text:
Can phenotype change without change in genotype?
If a person with lighter skin is to  live in areas close to the equator for a long amount of time, their skin would get darker, and hence their phenotype gets 'altered'.
If I'm to look at their gene that codes for skin color, though, I'd still see the one for lighter skin (which shows how it's not inheritable), but that would refer that the phenotype is also for lighter skin (when it's not the case in this situation)
'Phenotype' is defined as the morphological expression of characters on the basis of genetic constitution/genotype. How then, considering my example, is phenotype dependent on genotype?
I'm currently a high school student having mostly introductory/basic knowledge on genetics and heredity. I would appreciate some help in gaining conceptual clarity.

Even if a person gets a darker skin tone under these conditions, they are still pretty much different from people with a lot of pigmentation.

Following what David writes, if your book or something says "phenotype is dependent on genotype", be careful that you don't misinterpret this as "phenotype is entirely dependent on genotype". Entirely, completely, absolutely, whatever synonym you might choose it is not in the statement so do not insert it on your own to make the claim stronger than it is.

I thought it useful to provide an answer (more for the general footnote, which is relevant to other questions), but the logical fallacy is anticipated in the comment made by @BryanKrause .

The Logical fallacy

‘Phenotype’ is defined [by the poster] as the morphological expression
of characters on the basis of genetic constitution/genotype

There is no reason to accept this particular definition, but I find it reasonable enough. However I maintain that it is a logical fallacy to say — as the poster does — that it implies that if a morphological characteristic of an organism can, in certain circumstances, be caused by non-genetic factors, then it can never be a ‘phenotype’. To allow that implication the definition of phenotype would have to be something like:

A morphological expression of characters arising solely from the
genetic constitution of an individual.

which it is not what the definition states.
The term phenotype was coined and is used, solely in the relation to genetics. Hence, if the presence or absence of a particular gene causes a particular morphology, that morphology can be regarded as the phenotype of that gene or allele. This does not exclude the morphology also being the phenotype of another gene/allele, because the term is employed in relation to a specific gene. (Of course, some morphological features have a multigenic cause, and some genes have no observable phenotype, but that is irrelevant to the poster’s proposition.)
Incidentally, Mendel — who never used the term phenotype but a more cumbersome (Czech or German) phrase instead — would have been well aware that the size of peas could be affected by their access to nutrients and the weather. This did not invalidate his using size to access the effects of various breeding crosses and make conclusions about their origin in terms of invisible ‘factors’, only later called ‘genes’.
Footnote: Terminology in the biological sciences
Students from the numerical sciences (especially physics and mathematics) are in the habit of thinking in terms of definitions relating to the laws of the universe, and in this sphere a legalistic dissection of terms is often valid. The biological sciences are experimental sciences in which there are few, if any, universal laws. Ideas about biology develop from a limited number of observations (historically on whole organisms, rather than at the molecular level), and are refined as more observations are made and it becomes possible to provide molecular explanations for them. To communicate ideas it is necessary to make formal proposals and often to devise new terms to express them. Such proposals are not like laws or theorems in the numerical sciences. They frequently require modification as greater complexity is revealed and the anarchy of biology throws up exceptions. Biological scientists do not spend time debating the meaning of terms devised years previously. When new discoveries emerge they modify their picture of science and either modify or add riders to their terminology. They certainly do not spend their time shouting that a particular giant of the past had feet of clay. (Only seldom is there a complete revolution in ideas, or yesterday’s hero declared a charlatan.)
An example of the way genetics adjusts can be seen in Beadle and Tatum’s historic proposition: “one gene—one enzyme”. This was a made in 1941 at a time when the molecular nature of genes was still in debate (many, if not most, still thought that they were protein in nature) and not a single protein had been sequenced. The importance and originality of the proposal was in formulating a molecular relationship between nebulous entities, genes, and known molecules, enzymes.
Of course, we now know that not all proteins are enzymes, and some genes encode RNA (the structure and functions of which were unknown in 1941). Moreover with structural determination it became evident that some enzymes and proteins have more than one polypeptide chain, encoded by distinct genes (two genes—one enzyme). More recently, the discovery of alternative splicing means that in certain cases the situation is one genes—many enzymes.
Does this in any way diminish the contribution Beadle and Tatum made with their one gene—one enzyme hypothesis? I, for one, would wish to have half their insight.

Perhaps at some point we should turn the second half of your answer here into a canonical one for misunderstood definitions in biology. I think this comes up a lot, for example just recently https://biology.stackexchange.com/q/114739/27148 is effectively the same issue.

@BryanKrause — That would be fine with me.

@David Thank you for the insight you provided with the footnote. I am, obviously, new to this field and realise my mistake. I've been rather accustomed to physics and chemistry, and hence had such a doubt.

