important in its function (Clark et al 2012 Comput Struct Biotechnol J). So to answer your question in short, phospho-protein binding domains such as BRCT do not necessarily bind to their target proteins through phosphorylation.
Hope this helps.


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variance in zygotic gene expression across species
I found this review on the Maternal-to-Zygotic transition (MZT), describing how developmental control switches from maternally deposited RNAs to zygotic expression. I was struck by figure 1, and the apparent difference between viviparous and oviparous life histories.
My maybe naive question is, Could the sharp increase of zygotic expression reflect conflict between the maternal and zygotic genomes?

MZT review

In this figure only the Mouse is viviparous.  I don't have a clear sense of what you mean by "competition." In sexually reproducing species, like these five, fully one half of the zygotic genome is identical to the maternal genome.  I suggest that you try thinking about like this: the main purpose of oogenesis is to create a cell that will provide everything that the zygote needs following fertilization.  The eggs are getting loaded up with proteins and mRNA the zygote will use until its own genes get transcribed. In mice and worms it only takes 1-3 cell divisions for the embryo to take over.

What seems so striking to me is that the length of a single cell cycle is so drastically long in the viviparous species. That tells us that if your mom lays eggs then those first cell cycles are incredibly fast, which really means that oogenesis is stuffing those eggs full of DNA polymerase and dNTP's.


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About excessive cellular growth
When there is 'excessive' cell growth 'ordered' by the human body in some specific part of the body that is not part of the usual repairing mechanisms, does this cause extra telomere 'shortening' or damage even though a lot of cell growth and repair is 'required'. If a lot of cell growth is 'activated' with problematic telomeres does this cause telomerase to be formed which then might shut down the apoptosis mechanisms and keep the cell 'going' indefinately. Note; I read some acid reflux problem causes parts of the throat to scar or be damaged causing excessive cellular repairs on those parts of the throat where tumors have later developed. When someone gets sunburned on the shoulders say, and this damages the skin there, then does every future time the persons shoulders get in the sun ,do those same areas get further damage causing excessive growth and repair of skin cells on the shoulder. With a lot of excessive repair tumors might develop. SO could excessive cell growth (that might be caused by many different factors ) help to cause cancer??

Long story short: Absolutely.
Short story long:
While your intuition that growing a lot of cells can increase the risk of damage that might cause cancer is spot on, your specifics are a little off. It's not the telomeres themselves that are the problem, but broad spectrum DNA damage and transcriptional changes. The condition of the telomeres doesn't directly affect the likelihood of a cell growth becoming more cancer-like. A cell with perfect telomeres fresh from a telomerase-expressing stem cell and cell with shortened telomeres have an equal chance of becoming cancerous. Cell populations with longer telomeres have 'more time' or more chances to develop mutations and cell expression damage, however. You're more likely to get in a car crash if you go to the store across town  than the neighborhood convenience store, even though it's not intrinsically more dangerous per mile driven.
The sunburn example can be a little misleading. It's not cell regrowth that's the key carcinogenic factor, but instead the direct DNA damage UV radiation can cause. In a particularly bad sunburn your skin cells may be killed or commit suicide(apoptosis) because of the DNA damage they've sustained. If the cells are damaged but do not die, they're likely to recover. Over time and repeated sun exposure, the skin cells that are most resistant to orders from the body to stop growing or die stick around and may grow and divide. Freckles are when this happens to a population of skin cells that ignore orders about how much brown pigment to be, but still listen to the orders that instruct them on how to be skin. When they stop listening to the skin orders, they officially become precancerous.
The acid reflux example is excellent. There are populations of stem cells throughout the adult body that produce skin cells and hair follicles and blood cells and all the other kinds of cells that are more or less expendable. Generally speaking these stem cells don't have do very much work replenishing esophagus cells, so when they are taxed by something killing off the esophagus lining regularly, they can 'break down' and lose control of their own replication.
It seems like you're both pretty interested in cellular mechanisms of cancer and a little shaky on current theories of cancer formation(there are a few), so if there's a section of this answer that needs to be more detailed or followup questions please let me know.

Are there ways to retard or slow down excessive cellular growth? Can telomere damage cause the apoptosis mechanisms to malfunction? I'm fascinated with Biology but am shaky on a lot of theories..

Depends on the kind of growth. In the case of acid reflux, no. You need to replenish that lining once it is damaged. Telomeres are rarely 'damaged', as they're very long highly repetitive sequences. Think of them as 'margins'. When the margin is missing, you start to lose words off the page, and indeed telomere shortening is used as a trigger for apoptosis. If damaged or short telomeres interfered with apoptosis, very little apoptosis would every happen.


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About sharks and how they find fish
Other than olfactory senses do sharks use some kind of sense that uses electromagnetic waves? Is this similar to an electric eel? I saw a book with the cover statement 'Sharks never get cancer'. IS this possible or just 'quackery' ? Could being constantly 'bathed' in some kind of electromagnetic field cause pre-cancer cells ( that are already unstable) to be 'disrupted'?

Sharks do get cancer.. See also, "Shark cartilage, cancer, and the growing threat of pseudoscience". Contrast, this nonsense.

Oops, the link was wrong: Shark cartilage, cancer, and the growing threat of pseudoscience

I didn't say it was 'sense or nonsense'. Notice I asked if this was just quackery? But is cancer in sharks rare? What about electric eels, do they get cancer; is it rare? I read on wikipedia there is a biological paradox related to whales. They obviously have alot more cells than humans yet they don't get cancer as much as a random process would 'cause' if cancer causes are 'random'. Is this true? Why is cancer in the Heart rare?

Sorry, I didn't mean to imply that you were endorsing that view; just making an observation about the available literature on the topic.

Thank you for the response but what about my other questions?

I don't know the answers, sorry. I think that's probably best left for the answer space rather than comments anyway.

Sharks sense their prey with the normal senses, they see, hear and smell them.
They have a remarkable sensitive sense of smelling, which enables them to sense highly diluted traces of prey. They can also use their smelling to determine the direction where a certain smell comes from. This is achieved by the timing in which the senses arrive in different parts of the sharks nose. See references 1 and 2 for more details.
While sharks have eyes which are similar to that of vertebrates, they have an additional reflective tissue called "tapetum lucidum" behind their retina, which reflects the light back and therefore raises the sensitivity of the eye. It seems that a lot of shark species are either colorblind (because they only have rod cells but no cones) or they had only one kind of cone cells which allows them only to see one color. For sharks it is obviously more important to detect objects than to see colors. See references 3 and 4 for more details.
The sense of hearing of sharks is also highly sensitive and is able to detect sounds from far away. See also references 5 and 6 for more details.
The most interesting sense of sharks is their electrosensory organ. This is also called Ampullae of Lorenzini which is a number of sensory cells along the head and which are able to detect the weak electric fields that exist around living animals. This sense only works on a very short distance. See references 7 and 8 for more details.
Finally sharks have the so-called lateral lines (which are present in most fish), which is an organ which detects movements and vibrations in the water around the shark. See the Wikipedia page for more information.
And for the sake of completeness (already quite nicely answered by @Susan in the comments), sharks do get cancer. All cures which are made from shark and claim to be able to treat cancer are pseudoscientific nonsense. This also endangers many shark species as they get radically overfished. See references 9 and 10 for more details.

References:

Smell and Taste
The Function of Bilateral Odor Arrival Time Differences in Olfactory
Orientation of Sharks
Microspectrophotometric evidence for cone monochromacy in sharks.
Vision and a Carpet of Light
Hearing and Vibration Detection
Functional anatomy of the auditory system in sharks and rays
The Shark's Electric Sense
Electroreception
Mythbusting 101: Sharks will cure cancer
Shark cartilage, cancer and the growing threat of pseudoscience.

Excellent information. Is cancer in sharks rare? If an animal has some type of 'function' like the Ampullae of Lorenzini that 'uses' weak electric fields could this de-stabilize pre-cancerous cells that are already unstable to some extent.

As far as I am aware, cells are not destabilized by weak electromagnetic fields. This is different for high energy, but then we are talking about denaturating proteins.

Are they de-stabilized by microwaves or M.A.S.E.R.s?


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Correlation between threat and odour, taste
Is there any sort of correlation between threat and taste/smell?
Are we evolved such that things which are harmful to life taste and /or smell bad and things(food) which are useful to us taste, smell good?
How far this conjecture correct?

interesting question, if that's true the additives in food messed everything up

The compounds that smell bad to us are often the same ones produced by the anaerobic metabolism of bacteria, such as hydrogen sulfides or butyric acid. These types of compounds are the ones that make excrement and rotting food smell bad, and if something is giving is giving off a lot of them it's a pretty good signal to not put it in your mouth. Vomit also has quite a lot of butyric acid in it, so we may be particularly sensitive to it.
Plants produce toxic compounds to stop herbivory, many of them taste bitter. Alkaloids are often toxic and uniformly bitter, terpenoids are another example.
There's nothing obviously different from a chemical perspective in chemicals that smell bad. Butyric acid is just a 4 carbon chain with a couple of oxygens on the end and reeks, while the compound propanediol (which is 4 carbons with an oxygen on each end) is used in deodorants. If a compound has a strong smell or taste to us, it is because that compound has been important to us during our evolution. That doesn't mean it's a perfect indicator; cheeses can stink and be totally edible, but that's because the compounds in that cheese usually are a sign of something dangerous.


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Is pure (100% H20, (near to no) solutes) water toxic to living organisms?

Possible Duplicate:
Death because of distilled water consumption

I know about the effects and myths about drinking distilled and/or deionized water. I'm not asking about such substances.
I wonder if a semi-immediate effect of drinking, say 1L pure 100% H2O is deadly or harmful.
My intuition says yes: either the reverse osmosis effect also present in distilled water is amplified so much that critical systems shut down due to extremely low concentrations in the organs/cells/... or the reverse happens, where the water is absorbed into cells making them burst, leading to among other things (massive) internal bleeding.
I'm particularly interested in scientific studies (if any) that were done (link to publication would be very welcome, my Web of Knowledge search-fu doesn't seem to work for this subject).

I don't know much about this subject but here are a few links you might find helpful.
http://purchon.com/wordpress/biology/?page_id=173
http://www.sciforums.com/showthread.php?s=d463b981152a76c85345e9164df85b9e&t=55440&page=2

@Kevin: Close, but not quite. The commercially available distilled water is not pure enough for what I mean. Unfortunately, I am unable to find any decent "purity classification" other than this little table that forgets to mention any solute concentrations whatsoever.

The distilled water you find in a chemistry lab is pretty much as pure as it gets... For a classification see the Wikipedia purified water article. Even if you were to ask about perfectly pure water with no solutes whatsoever I don't see how the answer would be different from that of the other question.


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Common site for atherosclerosis
My book( textbook of anatomy abdomen and lower limb 2nd edition - by vishram Singh pg.no:286) says:

Acute arterial occlusion: It is mostly caused by embolism or thrombosis. It usually occurs in the femoral artery where it gives off the profunda femoris artery.

So my question what makes this site more susceptible for atherosclerosis?
In general what are factors that make some sites more susceptible to atherosclerosis?

Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. "Homework" is interpreted to mean any academic or other assignment, test preparation, or task given in relation to a class, educational setting, or self-learning. There is plenty of information on atherosclerosis available easily online, starting with Wikipedia.

I can give you some facts about atherosclerosis, but I should warn you that--judging by your question--you may be making a false equivalence between atherosclerosis thrombus/embolism. The two are often very interrelated, but there are times when an atherosclerotic plaque is significant without causing an embolism (e.g. stable angina) and there are times when a thromboembolism forms without the presence of a significant atherosclerotic plaque (e.g. atrial fibrillation). The likelihood of thrombus formation is dictated by Virchow's Triad: Endothelial Dysfunction, Blood stasis/turbulence, inherent coagulability of the blood (factor problems mostly).
Now to get to your main question: atherosclerosis. The current theory is called The Response to Injury Theory. The general idea is that whenever there is damage to endothelial cells they will release inflammatory cytokines, and these will lead to a thickening of the wall. There are a lot of different things that can lead to this endothelial damage. There chemical factors: exogenous sources like cigarette smoke and endogenous sources like elevated levels of homocysteine. However the two most important factors that lead to endothelial damage are high cholesterol and hemodynamic factors (Robbins, 494). That second point hints at why atherosclerotic plaques are more common at branch points. As blood is going past a branch point it becomes more turbulent which makes it more likely to cause damage. This is especially true when blood is flowing more forcefully, as in the case of hypertension (another risk factor for the development of atherosclerotic plaques).
There are many other factors that play into the development of atherosclerotic plaques. For example, the abdominal aorta distal to the renal arteries has no vasa vasorum, which makes it more susceptible plaque formation(5). This is just a small sample though. There are a plethora of factors that go into plaque formation: literally textbooks full of information about he disease. If you're really interested in the topic and want to dive in, I'd suggest taking a look at Inflammatory Atherosclerosis.

Evolution of arterial wall changes in the response to injury hypothesis. 1, Normal. 2, Endothelial injury with monocyte and platelet adhesion. 3, Monocyte and smooth muscle cell migration into the intima, with macrophage activation. 4, Macrophage and smooth muscle cell uptake of modified lipids, with further activation and recruitment of T cells. 5, Intimal smooth muscle cell proliferation with extracellular matrix production, forming a well-developed plaque. (Kumar 495)
Kumar, Vinay, Abul Abbas, Jon Aster. Robbins & Cotran Pathologic Basis of Disease,  9th Edition. Saunders, 062414. VitalBook file.


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Secondary/ Acquired lactose intolerance

Acquired lactose intolerance may occur due to a sudden and high intake of milk-based diets. Lactase is an inducible enzyme.

So if lactase is an inducible enzyme then why increase intake of lactose is causing negative effect? Why more lactase isn't produced in more lactose intake conditions?

Searching for the quote you included led me to the original source.
I wouldn't spend too much time worrying about this particular source, and look at some other sources for more information on acquired lactose intolerance. I think there may be some translation/language issues with this section in this particular source. I believe what the author is trying to convey is not that the intolerance is coming from the increased intake, but that the symptoms of intolerance are coming from a sudden increase in lactose intake following a period of low/no lactose intake, where "sudden" essentially means "faster than lactase induction can occur."
That said, I think this is really more an issue of poor wording in a textbook. The whole section is a bit strangely worded, particularly the part on "flatulence" which this author describes as "characterized by increased intestinal motility, cramps, and irritation" - while these issues may certainly accompany flatulence, this definition of these symptoms characterizing flatulence is not correct, as one can certainly have flatulence with normal intestinal function.

You are right about the source. Iam currently reading that book. Could you please suggest a better book?

For biochemistry in general, or for lactose intolerance in particular? For the former, I just looked quickly and found a syllabus from my current institution using this book for an upper-level undergraduate/low-level graduate biochem course. Full disclosure: the textbook authors appear to be the instructors in that course, though I have no personal connection to those instructors or their department besides sharing a university. For the latter, I would suggest a scientific review article rather than a book.