Yes, phenotype maps only noisily onto genotype. I recommend looking into the concept of phenotypic plasticity.
For example, temperature or food availability has regularly been used to alter phenotypes in clonal (~same genotype) populations of organisms, such as flies, plants, or Daphnia.
In one dramatic example, high population densities of tadpoles leads some of them to adopt cannibalistic behavior and morphological changes for preying on their siblings.
That said, genotype can itself control the way in which phenotype will change. This is the idea underlying the "reaction norm" first described by Richard Woltereck in 1909. He famously wrote "Reaction norm = Genotype", to describe that what is inherited in the genotype is not a deterministic program for creating phenotype, but rather a set of possibilities for what your phenotype can be.
This is not dissimilar to what MakM says, but the idea of plasticity is a core concept in biology that should be underlined as a common theme.
Interested to see what David writes.

Skin color is a polygenic trait. This means that it is controlled by multiple genes. (This can make it a little more complicated than some of the traits you learn about in your introductory classes).
If I understand correctly, you are asking about a single person that temporarily lives in another region of the world. During that time, their skin color darkens but their DNA stays the same. Now, I am no expert, but I am pretty sure that if they moved back, their skin color would eventually lighten again. This is due to skin tanning which is caused by melanocytes present in your skin. They produce a dark pigmentation in the skin to help protect against UV damage. (This is why increased sun exposure increases the risk of skin cancer. The UV rays damage your DNA and to prevent this, your body builds up melanin)
The way that I understand it is this: The genetics of skin tanning are always present in your DNA. If you have albinism and do not possess the ability to produce much melanin, regardless of where you live, you will still have the same (or near same) skin tone. The genes for the response to UV damage are always present in your DNA, but they are expressed only at certain times (after sun exposure).
Thingnes J, Oyehaug L, Hovig E, Omholt SW. The mathematics of tanning. BMC Syst Biol. 2009 Jun 9;3:60. doi: 10.1186/1752-0509-3-60. PMID: 19505344; PMCID: PMC2714304.
Visconti, A., Duffy, D.L., Liu, F. et al. Genome-wide association study in 176,678 Europeans reveals genetic loci for tanning response to sun exposure. Nat Commun 9, 1684 (2018). https://doi.org/10.1038/s41467-018-04086-y
Lucock MD. The evolution of human skin pigmentation: A changing medley of vitamins, genetic variability, and UV radiation during human expansion. Am J Biol Anthropol. 2023 Feb;180(2):252-271. doi: 10.1002/ajpa.24564. Epub 2022 Jun 25. PMID: 36790744; PMCID: PMC10083917.

We were given only definitions related to polygenic traits and non-mendelism under classical genetics but I did not think of it this way. I think the only way to confirm that the phenotype is altered is crossing with another individual and studying the progeny, right?

DNA methylation: When a methyl group is added to a promoter region of a particular gene, expression of that gene may be suppressed. For example, when two cells have the same genotype, one may exhibit a different phenotype because no particular gene is expressed due to DNA methylation.
Histone modification: Chemical modifications of histone proteins (e.g., acetylation, methylation, etc.) regulate how closely the DNA adheres to the histone. This can regulate the expression of genes and alter their phenotype


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What are ways to measure carbon fixation of microalgae?
So I am conducting a very simple experiment about microalgaes, particularly their biofixation of carbon dioxide. In a small compartment, where microalgaes are suspended in water with an air pump that supplies carbon dioxide for growth and development.

What are possible techniques to measure the biofixation rate that utilizes less highly specialized equipment as much as possible?
Is it also possible to conduct gravimetric analysis to measure biofixation?

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Chromosomes in humans and chimpanzees
I am reading a book titled 'Critical Thinking Skills for Dummies' by Martin Cohen, in which I came across this passage:
'Although humans share 98 per cent of their genes with chimpanzees, they share precisely 0 per cent of their chromosomes -and chromosomes are what actually do things.'
Is this correct?

List item

If he did, that's a really dumb thing to say, and there is an extreme lack of critical thinking present in that statement. Chromosomes are a bit like houses, houses where genes live. Genes are "what do things"; chromosomes themselves are inactive. Here you can see an example of a human and a chimpanzee chromosome, and an brief explanation of chromosomes and genes.

@anongoodnurse that (that chrs are inactive) is an odd statement. Chromosomes and genes are not distinct things, genes are DNA sequences, and chromosomes are large stretches of DNA sequence. Genes are chromosomes in the sense that my arms are me. So no, chromosomes are not inactive. Perhaps a closer analogy would be that chromosomes are books that contain many sentences. Some of the sentences are nonsense, and some carry meaning (genes). Yes, it is the ones that carry meaning that "do things" but the book isn't inactive as it is made up of the bits that carry meaning and those that don't.