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How greater magnitude implies greater frequency of action potential?

Greater the magnitude of receptor potential, greater is the rate of discharge of action potentials in the nerve fibre.1

Now consider a case where stimulus ( strength ) is large , so there is more accumulation of positive charges near the spike generator region, this would then form action potential , this action potential should then travel in both directions just like at initial segment , where SD spike clears the existing EPSPs, so if I apply same logic here then antidromic Action potential should clear those generator potentials. If I am right then how is more stimulus causing more frequent action potentials?
Case2: If we take the scenario where there is no antidromic conduction of action potential ( for some unknown reasons) then more and more generator potentials are coming at spike generator region(1st node of ranvier) then also how it is causing more frequent action potential generation , if we consider that fact refractory period is constant for all action potentials( in a particular neuron)?

There are several important points to answering your question, each somewhat independent of the others. First, lets think about this problem from the perspective of the axon hillock, where action potentials are thought to be generated.
Conduction of action potentials requires voltage-gated sodium channels
When you talk about antidromic action potentials, you mean when they start at the "end" of an axon and return towards the cell body. You can also get backpropagating action potentials into the cell body and dendrites, but these are impaired by two things: 1) fewer voltage-gated sodium channels, so the action potential is weaker or not really an action potential at all, and 2) impedance mismatch. The axon is very narrow; the soma is very big in comparison (this is less of a factor in the context of peripheral sensory receptors where the soma is located far from the site of action potential initiation, but it is still true for the neurites there). A few sodium ions coming in around the axon hillock is enough to depolarize that membrane enough to start an action potential, but when those ions diffuse passively into the rest of the soma, they have a lot more membrane area to cover, and they don't cause as much depolarization.
What all of this means is that the "strength" of a backpropagating action potential isn't less than that of an action potential in the axon.
Frequency is relative
When people talk about frequency coding of intensity, they are talking about a gradual increase in frequency, not going immediately to refractory period. For example, a cell may fire at 1 Hz, then fire at 4 Hz, then fire at 16 Hz, then fire at 64 Hz. If the cell has a refractory period of 5 ms, even at 64 Hz it is nowhere near it's theoretical maximum firing rate.
Related to that point...moving ions takes time and cells are not isopotential
Threshold isn't reached immediately in the axon hillock when a "refractory period" ends: that's the difference between an absolute and a relative refractory period. Ion concentrations and ion permeabilities set an equilibrium potential, but, it takes time for the potential to actually reach that equilibrium, and both the present voltage and equilibrium potential can be different in different parts of the cell: this leads to current flow, which takes time.
After an action potential, the axon hillock typically hyperpolarizes for a bit, sometimes followed by a brief depolarization. During that time, if there are other parts of the cell (such as dendrites) that are still relatively depolarized from a receptor potential, ions will be flowing from those areas into the axon hillock. This depolarizes the axon hillock, but again, this takes time (I'm purposely repeating that to convey a feeling of this all being a dynamic, moving process, with ions moving through each step). The amount of time it takes will depend on the voltage difference, so a bigger depolarization in the dendrites will bring the axon hillock back to threshold sooner.
Not that many ions flow during an action potential
This has been a recurring theme here, see this answer: Why is it possible to calculate the equilibrium potential of an ion using the Nernst equation from empirical measurements in the cell at rest?
The change in membrane potential isn't just because ions flow: it's because permeabilities change, briefly creating a new equilibrium potential. If you have in your mind massive quantities of sodium and potassium ions flowing, completely upsetting the ionic balance in the cell and drowning out all other electrical activity, you have it wrong.
Stimuli are often long-lasting
Especially if you are talking about a mechanical stimulus, most will last a lot longer than an individual spike, which is only ~1ms long. So although one transient stimulus can cause several action potentials, often what actually happens is that those receptor potentials are quite long lasting. Effectively, they set a new "resting potential" for the cell which is above the cells' firing threshold.
In summary:
Receptor potentials depolarize the cell, bringing them to or beyond firing threshold. An action potential starts in the axon hillock and propagates down the axon, but only has a minor impact on the rest of the cell. Importantly, the action potential is really brief, not many ions move, and there is current flow in both directions, so the depolarized parts of the cell are still depolarized somewhat even after a spike. As the initial axon segment recovers from post-action potential hyperpolarization and sodium channels leave their inactivated state, current from the receptor potential is flowing in, depolarizing the cell to threshold and causing another spike. Repeat.

"So although one transient stimulus can cause several action potentials, often what actually happens is that those receptor potentials are quite long lasting. Effectively, they set a new "resting potential" for the cell which is above the cells' firing threshold." --> Would this mean that it then takes less for cell to fire next (as the new resting potential is above the initial resting potential)? I am asking because that would be not consistent with adaptation (which I assume would increase the threshold)

@Pugl Both are possible, on different time scales. When held at a depolarized potentials, cells can somewhat paradoxically become less excitable: this is because of voltage-gated sodium channel inactivation. The more VG Na channels are inactivated, the fewer are available to open, so more depolarization is required to reach the positive feedback underlying an AP (it's possible to depolarize a cell enough that it can never spike, called "depolarization block"). Adaptation can also occur at multiple stages. I can't say much more about a general case.


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Why Cerebrospinal fluid is not heated for VDRL?
For performing VDRL of serum , we heat serum to inactivate complement proteins which may otherwise interfere , but why don't we do same for CSF even though it too has complement proteins in it?
Is it because of lesser stability of WBCs in CSF( which is hypotonic) and on heating may rupture to release cardiolipin? But I can't comprehend how its worse than having complement proteins?


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About a mechanical aid to the heart
I saw a news story a few years ago (I think) about a girl with a poor heart having a device implant that took over only some of the functioning of her heart ( I think they called it a piggy-back device , or something like that). The extraordinary thing is that it not only helped her live but all the heart functions started to improve. It was as if giving part of the heart a chance to 'rest'  allowed the whole heart to improve. If this procedure works could it be applied to other organs? Could a Piggy-Back device be made for the liver taking over only some of its functions for instance?  Could such a thing help the liver functions to 'regenerate'?

The function of heart is just to pump blood and nothing else. Though, it is a vital organ, its functions are limited. The device that you are talking about is a battery powered mechanical pump that performs the same function as heart.
Liver, however has a more complex function. One of its function is to synthesize and secrete certain molecules. A small artificial device cannot do that (you would need a bioreactor !!!).
We still haven't developed and artificial cell. Perhaps a consortium of bacteria can do some of the liver's functions but to culture them in right proportions and implant them without the risk of infection or their elimination is almost impossible as of now. You can clearly see that there are too many steps to be optimized.

There was a news story about a device that took over some of a young girl's heart functioning and the girl's heart did improve. It was not  a heart pump that took over all its functions.

if you can then please post a link to that story.

See this, tell me which one are you talking about ?
All artificial hearts do nothing but pump. Even the real heart has no other function.
Or do you mean the pacemaker (that is for controlling arrythmic beating)

@user128932 - you can have an implanted assistive device that helps by pumping some of, but not the entire, volume of blood. These are used by patients (and I assume this young girl is one) whose hearts can still pump blood on their own, but for whatever reason are unable to do it under optimal conditions (low pressure and/or low volume caused by incomplete chamber contraction/expansion, backflow from issues like leaky valves, etc.).