Minor nitpicking aside, I have to agree with anongoodnurse's sentiment: that sentence is nonsensical. I don't understand how the author decides to quantify whether or not chromosomes are "shared". Is that in terms of sequence? Gene complement per chromosome? Order of the genes? Can you clarify what the specific claim you are asking about it? The statement as a whole is neither true nor false because it is nonsensical. Is there some context to clarify?

@terdon - Your analogy is better, true. Chromosomes are "inactive" in so far as switching to your analogy) the book is closed. You can't read a closed book; it must be opened in order to have phrases read and meanings understood. So, too, must the chromosome be "opened" to let the genes out. The book houses (and contains) the words. Chromosomes house (and contain) the genes. But yours is the better analogy. Regardless, we are both aware of the stupidity of that statement alone. It may be explained further, but I couldn't locate it with searxching.

Perhaps the author is suggesting you should critically think to ignore his book.

This might be an exercise in logical fallacies and arguments. I wish we had the exact wording so that the context could be read. All we have is a paraphrase. The author doesn't seem to be an idiot, although he appears to deny climate change as an argument from authority...

@anongoodnurse or terdon (sorry only 1 tag allowed), I do think it would be helpful if one of you could write an answer, since this is a good faith question and there is a clear answer. Then that could settle it. No one seems to be of the opinion that this is a homework-style question, if only due to the incredulity that we collectively feel towards what this Cohen character is saying.

@terdon see above

@MaximilianPress I can't answer since I don't understand the question. If the question is "is it actually chromosomes that 'do things'?" then it isn't even answerable since that is a nonsensical question. If it is "do humans and chimps share their chromosomes", then we would need an explanation of what is meant by "shared" in this context. In its current state, the question is too unclear to be answerable.

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How do we see the violet color?
Here is exactly the same question with an accepted answer. However, that answer looks wrong (I can’t find the “alert moderators” button). Firstly, it refers to a dubious source. Secondly, it contradicts this answer, which states that L cones do not have increased sensitivity in the violet area. This is also evident from the pictures on Wikipedia [1] [2].
The question is further complicated by this source. In it, the relative sensitivities of the M and L cones are exactly the same for violet.

How do we distinguish the color violet from blue? If a source of monochromatic deep red color is added to a source of monochromatic far blue color, will the effect be equivalent to the violet color?

Does the answer at https://biology.stackexchange.com/questions/51870/can-red-cone-cells-actually-see-much-red-light help?

Or https://biology.stackexchange.com/questions/26216/advantage-of-opponent-color

Or note that while "the relative sensitivities of the M and L cones are exactly the same for violet" may be true, this is not true for blue, and that's how you tell them apart.

Links are useful and I agree with the assumption. But here https://biology.stackexchange.com/a/85105/80210 the adopted answer with a positive rating contradicts this.

Okay; this isn't a very good place to complain about that. 4 users including the question asker found it useful, that's what the "rating" means. Other commenters have also pointed out an issue with it. Note that various plots of "cone sensitivity" come with different assumptions: with the eye or in a dish, for example, so you wouldn't expect them to all look the same.

Another related question: https://biology.stackexchange.com/questions/56385/how-are-colors-outside-the-standard-rgb-color-scheme-perceived

The fact that an accepted answer is incorrect does not justify reposting the same question. Acceptance is in the gift of the original poster — it doesn’t mean the answer is correct. Upvotes for an incorrect answer are annoying, but a limitation of the SE model. All you can do is downvote the accepted answer and explain why it is incorrect. To bring it to the list attention, provide an answer yourself, or perform a minor edit on the question (add or remove a tag, if you have the privilege or ask one of us).

Does this answer your question? What is violet color?

That answer looks wrong. It refers to a dubious source beause L cones do not have increased sensitivity in the violet area.

Color perception: There are several competing/complementary theories of color perception: the most popular, trichromatic theory, being complemented by the opponent process theory. There is also Land’s Retinex theory and Goethe’s (yes, that Goethe) Theory of Colors.
According to Peter Vishton: (Teaching Company, Secrets of Human Perception)
Overall, the opponent process theory of color complements the
trichromatic theory of color. The trichromatic theory explains the
retinal receptor level, whereas the opponent process theory explains
processing in the lateral geniculate nucleus and the visual cortex
The perception of color by the human brain is an extremely complex interplay of many functions of which the frequency and intensity of light entering the eye is only one. (Do you remember The Dress)   Color is an artifact manufactured by the brain. How the brain interprets color depends on, amongst other things, the ambient light, surroundings, shadow and contrast.  A white table cloth appears white when illuminated by daylight, but also when illuminated by a yellow light for example a candle.
Edwin Land (of Polaroid fame) performed many experiments: Land
In one set of experiments, the illumination was adjusted so that, for example, a white area of one Mondrian sent to the eye exactly the same triplet of radiant energies as a green area of another Mondrian. The two areas continued to appear white and green. Retinex Theory
However, to answer your question from trichromatic theory:
The receptors send a series of impulse to the brain proportional to their response to the frequency and intensity of the light striking them. The brain interprets the color it sees by comparing the levels of response from the various receptors. Different relative levels are interpreted as different colors. So, from your diagram S=10%, M=0.5%, L=0.5% activation is interpreted as violet. Rods will give a measure of the total intensity of light for comparison.