Yes , this (I think ) was it , an implanted assistive device. The news story even said the young girl's heart improved in function. Could there be an implanted assistive device for the lungs? Thank you MattDMo

I heard cows and salmon and sheep have been cloned ; so if they can clone a large animal can they clone a cell? Can a liver cell be cloned or would it have problems with longevity like the sheep did? Could blood be cloned?


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Regarding signalling pathways
Do all signalling pathways have something that can inhibit them? If the signal pathway is benefitial  and it is inhibited would the inhibitor be caused by a biological problem?  Are all inhibitors controlled by some subcellular  mechanism?

Do you think about "artificial" inhibition or an inhibition that occurs naturally in the cell?

There are some inhibitors in the cell, which have specific effects on signal transduction. These are mostly second messengers (like cAMP, cGMP, calcium ions,  inositol 1,4,5-trisphosphate and others), which are then able to diffuse relative fast to other proteins. There they can either amplify a signal or cause inhibiting processes to start which then terminate the activation of the signal transduction cascade.
The problem is that these inhibitors that they work unspecific in their inhibition and termination. Signal transduction is tightly controlled as they directly influence the expression of various genes.
A lot of the proteins in these cascades are kinases which are activated upon phosphorylation and then carry on by phosphorylating the next step of the cascade. The activity is stopped by phosphatases which remove the phosphorylations from the kinases and thus inactivate them until the next signal is passed down the cascade. It works like in this figure (from here):

Specific inhibitors for single proteins in the signalling cascades are available as drugs against cancer. Since these signalling cascades regulate gene expression including cell cycle control, they are important targets for dysregulation in cancer. A numer of kinases in the MAP kinase pathway for example are mutated there and constantly active. The so called small molecule inhibitors bind to the protein and inhibit the kinase activity, preventing a permanent signal. See this article for more information:

Targeting cancer with small molecule kinase inhibitors

"There are no inhibitors of signal transduction occuring in cells." Are you talking about small molecules? There are plenty of specific inhibitors of signal transduction, they just happen to be proteins for the most part, and not all of them are phosphatases. Each signaling pathway is very tightly regulated by a variety of mechanisms, including second messangers (which are technically small molecules).

Ok, that's right. I was thinking about molecules like the small molecule inhibitors (like all the kinase inhibitors in clinical trials or already licensed like vermurafenib) which specifically inhibit one kinase. And there is no analogon to these in the cell to my knowledge. I will make my answer more precise.

Could a cell be considered like an EXTREMELY complicated subcellular and intracellular signal processing 'machine'? Where any signal pathways are tightly regulated..

If you like this, why not? A cell is a extremely complicated mechanism...


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About stem cells and Cancer
Do stem cells have an apoptosis mechanism and , if they do could this be used to repair the  cell self-destruction pathways in a cancer cell?


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Why proximal muscle weakness is seen earlier than distal muscle weakness in Dermatomyositis?
It is said that in dermatomyositis(DM) , proximal muscle weakness is seen earlier than distal muscle weakness. It is also said that , DM is due to damage to small blood vessels contributing to muscle injury.( from Robbin's textbook of pathology pg.no: 1238-1239, 10e)

Shouldn't the distal group of muscles being smaller show weakness earlier? Why inclusion body myositis does not follow the pattern as in DM?

Usefull links:
https://www.mda.org/disease/dermatomyositis/causes-inheritance
https://emedicine.medscape.com/article/332783-overview#a1
My hypothesis are
1) Since skin, is commonly involved in sunexposed areas, may be enviornmental factors do play a major role. So, Proximal Muscles are more used in day to day work, so are more favourable site for drugs, autoantibodies to act upon.
2)May be, in case of due to drugs or vaccines, proximal muscles may be are preferrential site of action of these, making these group of muscle more suceptible.
By the way correct answer would be: Its under research.


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How nasal hairs filter particles of micron size?
This book says:

The larger particles (> 10 μm diameter) are filtered by hair in the nostrils

If we see the anatomy of nasal hairs and its density in the nostrils then it seems that its impossible for such a structure to filter particles in micrometers, So how does the nasal hairs filter them?

That's not strictly true. Particulate matter of less than 10μm in diameter (expressed as PM˘10) reach lower airways, and 10μm diameter reaches the bronchial tree, Hair disturbs airflow allowing for deposition, is moist and can catch small particles; mucus on surface epithelium and hair can as well. But it's a combination of a lot of mechanisms that keep out larger particles. Shape of the particle also matters. But pollen of 20μm has been found in lung periphery.


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DNA replication : binding
Regarding an activator, does the C amp cap complex, bind to the coding strand, the template strand, or both?

Your question makes it sound like the coding strand and the template strand are single-stranded when the cAMP CAP protein is bound. In fact, the recognition site for transcriptional activators and repressors are usually double-stranded, so the answer is both.

I agree with you but it's technically possible for a protein to make meaningful contacts with only one of the strands, although this is probably not what he meant.

*she .... you can't edit comments?

Both. You should note that activation in this case involves recruitment of RNA polymerase to drive transcription, and that this process is irrelevant to DNA replication. B in the figure shows amino acid contacts (from CAP) with specific nucleotides in the DNA duplex.
DNA binding by CAP: structure of the CAP-DNA complex.
(A) Structure of CAP in complex with its consensus DNA site (PDB 1RUN) [14], showing primary- and secondary-kink sites. CAP is in cyan; DNA and cAMP bound to CAP are in red. The crystallization DNA fragment contained a single-phosphate gap between positions 9 and 10 of each DNA half-site (Fig 1b).
(B) Summary of CAP-DNA interactions. Shaded boxes indicate positions at which CAP exhibits strong sequence preferences [11,15,16,17]. The black circle, black rectangles, and black diamonds indicate, respectively, the two fold-symmetry axis, the primary-kink sites; and the secondary-kink sites. The black vertical lines indicate the positions of single-phosphate gaps present in the crystallization DNA fragment. The cyan ovals and cyan circles indicate, respectively, amino acid-base contacts and amino acid-phosphate contacts.
Figure from:
Catherine L. Lawson, et al. 2004. Catabolite activator protein (CAP): DNA binding and transcription activation. Curr. Opin. Struct. Biol. 14:10.


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Understanding the dissociation constant of a ligand - receptor complex?
I am learning about dissociation constants in Lodish's Molecular Cell Biology and can't follow an example in the text - specifically, how he calculates [P] in the cell to be ~111x10^-10 M and the ratio to be 99% (text below). I feel like this example is supposed to be easy and that I am missing something super obvious. Any guidance would be greatly appreciated!
Text Excerpt
"Typically, a protein’s binding to a specific DNA sequence exhibits a Kd of 10–10 M, where M symbolizes molarity, or moles per liter (mol/L). To relate the magnitude of this dissociation constant to the intracellular ratio of bound to unbound DNA, let’s consider the simple example of a bacterial cell having a volume of 1.5 × 10–15 L and containing 1 molecule of DNA and 10 molecules of the DNA-binding protein P. In this case, given a Kd of 10–10 M and the total concentration of the P in the cell (∼111 × 10–10 M, about a hundredfold higher than the Kd), 99 percent of the time this specific DNA sequence will have a molecule of protein bound to it and 1 percent of the time it will not, even though the cell contains only 10 molecules of the protein! Clearly P and D have a high affinity for each other and bind tightly, as reflected by the low value of the dissociation constant for their binding reaction. For protein-protein and protein-DNA binding, Kd values of ∼10–9 M (nanomolar) are considered to be tight, ∼10–6 M (micromolar) modestly tight, and ∼10–3 M (millimolar) relatively weak."
Link to Text

This is all just algebra and some basic chemistry, the author is giving you an equation and expecting you to be familiar with algebra and chemistry and use that knowledge to follow along with the equations.

a bacterial cell having a volume of 1.5 × 10–15 L and containing ... 10 molecules of the DNA-binding protein P

Concentration is molecules per volume: the volume is given, the  concentration is given. To go from molecules to molar, divide by Avogadro's number.
10 molecules/(1.5 * 10^-15 liters) * (1 Molar/(6.02214 * 10^23 molecules/liter)) = 1.11 * 10^-8 M = 111 * 10^-10 M

given a Kd of 10–10 M and the total concentration of the P in the cell ... 99 percent of the time this specific DNA sequence will have a molecule of protein bound to it and 1 percent of the time it will not

Kd = [P][D]/[PD]
If [P] ~= 100 * Kd, we can substitute for [P]:
Kd = 100 * Kd [D]/[PD]
Do some algebra: multiply both sides by [PD]/Kd
Kd * [PD]/Kd = (100 * Kd [D]/[PD]) * ([PD]/Kd)
cancel:
[PD] = 100 * [D]
The bound concentration [PD] is going to be 100 times the unbound concentration [D]. We've done some approximating to get there so might as well say roughly 1% as D and 99% as PD.

Thank you Bryan, that was a very helpful explanation (and yes, it's been a while since I took gen chem, I definitely need to review!)

@user123429 Probably also worth noting that, while you should be able to do the algebra, from a biology perspective we're usually more concerned with rough order of magnitude and a conceptual understanding. Here, you should be focused on understanding that when concentration of [P] is much larger than the Kd, that means most D will be bound with P as PD. If [P] = Kd, then only half of D will be bound as PD.


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Does alcohol really do more damage to the body of a child compared to an adult?
Beside the fact that children and teens (people under the age of 18 year) usually have less body weight than the average adult, is there a   biologically fundamental difference between the damage done to their bodies compared to an adult when drinking alcohol?
I often read that their organs are still developing and thus alcohol will do more damage, but has this actually been proven?

As is stated in this article by Hiller-Sturmhöfel and Swartzwelder from the National Institute on Alcohol Abuse and Alcoholism, there are ethical issues surrounding research on human subjects that preclude direct testing, however studies in model mammals and observational studies do find that "adolescence is a unique stage of brain development which is particularly sensitive to the disrupting effects of alcohol."
A research review by Tapert, Caldwell, and Burke, also finds that studies support the conclusions that alcohol use by adolescents and young adults has a negative effect on cognitive abilities.
Hope that begins to provide you with an answer to your question.

Is the cognitive damage by alcohol uniquely restricted in "the stage of brain development"? What if the fetus is in its embryo phase without neural system developed yet?


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Why do orcas eat only the tongue of whales, liver of sharks, etc.?
I noticed that although killer whales are clearly the top predator living in the present oceans, some of them appear to be very picky with their meals.
After spending hours hunting down a whale, pretty much the only thing they eat is the tongue. I'm not sure how that satisfies their hunger, especially considering how long and arduous the hunt took.
Then there are orcas hunting sharks and eating virtually only the liver. For such a dangerous prey, is such a delicacy worthwhile? I mean, what happens if they're starving after the hunt?
Any relevant comment will be greatly appreciated. Thanks!

Could you add a link to these data. I know, e.g. that grizzlies eat only salmon heads (the fatty brain tissue) when salmon is plenty available. They just sit by the river bed and grab the exhausted, tired salmon straight out of the stream one by one; bite the head off and throw the rest away. They stop doing this when salmon is getting scarce and they start to eat the whole thing. I can imagine the same goes for other predators and humans too. During the "hongerwinter" (literally hunger winter) in '44-'45 during WWII, Dutch folks would eat anything, while now they can be pretty picky :)

Welcome to Biology.SE. Can you please link your sources? That would help

I've got to admit that most of it is memory, but Google gave me these results:
http://www.learner.org/jnorth/tm/gwhale/EnemyOrca.html
http://voices.nationalgeographic.com/2011/11/25/nat-geo-wild-the-whale-that-ate-jaws/
http://www.pbs.org/wnet/nature/killers-in-eden-face-to-face-with-a-killer-whale/1045/
http://knowledgenuts.com/2013/11/19/orcas-can-eat-great-white-sharks/

I really have no idea about this, but consider that orca's are very social and intelligent animals, they may hunt 'just for sport'

Killer whales have a wide range of prey. They hunt in coordinated packs called pods. They are very organized on a hunt and each has a specific job before the kill.
Where the confusion might be coming from is that different pods have different habits. It is true that orcas have been witnessed eating only the tongue, but this is not the norm. They tend to eat the tongue first because it is muscle, rich in protein. In addition, they like the tongue, just as humans may like a good steak. However, in most cases they will consume as much of a whale (typically baleen, or blue whales) as they desire. In fact, whalers hate them because they will follow whaling ships and wait for the fishermen to harvest a whale. They will then rush in and gorge themselves. Another case of their only eating the tongue is when they are well fed. In this case, they can afford to be picky and may only eat the tongue, which on average is the size of an elephant. So, it's no small meal.
As for sharks, it's pretty much the same scenario. However, there are many cases of orcas eating only a great white shark's liver. The reason they target the liver (and they do it with surgical precision) is because it contains large amounts of a compound called squalene. Squalene is important for the synthesis of certain chemicals in the orca's body. They will also target the heart. The attacks on great whites is a more recent trend among killer whale pods. They are quick learners and once they feel the benefits of these organs, they will then focus on the sharks when their bodies tell them they need the squalene. Of course, they don't know that. They just feel better and stronger after consuming GWS organs.
There may be pods that tend to have these habits (outlined above) more than others. Resident pods (staying in one area) seem to be calmer and are not as likely to have the tongue activity, but it is the residents that kill the GWSes for their organs.
Transients are far more aggressive than residents. They are likened to pack wolves and will do some extremely cruel things (by human standards). These are the ones who are far more likely to eat only the tongue of a whale. It could be that since the shark organ habit has not been happening for very long, it's the residents who made the connection between health and these shark organs.
Another factor that could come into play is that scientists/marine biologists tend to believe that there are different species of killer whale. This may play a role in dietary habits as well.
Killer whales are the top (known) predator in the water. While a much larger whale, or GWS could potentially kill one, they are typically no match for a pod and will instead steer clear and only fight if no other alternative presents itself.

Can you cite some of that research?

They eat the tongue and sometimes lower jaw of larger whales because they are the easiest parts to eat. They are soft, unlike the rest of these whales’ bodies. I’ve heard a scientist compare an orca attempting to bite into a grey whale’s body to a human attempting to bite into a whole watermelon. The grey whale’s skin is very hard and thick, and it also has a very thick layer of dense blubber, if an orca tried to take a bite out of, let’s say, the back or side of a grey whale, they would basically only scratch the surface. So the obvious solution is the soft tissue of the lower jaw and tongue. Like someone also said before, the tongues are huge! I’ve heard a scientist say that the tongue of a California Grey Whale calf could feed a family of 5 adult orca!

Can you please add some references to support your answer?

orca have only one set of teeth and i would guess culturally they are aware of the consequences of losing any of them or maybe simply it hurts their teeth to try to eat other parts of the shark -- I mean orca no doubt have nerves in their teeth as we and other mammals do.


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Bradford Reagent Disposal
I am a graduate student volunteering in a professor's lab being tasked with finding out how to dispose of certain hazardous materials. I have encountered a problem with disposing of Bradford's Reagent. I have checked online, but am running into problems due to the methanol component of this compound. Can someone help me with the proper disposal procedure? Thank you in advance.