If you consider the sensitivity of the different receptors to violet light, the output from these is a unique combination that is sent to the visual cortex. There is no other possible light source that will produce this array. The brain has no trouble labeling this as violet.
Blue light would send S=100%, M=10%, L=5%    (This assuming log10 scale)
Adding blue light to red will give magenta - for which there is no single monochromatic color.

I refer to the comment of Bryan Krause and the data you provided:
If the M and L cones respond similarly for violet, and dissimilarly for blue, then that is a simple explanation for how you tell them apart.

Ryan Unfortunately that statement is also true for green (550nanometers) although the blue S is much less intense.

Your answer is excellent, Rich, especially in explicitly naming trichromatic theory. Besides upvoting it myself I don't have much more to do here; this answer was never developed properly, and was just drawing attention to a comment


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What is on these Dryas leaves?
I saw these Dryas (octopetala or integrifolia, I'm not sure) in Svalbard. They have some white substance on them. At first I thought it was a fungal infection, but then looking at them under the microscope it looks like salt excretion. Is that something Dryas can do? What's going on here?

Is the Dryas healthy? It could still be fungal, just internal and starting to break out of the leaf. Could be salt secretions (don't know if Dryas does this), could be wax. Since you have a microscope, could you put some on a slide and take some photos?

Crystals look like crystals (especially under magnification), fungus looks more like fuzz/hair. A wet prep is easy; make a saline solution (1 tsp. table salt in 2 cups water), scrape the fuzzy stuff and stir it into solution. Put a drop on a clean slide and cover with a cover slip or another clean slide. Hyphae have a very distinct appearance. Let us know what you find!

Unfortunately these pictures are all I have. I took them when I was still on-site, and Svalbard prohibits taking plant samples off the island, so I couldn't bring any home with me. I tended to see the white substance on all the leaves of an individual plant, rather than on individual leaves on different plants. I haven't found any mention of salt excretions in Dryas literature, but I may be looking in the wrong places.


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Number of autoregulation and FFL motifs in a network
Suppose we have a network with N* nodes (N* is the number of internal nodes). Every directed link in this network exists with probability p. What would be the number of:

motifs that are auto-regulatory?
feed-forward loop motifs
feed-back loop motifs

that looks like a homework problem. please see http://biology.stackexchange.com/help/homework on how to modify your question

Yes it was a homework problem. Thank you for the link. I am new in the whole stackexchange thing. I read it's ok that I answer my question though, now that I know how.

The average number of auto-regulatory motifs (self-edges), is equal to the number of edges E times the probability that an edge is a self-edge which is $p_{self}=1/N$, with N being the total number of nodes. Therefore, $<N_{self}>_{rand} \approx E/N$
& 3. According to U.Alon's book ("Introduction to Systems Biology"), the mean number of times that a subgraph G occurs in a random network is given by the following formula: $<N_G>\approx a^{-1}N^n p^g$.

Explaining what each term of the formula means:

α: is a number that includes combinatorial factors related to the structure and symmetry of each subgraph, equal to 1 for feed-forward loop (FFL) and equal to 3 for feed-back loop (FBL)
$N^n$: is the number of ways of choosing a set of n nodes out of N. Because there are N ways of choosing the first one, times N-1$\approx$N ways of choosing the second one, and so on..(this approximation is true for large networks)
$p^g$ : is the probability to get the g edges in the appropriate places (each with probability p)

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Why is iodine used for metabolic hormones?
Iodine and related biological iodine-carrying hormones are phylogenetically very old, at least according to Wikipedia. Humans use iodine as a metabolic indicator, as do axolotls and apparently most multicellular life.
So why? Growth hormones, sex hormones, et cetera don't require strange heavy elements not used for anything else. It's not a requirement of transcription factors that they contain iodine.
All I've got for hints is that selenium forms an essential part of deiodinases, as well as forming an essential part of thioredoxin reductase. Thioredoxin is a component used to reduce things around the cell, like thiols and RNA bits and so on and so forth, which I could see being worth the evolutionary cost of running down some selenium.
What's the point of iodine? People have iodine deficiency 'all the time' (it's common enough to be named). Is that a product of agriculture somehow? Are there any advantages to using iodine for metabolic hormones? If there are, what are they?

It's an interesting question, though I'm not sure it's answerable. This may be vaguely insightful (I have only read the abstract): http://www.ncbi.nlm.nih.gov/m/pubmed/7381861/?i=2&from=/684433/related

It may not be correct to say that iodine is a requirement of metabolic hormones; I imagine that the evolution of another system is entirely feasible. Perhaps it's a remnant of some species that had access to excess iodine, which provided a mechanism to easily create a different tyrosine-derived hormone to fill some niche.