I would strongly suggest to ask someone in your lab about this, they will have a better idea about the different waste disposal methods you have available.
In general you would dispose anything that contains organic solvents like methanol in a waste container for generic solvent waste. You should have something like that somewhere in the lab.
One thing you always have to keep in mind is to never put anything still reactive into your waste container. A popular example would be a strong oxidizing agent, putting that into a solvent waste container is dangerous and could e.g. ignite the waste. This is not an issue in this case, but you should always keep that in mind.
Another aspect is the pH of the waste, in many cases the waste disposal facility will only accept reasonably neutral waste, so you should neutralize your waste before putting it into a container. Neutralizing it inside the container can be much more annoying. This might not be necessary if you have a dedicated acidic waste, you'll have to ask someone in your lab about that. The Bradford reagent is strongly acidic, so you'll have to pay attention to this aspect.

@wingsfan1340 If this answer addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered.


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Is it possible there were multiple origins of life? And, if so, why did the one which became the common ancestor between all organisms prevail?
I have learned that all currently-living organisms come from a common ancestor, which I theoretically understand. However, my professor in a class mentioned that there is a chance that there were multiple origins of life, but that all the creatures living today all came from the same one and the others died. How can we be sure that before the other origins of life died, they didn't somewhat evolve, and the species from that origin didn't just evolve in convergence with those of this one since through natural selection both would need similar characteristics to survive on Earth?

That is an interesting idea. Are you sure that your professor was saying that all life today descends from several ancestral cells, or that ancestral life was eradicated many times before our ancestral cell came into being?

Closely related: http://biology.stackexchange.com/questions/14175/why-did-abiogenesis-only-happen-once

It is interesting that all forms of life use the same genetic code. The nucleotides composing DNA and RNA are universal. Eric Lander, geneticist from Harvard/MIT cites this as evidence for evolution from a single ancestor. I think your instructor may be saying that it's possible alternative adaptations for initiation of life may have occured and perhaps not worked out. They become just another of nature's experiments that ended in extinction. I seem to recall reading somewhere all but 2% of species have ended in extinction.

I believe that the answer to this question would be that we cannot tell for certain that there were multiple origins of life.
In order to determine that there were multiple origins of life, we would almost certainly need to look into the molecular biology side of these organisms, since convergent evolution makes it extremely likely that these differently originated organisms would be very close to each other in outward appearance. However, the basic molecular machinery would have much less of such selection pressures, allowing them to be maintained.
However, this would be impossible if the organisms have already gone extinct, as fossilisation generally does not preserve the structures of the proteins and DNA (or equivalent information storage molecules) that are used by the variant organisms.
If such an animal was alive, however, it would then be possible to determine the animals' variant origins by detecting a specific biochemical trait that they alone possess. For example, an animal which used D-amino acids for its proteins would certainly be determined to have originated from a different common ancestor.


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where can I find estimated costs of laboratory equipment?
Often when I am curious about purchasing new laboratory equipment I cannot find a ballpark figure for the price.  Companies that sell expensive lab equipment prefer if you contact their customer service or sales teams to inquire about prices.  I don't want to go through all of that hassle, as well as exposing myself to  potential marketing emails.  Is there any website that lists ballpark figures for lab equipment?  The type of equipment I am talking about are things like PCR thermal cyclers, Flow cytometers, nucleofection devices, centrifuges, etc.
Thanks in advance.

Yeah, it is annoying that nobody lists prices. Call them using a temporary forwarding e-mailadres.

Yeah, but calling them is what I'm trying to avoid..... I Just want ballpark figures, not exact price quotes based on all the details of my institution/grants etc.

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

The best way (if you're buying new) is to contact the manufacturer/distributor. Sales people get inquiries like this all the time, and are generally more than happy to accommodate you (because they get commission on any sales they make). Most items have customized pricing depending on the customer, their order history, the number of items being ordered, add-ons like maintenance contracts, reagents, etc. Many complex instruments like flow cytometers have many customization options, including the number and type of lasers, different types of filter sets, tube vs. plate-based acquisition, type of computer, licenses for software, etc. Sales people know their company's product lines the best, and are willing to talk to you to figure out your needs and then recommend the product that works best for you, which may not necessarily be the one you were originally thinking of.
You can always ask to not be added to any email lists, and if you are added, commercial emails (in the United States, at least) are required to have an unsubscribe link in every email. Check out the CAN-SPAM Act of 2003 for details.

I specifically asked in the question how to get ballpark estimates for prices without contacting the company, so I cannot accept your answer.  I do agree with you based on my experience, that calling the company is the best method of getting this info, but I think that is ridiculous and annoying.  I don't want to spend that much effort/time when I am just brainstorming about potential possibilities.  It would be nice if the companies just had a price range listed for each machine, that would be a good starting point.

@Reilstein unfortunately, I don't know what else to say. Companies generally don't publish list prices for big-ticket items, although you may be able to find some info if they distribute through ThermoFisher or VWR or some place like that. There are sites that sell used equipment, so you could google them for ideas. But, if you're looking to buy new, contacting the company is the only way to go. Remember what I said, sales reps get these kinds of questions all the time, and if you clearly state you're just pricing options at the moment, they should be able to accommodate you. Good luck!

I Hear you, and thanks for your tips.  I will keep it in mind for when I get more serious about my equipment.  I was hoping for someone to have a website that users contributed their prices for equipment recently purchased, but apparently that does not yet exist. Thanks again.


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Choice of primers for PCR
This exercise was given by my professor but I am struggling to understand the solution.
A PCR is performed on the following sequence (in order to replicate the chain and thus have a greater quantity of DNA so to be able to analyze it):

The main sequence belongs to a horse and differences are indicated below with dna belonging to a cow.
1) Choose appropriate primers in order to analyze some lasagna, which is suspected to contain both horse and beef.
Given Solution:
The primers should be:

I understand how these primers would work in this case, but why not just have the second pair of primers which would make it possible for the whole chain to be analyzed at once?

Welcome to BiologySE - we have some specific home work question policies that you should look at when posting questions. Check this out and edit your question appropriately. http://biology.stackexchange.com/help/homework

You do need two pairs of primers one unique to each species as you need a positive result to be confident that the thing you are looking for (cow or horse) is there.
There is no limitation on them being in the same place (with a different last base).
Usually this would be analyised by gel-electrophoresis and not by sequencing so you don't have to worry about getting the whole thing. This is because you are only looking for the presence or absence of PCR product.
When you do the PCR you will have 4 reactions, one which amplifies horse only, one which amplifies cow only and their negative controls (adding water instead of lasagna DNA extract). After the PCR you take a small amount of your PCR product and run it on a gel (gel-electrophoresis). If you see amplification in the negative controls then you have contamination and can't trust the result. Otherwise if you see amplification by the cow primers then cow is present in the lasagna and if you see amplification by the horse primers then you probably don't want to eat the lasagna. If you used both options for the first forward primer you suggested (blue) then all your bands would be the same size, if you used both the first (blue) and second (yellow) then you would get different band positions on the gel due to the different sized products which makes you feel more sure that you didn't make the mistake of adding the same primer pair to both tubes (it happens).
In the end it's simply a matter of style.

I'm not quite clear what the question is asking, as far as I can see, one pair would be enough..  Since your primers don't include the distinguishing base (and it would be dicey to e expect a PCR reaction to totally fail because of a one base difference) I assume you are going to do sequencing or digest after the PCR to distinguish between the species?