There are two possiblities. Either iodine is useful in its own right in some way, or lack of iodine is not a concern. I don't know enough about iodine metabolism, excretion etc to know if iodine deficiency is even a thing in nonhuman animals. If it's not a thing, what is it about humans that makes them susceptible? Is it agriculture or something?

Thyroid hormone functions generally require they bind to specific receptor proteins, and some of these receptors undergo specific conformational changes that alter activation/repression dynamics in the nucleus. Iodines might assist in that respect, esp. given Canadianer's article.
http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/thyroid/receptors.html

The specific receptor proteins are tuned to recognize thyroid hormones containing iodine, yes. Most transcription factors don't require a rare trace element, and there's a distinct fitness cost to it(at least in modern humans). So what's the payoff? Why do most multicellular organisms use such a specific and rare element? HGH, leptin, ghrelin, etcetera all don't require iodine. Other evolutionary solutions are possible

Interesting, but the question is too broad I think -- not all metabolic hormones contain iodine. (Insulin, glucacon, glucocorticoids, leptin are examples.) And thyroid hormones have effects on growth and development too. It would be better to phrase it specifically about thyroid hormones.

@Roland That's precisely what I mean. Not all metabolic hormones contain iodine, but some do. For some reason iodine is conserved even though it's not actually required for signaling, as demonstrated by HGH, leptin, etc. There's a drawback to using iodine(sometimes it's not there), and yet it's conserved. What's the benefit that balances out the fitness penalty of requiring iodine to grow properly?

Iodine in us
Iodine is found in two main hormones, T3 and T4. They affect every part of the body, and are important for cell-cell signaling. Wikipedia says:

The thyronines act on nearly every cell in the body. They act to increase the basal metabolic rate, affect protein synthesis, help regulate long bone growth (synergy with growth hormone) and neural maturation, and increase the body's sensitivity to catecholamines (such as adrenaline) by permissiveness. The thyroid hormones are essential to proper development and differentiation of all cells of the human body. These hormones also regulate protein, fat, and carbohydrate metabolism, affecting how human cells use energetic compounds. They also stimulate vitamin metabolism. Numerous physiological and pathological stimuli influence thyroid hormone synthesis.

Why do we have iodine in these hormones?
This is really what your question is. I have found several articles about this and what I found is Iodine is an important catalyst, and Iodotryosines evolved to be important hormones
First, of all, the use of iodine in organisms was ancient. Many prokaryotes and protists used it as a way to deal with reactive oxygen species. Iodide peroxidases were present in primitive oxygenic and photosynthetic Cyanobacteria about 3 - billion years ago. This is because Iodine is one of the most ancient antioxidants.
The thyroxine-like hormones seems to have evolved some 4 Mya in unicellular algae. However, its original function was not for cell-cell signaling as is the case for T3 and T4. It was originally to catalyze other biochemical reactions and scavaging  free radicals. This all came about when tyrosine was first created. Iodine reacts with the tyrosine, and forms iodotryosines that were important catalysts for many biochemical reactions.
The first use of Iodotryosines for regulation could have been for ATPase in the mitochondria for non-verterbrate organisms. Also, for vertebrates, the regulation of mtRNA was regulated by iodotryosines.
Iodotyrosines can diffuse between cells very easily, and the development of TH-receptors leaded to the development of thyroxine hormones. Such hormones were used first for embryological development, metamorphosis (if this is the correct term) of amphibians, and more. The rest is really evolution! These hormones are present in virtually all organisms (except prokaryotes).
Summary
In summary, the use of iodine in hormones started with iodine in the first cells as they provide protection against free radicals and reactive oxygen species, while catalyzing biochemical reactions. Iodotyrosines evolved to be important for regulation in cells and finally important in cell-cell signaling.
If you have any more questions, please ask in the comments or we can chat in the Biosphere.
References
These are my sources and there is much more information on these articles. Note that I am not chemically correct about the form of iodine used so these articles have the correct information
http://m.icb.oxfordjournals.org/content/early/2009/06/23/icb.icp053.full.pdf
http://ign.org/cm_data/2011_Venturi_Evolutionary_Significance_of_Iodine.pdf

Iodine helps balance out ROS production of metabolism, so when iodine is present, grow. That helps explain pretty much everything, I think. Nice answer.

Classical thyroid hormones implement a very flexible signaling mechanism. Basically, they comprise two aromatic rings that are connected via an oxygen atom. Optionally, they may contain organic side chains and inorganic iodine atoms.
In the case of iodothyronines, which are represented e.g. by the well-known thyroid hormones T4, T3 and 3,5-T2, the side chain contains an amino group and a carboxylate group. Therefore, iodothyronines are amino acids. Up to four different hydrogen atoms (two at every ring) may be replaced by iodine atoms, and the resulting pattern of iodination determines their biological activity. Generally, iodination of the inner ring and deiodination of the outer ring results in high biological activity (e.g. in T3 and 3,5-T2), whereas iodination of the outer ring and deiodination of the inner ring delivers a receptor-blocking thyroid hormone (e.g. reverse-T3). There are three deiodinases encoded by the DIO1, DIO2 and DIO3 genes that catalyze the "step-up" and "step-down" reactions to active or inactive thyroid hormones, respectively. Multiple molecular processes are able to differentially upregulate and downregulate tissue deiodinases. Therefore, thyroid hormones are subject to both global and local control.

Removal of the amino group results in iodothyroacetates. Their biological effects are similar to those of iodothyronines, but in addition to nuclear receptors they also have a strong effect on membrane-bound receptors, which are only weakly activated by iodothyronines.

Thyronamines lack the carboxylate group. Their biological effect is different to that of iodothyronines and iodothyroacetates. By activating the membrane-bound TAAR1 receptor they have an effect that is in most respects antagonistic to that of classical thyroid hormones. Thyronamines seem to be most active in deiodinated state.

Summarizing, both organic and anorganic modifications are able to modulate the effect of thyroid hormones. This mechanism is a very effective way to encode a high  grade of information entropy in rather small molecules.
References
Gereben B, Zavacki AM, Ribich S, Kim BW, Huang SA, Simonides WS, Zeöld A, Bianco AC. Cellular and molecular basis of deiodinase-regulated thyroid hormone signaling. Endocr Rev. 2008 Dec;29(7):898-938. doi: 10.1210/er.2008-0019. PMID: 18815314
Engler D, Burger AG. The deiodination of the iodothyronines and of their derivatives in man. Endocr Rev. 1984 Spring;5(2):151-84. PMID 6376077.
Piehl S, Hoefig CS, Scanlan TS, Köhrle J. Thyronamines--past, present, and future. Endocr Rev. 2011 Feb;32(1):64-80. doi: 10.1210/er.2009-0040. PMID 20880963.

This answer is great. It's technically complete and well-sourced. It doesn't actually answer the question I asked, but that is its only fault.

here is an interesting article:
The accumulation of radioactive iodine by Amphioxus
summarizing the abstract: it's about cephalocordates that are not vertebrate, so they are close relatives (most related to the ancestors of) the vertebrate. The specific cephalocordate in question is amphioxus.The article talks about a specific gland called the "endostyle" of Amphioxus and it explored the homology with the subpharyngeal gland of the larval form of lampreys (an agnathan, the most primitive of vertebrate) called ammocoete. The sub pharyngeal gland is sort of the same thing as the thyroid. In fact this sub pharyngeal gland or thyroid is a defining characteristic  of vertebrate. The abstract describes an experiment where they took the endostyle from amphioxus and implanted it into a salamander (and amphibian) and it had effects similar to the thyroid gland. This means that this mucous producing gland in the cephalocordates produces compounds that have effects similar to the thyroid
Why does the endostyle produce mucous? Because it is essential for their filter feeding (feeding by straining suspended matter and food particles from water).
Why concentrate iodine in the mucous, I don't know.
The other answers explain the function of iodine. This answer was to explain the evolution of iodine concentrating glands at the very beginning of our vertebrate ancestors.

Have a look at the article, I found an open source (linked above).

nice! full text definitely beats abstract...

I went back and reread this paper, and it looks like the thyroid started as a gland that secreted mucus into the gut, so any signaling molecules would have to be gut-resistant, ruling out proteins and so on. Still not sure why iodine exactly, but this has helped narrow it down for me substantially. Nice find.

yea, and just for a comparison I guess GI peptide horomones are secreted into the blood (or lymphatics?)... given high blood flow to the GI when eating the guts get some of the peptide horomone back... presumably endostyle secretions were secreted into the gut and not the blood...

you know I've never read anything about GI peptide horomones (CCK, secretin, gastrin, GLP, etc) in primitive cordates...

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text:
How does a virus take control over the host cell?
When the virus integrates its DNA with the hosts and enters the lytic pathway, do the viral proteins that produced destroy the cells DNA? Do they deactivate it? Also does the cell function in the same way as before?