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RNA interference and the former Petunias experiment >
I'm having problems trying to understand how RNA interference works.
From what I understood, in simple terms there is this  dsRNA which is fragmented into siRNA by the enzyme called Dicer, and those siRNA make the RISC complex active, which leads to the degradation of mRNA which are complementary to one of the strands of the original dsRNA.
Said this (which I don't even know if it is correct), how this relates to the petunias experiment? From what I understood the researchers put into the petunias an enzyme that coded for the pigment and not strands of dsRNA which then would have created the inhibition...
What am I missing?
PS. I don't have technical knowledge about Technologies so excuse me in case I said wrong things.
Thanks in advance everyone.

Can you please provide a citation for the "petunias experiment"?

By Andrew Fire and Craig C. Mello - For the petunias pigments.

They introduced a foreign gene responsible for petunia leaf colour, with the intentions of up-regulating gene expression for this colour, which was purple. What was observed however was intriguing. Rather than an up-regulation of the purple colour, the leaves were all white instead. This finding showed that the RNAi system in plants recognised the foreign gene and degraded it. Not only that, but the RNAi system also identified the endogenous equivalent of the foreign gene and down-regulated this also thinking it was foreign. This is how they discovered this miraculous finding :)

Hi Chris - on this site when you answer a question you need to include some background information and references to back up the claims you make in your answer. Without this important information your post will potentially be voted down and you will lose reputation points or deleted altogether. Looking forward to see your edits - thanks for your contribution.


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Can a stationary eye with a moving pupil exist?
I am making a sci-fi web-comic set on an alien world and I thought up an idea for an eye that works much like an eye from a mammal, but instead of moving the whole eye, only the pupil moves. This idea sprouted from the eyes of mantis, though their moving pupil is possible because of their compound eyes, I would like to know if my idea could be physically possible. (And yes I know this is a strange question compared to others on this site).

Although this is an interesting question, it doesn't look like it can be answered without being opinion-based. Perhaps this fits better on Worldbuilding.

what do you mean with "physically possible"?

What I mean is can there be a structure capable of this function.

Also, thanks for the forum recommendation I'm new to these and your help is much appreciated.

Mmmm.... You wish to know whether theoretically an eye could exist that features a moving pupil? Everything is possible, right? I think this question is too theoretical and will give rise to primarily opinion-based answers. I vote to close.

@Jesse There is a Stack Exchange forum where questions such as yours are not only welcome, they are actively discussed. It is Worldbuilding SE. You should join that SE and post this question there. It is populated with creatives who are trying out ideas as well as trying to find out how scientifically accurate their ideas are. There is also a Science Fiction & Fantasy SE where this question would likely generate a discussion, but I would try Worldbuilding SE first.

@Jesse also think of the function of an eye and the pupil. The pupil is an aperture that regulates the amount of light that is allowed to enter and project onto a photo sensitive surface, it the eye's case the retina. The retina is tuned mostly in the center of the rear curve of the eyeball. Moving the pupil would change the plane of the projected image and would be reflected on a different spot on the eyeball with likely a certain amount of diffraction as the lens is still set to focus on the rear of the eye...

... Now if your alien life forms evolved to see white light when their pupil was centered but then had other focal planes that allowed them to see more sensitively in the infrared spectrum or with another positioning and ultraviolet spectrum, then maybe a shifting pupil would be an interesting device to harness this ability. It could be analogous to night vision goggles only built into their eyes, where they can shift their pupils to see under different conditions.


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Differential gene expression analysis between species
I have RNA Seq data from mouse and human skin ( 2 replicates each) and want to compare the expression of the orthologous genes to find any which are differentially expressed.
I have quantile normalized the gene expression matrix across all 4 samples (2 mouse + 2 human). I eventually want to calculate the log fold change in expression of all orthologous genes between the 2 species. However before I do this, I should control for gene length, right? Will this be enough to give me an idea of the differentially expressed genes or should I be employing more sophisticated methods?
Any comments would be helpful. Thanks a lot.

This might be better suited at [stats.se].

It depends on what type of data you have, really. There are methods developed solely for quantifying relative expression based on count data, such as using edgeR or limma-voom.
You don't need to correct for gene length to estimate fold-changes of relative expression, what you need to do is normalise by library size first (and in the process obtain log2 ((counts + 0.5)/1e+06) and then, following quantile normalisation, you can just calculate mouse - human or human - mouse to give you an estimate of fold change.
I still would recommend using something a bit more sophisticated like limma-voom for this task, though, because that also will enable you to get stuff like false-discovery rates for your fold changes.

I have count data. However the reason I am hesitant in using packages like edgeR or DESeq2 is because they are meant for comparing expression of same gene between 2 conditions. I on the other hand want to compare the expression of orthologous genes (diff genes with diff lengths) between 2 species.  Also if I am doing quantile normalization (i.e. imposing the same distribution on all samples), do I still need to control for library size?

Yes it is the norm to control for library size and then quantile normalise - you always need to control the number of counts for how many reads were sequenced per sample.
Orthologs with different lengths should be fine - I mean, in any case limma-voom for instance estimates gene level differential expression without consideration of isoforms (which have different lengths). Orthologues can technically be regarded as variants of the same genes so maybe give it a go.

Thanks for your answer. But the fact that limma ( & other count based methods) does not account for diff transcripts is a limitation (e.g: if gene A transcript 1 has 20 reads in condition A & gene A transcript 2 has 20 reads in condition B, it will not find transcript 1&2 as differentially expressed...whereas depending on the gene this can be biologically relevant.) this is why I am hesitant to use these methods for my analysis.

You are going to run into similar problems anyway if you are comparing orthologues by fold changes alone - the only way to get round this is to derive exon specific counts,  in which case limma has a diffsplice function to check for differential splicing.
or you could use RSEM to estimate counts for comparable isoforms in your organisms and then instead of gene counts use isoform counts.


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What do HG and NA mean in Geuvadis project RNAseq sample labels?
I'm looking at RNASeq Data from Geuvadis website e.g. the file GD660.GeneQuantRPKM.txt.gz.
The samples are labeled by e.g. HG00105.1.M_120209_7 or NA20812.2.M_111216_6
What do HG and NA mean? Are they ethnic backgrounds?
If not, how can I look up the ethnic mapping to the samples?
Thanks!

If you google HG00105, among the first hits is geo accession GSM649517 with the title HG00105/NA12878.
Channel1:
Characteristics gender: Male
cell line: lymphoblast cell line HG00105
ethnicity: British from England and Scotland, UK (1000 Genomes codes: GBR)

Channel2:
gender: female
cell line: lymphoblast cell line NA12878
ethnicity: Northwest European American from Utah (HapMap code: CEU)

So no, they are not coding for the ethnic background but are part of the unique identifier of the sample.


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B cell clones and affinity maturation
As B-cells undergo affinity maturation, their BCR sequences change. Are they still considered to be part of the same clone?
I couldn't find a clear answer in response to this very similar question:
What is meant by clones of B-cells?

There are different opinions on this, since it's about usage. You could make an argument that, if you're talking about a B-cell clone, it is the product of a specific VDJ recombination (a mature, but naive B-cell), and refers to B-cells that produce antibody to one antigen. However, the term was originally proposed in this context:

...the expendable cells of the body can be regarded as belonging to clones which have arisen as a result of somatic mutation or conceivably other inheritable changes. Each such clone will have some individual characteristic and in a special sense will be subject to an evolutionary process of selective survival within the internal environment of the body.

In this case, I'd argue that, when the BCR sequence changes in progeny from that original naive B-cell (as in affinity maturation), you end up with different clones.
You do have to be careful, though, because people use this term differently.