A virus does not typically destroy its host's DNA. Rather, the virus makes the host cell express viral proteins at an elevated rate compared to the host's own proteins. This is usually achieved because the viral genome contains a strong constitutive promoter, possibly coupled to an enhancer sequence. The virus may also preferentially insert itself into transcriptionally active sections of the host DNA.
As I said earlier, expression of the host's own genes as a whole is not directly regulated by the virus, though specific genes may be up- or down-regulated (immune-system related genes are often primary targets). However, the host's genes will usually be expressed at a reduced level because of the resources being diverted to make virions.
Remember however, that the virus relies totally on the host's machinery to make viral proteins. So, anything that kills the cell before sufficient viral particles are assembled is going to be selected against. This doesn't mean that the cell is healthy though. A significant chunk of the cell's resources have been hijacked by the virus, and a virus infected cell is typically just limping along, clinging to life, as it were.
Depending on the virus, once sufficient virions have been assembled inside the cell, the virus may enter a lytic phase, where the cell literally bursts to release the virions into the surrounding environment to infect new cells. At this point, the cell is obviously dead.

"The virus may also preferentially insert itself into transcriptionally active sections of the host DNA." I'd be interested in reference, it doesn't sound familiar to me. Any text book should do.

"However, the host's genes will usually be expressed at a reduced level because of the resources being diverted to make virions." Is there some textbook page addressing this?

RE "So, anything that kills the cell before sufficient viral particles are assembled is going to be selected against." Very interesting, refering to the question which erroneously sees integration of DNA into host genome as a rule and not the exception: "selected FOR" then should be the integration of DNA into the genome, as well as replication of virus by live replication of the host. Interestingly, it does not at all seem clear in science that integration into DNA depends on or is made possible by  the cell dividing.  "Transcriptionally active" : with the intention to divide, to cross-over?


text:
Non toxic low melting point alloy
I am looking for an alloy with low melting temperature (< 350°C) which is not toxic when in direct constant contact with skin, food and overall in domestic environment. My application is a solder that can be used for soldering a ring.

I'm not a metallurgist, which you should probably ask... but there is this that I found:
Low Melting Fusible Alloys
Both Cadmium and Lead are toxic, but Bismuth, Indium, and Tin are not. An alloy of those might be what you're looking for. Indium raises the price-point considerably, as it's a few magnitudes more expensive than Bismuth and Tin.

Metallurgist will most probably tell that toxicity is for biologist or toxicologist and there is no stackexchange for metallurgist yet

Rather than a metallurgist I would probably ask a jeweler... they should definitely know what they are allowed to use.

@nico: just tried contacting jewelers, though not sure if they use low melting point alloys

@tig: right, did not think about that


text:
What part of the brain controls depth perception?
Specifically the part of the brain that does depth perception based on binocular vision. I have searched all over the web and have turned up nothing. Is it the same part of the brain that processes all images from the retina?

Some regions of primary visual cortex (V1; physically at the very back of the cortex) respond to visual stimuli present in either eye. These are called "binocular" regions, for obvious reasons. Some of the neurons in these regions are "disparity-tuned", in the sense that they respond most strongly when a stimulus is present on both retina, at a particular retinal distance apart. This has been known for cats for some time (Fisher & Kruger 1978). The suggestion is that information from disparity-tuned neurons are used for depth discrimination (Ohzawa et al. 1990).
There may be other mechanisms as well, which use relative motion and ocular convergence to estimate distance.


text:
Modeling yeast biochemical pathway using enzyme kinetics
I need enzyme concentration and metabolites concentration values to en-corporate these values in my model and do some simulation.
I searched through some database
yeast metabolome database http://www.ymdb.ca/
brenda and other enzyme databases for enzmye conc
and also did some literature search
but couldn't find much of data
where possibly i can get these data ??
is there any other way to do simulation without data.

You should take a look at SGD (the Saccharomyces Genome Database), and in particular YeastCyc. Some protein information pages at SGD give estimates of molecules per cell taken from this Nature paper.
Added later in response to some comments:
The question asks about levels of metabolites and of enzymes, not of transcripts. Microarray data can be, at best, only a guide to levels of proteins. Estimating the levels of metabolites from microarray data is a complete non-starter since there are entire layers of regulation that will be ignored. Just to give one example of a pitfall in this approach: you could have high levels of transcript from which you could you could infer high levels of enzyme, but that enzyme could be inactivated by a post-translational modification.

can't find much of data on YeastCyc and even

try approximating from microarray or RNAseq data.. they are available in GEO and SRA

Can you elaborate or cite a paper how to estimate concentration of metabolites mainly present in  this pathwayubiquinone synthesis from microarray RNAseq data. If any body have done similar thing and documented it please let me know.


text:
Could cancer be in itself a evolutionary process?
Could cancer be in itself a evolutionary process? Maybe in some way could it be a process of variation? Or would this idea be completely without support, if so, why?
I don't mean that each case would lead to evolution, but that within an entire group of organisms, it could lead to case of of individuals developing ways to resist what caused the cancer, maybe in cases of individuals beating the cancer or in cases of successive generations of off spring from individuals with cancer?
Could it be possible that in rare cases it could lead to the development of new organs or specialized cells?