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Where to obtain metabolic pathway datasets
I've been looking through the files available at www.reactome.org along with some others but I only find images/pdfs of metabolic pathway diagrams. Where is the actual data these pathways are drawn from? I imagine there should be some kind of directed graph representation. I'm limited to freely available datasets, so unfortunately I'm not able to check out those such as KEGG.

KEGG should be open for anyone, if I am not completely wrong.

According to their download page, access to the ftp files for KEGG require a paid academic subscription (through http://www.bioinformatics.jp/en/keggftp.html). I suppose the tools on their website are free, but I haven't found the pathway data I'm looking for (that is, I see where I'm only able to browse pathway diagrams).

Well, now I see that KEGG has a XML markup of their pathways, but it is only available from querying their API (http://www.kegg.jp/kegg/xml/). I wonder if there is an easy way to grab all pathway files.

KEGG is definitely your choice!
It is possible to get the whole list(s) of pathways: http://rest.kegg.jp/list/pathway (reference pathways) or http://rest.kegg.jp/list/pathway/hsa (for human).
Then you can use these IDs to retrieve information about individual pathways: http://rest.kegg.jp/get/hsa00053 (GeneBank-like format), http://rest.kegg.jp/get/hsa00053/image (image), http://rest.kegg.jp/get/hsa00053/kgml (KEGG xml). It will take a while, of course, and I'd recommend not to overload their server and make delays between queries. With the GeneBank-like format batch querying is also possible: http://rest.kegg.jp/get/hsa00053+hsa00061
This should likely be a one-time or at least rare operation, because of the load on their server (and I don't think they make big changes very often). You can retrieve info for new pathways, once they appear in http://rest.kegg.jp/list/pathway/...

Yes, this is actually precisely what I ended up doing. I wrote a python script which iterated through the human pathway file, sent a get request to their API and just saved each kgml file to hard disk. For the GeneBank-like format, those don't indicate any relationship among gene or compounds involved right? It looks like it is simply a list.

@Aaron: as far as I know, they are just listed. It's a pity, the API has no batching for the xml output, but KEGG is great any case!


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If someone A has lung cancer
and the lung cancer has not spreaded to other parts of A, does transplant help to remove cancer?
If someone B transplants a lung 'contaminated' by cancer, does B necessarily get cancer too? His body may kill cancer?

The standard procedure for curing cancer (besides chemotherapy) is to surgically remove parts of the organ with the tumor in it (or the whole, depending where it occurs). You also keep some safety margin around the tumor to be sure you definitely removed it. But in principle removing the organ in which the tumor grows and transplanting a healthy one would help.
There is indeed a problem with tumor cells in transplanted organs. If small (and thus undetectable) tumors have formed in these organs, they will be transplanted with the organ. Since the patient receives high doses of immunosuppressing drugs to avoid a reaction of the patients immune system, the activity of the immune system is greatly reduced.
Since the immune system also plays an important role in detecting (and fighting) the malignant cells of a cancer, this is also reduced which favors the appearance of tumors. There are reports for example from cystic fibrosis patients who received a lung transplant from a smoker and later died of lung cancer (see here, at the moment I only have a news source for it).

To the best of my knowledge, the only solid organ neoplasm routinely treated by Tx, at the moment, is hepatocellular carcinoma (liver), and even that under very strict conditions. For the rest, transplantation is currently not a standard therapy because of the very real possibility of accelerated growth of micrometastases under severe imunosuppression after the transplant.
And yes... a tumour transplanted into a person would grow, and fast, again because of immunosuppression.
If you're asking this for a practical reason, I'd advise you to talk to the oncologist involved in treatment for a thorough explanation of why this wouldn't work / referral to an applicable study, if there is one.


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about the direct intervention of a child's gender
Can we determine the gender of a child now,I mean,not randomly?
There are equal amount of sperms with X chromosome and Y chromosome.
Can these two kinds of sperms be distinguished easily?
If yes,we can choose the kind of sperm to meet the ovum,then the gender of the child can be determined.

Sperms can and are sorted using flow cytometry to attempt to separate sub-populations carrying X or Y chromosomes. The technique isn't perfect but it is undergoing "clinical trials" in the USA.

Gender selection as an invitro fertilization method has been in limited use in the US for decades. i just found this link: http://chooseagender.com/Methods-Of-Gender-Selection.aspx

"Sex" is the right word when talking about biology.  "Gender" is about the cultural signifiers and differences that a culture puts on people depending on their sex.
There are transexual people and transgender people and intersexed people...so it's a little rude to them to act like biological sex is a binary thing, or that is it totally the same as gender.

yes, sex selection also helps. It is illegal in China and India,but not in most of the countries especially in western countries. It should be a basic human right for parents?


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How many coronavirus particles are in the body at the peak?
How many coronavirus (or other common virus) particles are in the body at the peak? How far it multiplies? Are there billions, trillions or other number of them?

This measure changes dramatically between viruses and infected individual but there are some estimates that have been done.

Bar-On, Flamholz, Phillips & Milo, Apr 2020, eLife
From MERS and SARS (similiar to the current coronavirus) we know that from each infected cell emerge around 10^3 virions and it takes them 10 hours from the infection of the cell. We cannot deduce that every 10 hours the magnitude of virions in the body increases by 3 because:

Not all virions infect a new cell
Some virions infect the same cell and the burst size depends greatly on the cell
Not all virions are viable or able to infect

Another paper from Sender et al. (Nov, 2020) that is still in preprint (this is a long time for Coronavirus related articles) estimates the number of virions in peak infection at 10e9-10e11.
This estimate was done by analyzing data from Rhesus macaques (a monkey).
Concentration of virions per tissue weight was multiplied by the tissue weight to get total amount of virions.
On the relevance of Coronavirus information
Since our knowledge of Coronavirus advances and changes all the time it is important to note the date and source of information. Also, to advance science many papers published preprint articles regarding Coronavirus. This articles are published before peer-review and should be taken with a grain of salt as every peer-reviewd paper gets many revisions before published to the public.


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Barr bodies in males?
This source states that there are Barr bodies in 0-4% of males.
Why isn't it complete 0%? why some males loose their only X chromosome? How does then their body compensates for those genes which are inactivated?

To understand how the X inactivation can occur in, it requires a bit of understanding of how Barr bodies come about.
The main key players to keep in mind are (From 1):

Xist: Xist   Required for initiation of X-inactivation
Tsix: Tsix (It's Xist spelled backwards!) Represses Xist expression by silencing the Xist promoter, also required for X-chromosome pairing, counting the number of XICs (X-inactivated chromosomes)

From 2, Here is a general diagram of how X-inactivation occurs.

X-inactivation requires first, count how many X chromosomes are present (n). Then, the (n-1) number of X chromosomes are inactivated. The choice for which gets inactivated is largely random.
Therefore, if a male has multiple X-chromosomes (as in the case of Klinefelter syndrome) then X-inactivation would occur in males. However, there is also the case that erroneous counting may lead to the inactivation of the only X chromosome in males early in a developing embryo. But this is lethal, and the embryo would die.
More about Kleinfelter Syndrome can be found here: Klinefelter syndrome

Guided by RNAs: X-inactivation as a model for lncRNA function.
Lessons from X-chromosome ina ctivation: long ncRNA as guides and tethers to the epigenome

So all males with Barr bodies are Klinefelter males?

If they only have 1 X-chromsome and is inactivated, they would not make it to full term. They can have more than XXY, however, there will always be multiple X's.