Probably, I could imagine these rebel cells as Che Guevara comrades trying to destroy the Big Brother police state. Alex Jones except of the fact that he is a CIA tactician could be easily a virus ;)

Interesting question. I believe it definitely is an evolutionary process. unicellularity breaking away from a multicellular life.
There are two examples that I can think of, which can support this argument:

Hela cells: Hela cells have been classified as a different organism because they have the ability to grow outside the host indefinitely and their genome is different from Homo sapiens. Hela cells also have a new scientific name- Helacyton gartleri
Transmissible tumors: two tumors have been known to infect other hosts and therefore can be called obligate pathogenic lifeforms. One is Devil Facial Tumor Disease which infects Tasmanian devils and gets transmitted by biting. Another is Canine Transmissible Venereal Tumor which infects dogs and spreads via sexual route.

Could it be possible that in rare cases it could lead to the development of new organs or specialized cells?

Cancer as of now has a pathogenic identity. It is a simplistic process which in a thermodynamic point of view can be described as maximization of entropy(disorder) and thereby increasing the stability [like the way solutes diffuse]. If a cancer has to give rise to a new functional organ then it has to be supportive of the ordered lifestyle which it is trying to break away from in the first place. It may adopt a pathogenic lifestyle initially and then may redevelop order. I don't know of any such evolutionary event but it may nonetheless be possible.


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Problem on finding sequence of Taq polymerase
As i know, Taq Polymerase can be found in Thermus aquaticus, so i do a search for protein list of Thermus aquaticus and have this : http://www.ncbi.nlm.nih.gov/genome/proteins/1724?project_id=55053 . After filter for 'polymerase' i found a lot of protein named polymerase :

DNA polymerase beta domain protein region
DNA polymerase I
DNA polymerase III, alpha subunit
DNA polymerase III, beta subunit
DNA polymerase III, delta subunit
DNA-directed DNA polymerase
-.....

I don't know what they mean and which is the protein i'm looking for ?

After click on one of them i have the sequence not in A-T-G-X format :
ORIGIN
        1 msgvdallll gvelsraiit aysvyaivli lggflarlpt rweervealg gsfylagvil
       61 wryyaggday dldlflrasg mallvlprlv rvvlreyggg r
What does it mean and how to working with it ?

According to the paper here "Taq polymerase" is the DNA polymerase I from Thermus aquaticus. (Incidentally the paper has the complete sequence of the gene in question.)
You can find a protein sequence entry at NCBI here. This shows the sequence of amino acids in the protein, not the DNA sequence of the gene. Several lines from the top you will see:

DBSOURCE    locus TTHDNAP accession D32013.1

with the last word highlighted as a link. Follow that link to the DNA sequence. That entry includes the line:

CDS             1..2499

which tells you that the initiator ATG of the gene is right at the start of the sequence shown, but that the 3026 bp sequence includes a lot of downstream DNA. If you click on CDS on that line it will highlight the coding sequence in the DNA.
A very cursory comparison of this sequence with the one in the paper that I linked to suggests that this is the same gene.

Thank Alan Boyd so much, below is the answer for these protein code mean:
    A  alanine               P  proline
    B  aspartate/asparagine  Q  glutamine
    C  cystine               R  arginine
    D  aspartate             S  serine
    E  glutamate             T  threonine
    F  phenylalanine         U  selenocysteine
    G  glycine               V  valine
    H  histidine             W  tryptophan
    I  isoleucine            Y  tyrosine
    K  lysine                Z  glutamate/glutamine
    L  leucine               X  any
    M  methionine            *  translation stop
    N  asparagine            -  gap of indeterminate length

Source from NCBI : http://www.ncbi.nlm.nih.gov/BLAST/blastcgihelp.shtml


text:
Why a repeat wasp sting cause an anaphylaxis shock?
I understand that an anaphylaxis shock caused by a huge dose of histamine. But why the first sting does not cause an anaphylaxis shock like the second sting? As i think there may be a relevant between antibody and histamine because the victim already have antibody presence in the second sting, is that right and what is it?

It probably has to do with the amount of toxin. It isn't alway a gradient, it can be like walking up a hill (mild response) until you get to the top and jump off the cliff (anaphylactic shock) on the other side.

The reason is the way anaphylactic shock is caused by massive release of certain cytokins as well as inflammatory mediators such as histamine by two types of white blood cells: mast cells and basophils. This release is triggered by the binding of immunoglobulin E (IgE) to the antigen (the foreign substance provoking the allergic reaction). Antigen-bound IgE then activates so-called FcεRI receptors on the mast cells and basophils. IgE molecules specific to the allergen provoking the allergy are not present in the blood in sufficiently large quantities until after the first (several) exposures to this foreign material. Initial exposure triggers IgE production by specific B-lymphocytes. Only once one or more exposures to the antigen have occurred will there be sufficient quantities of the relevant IgE to trigger this excessive mast cell and basophil reaction.


text:
Are there more/less favourable phases of menstrual cycle to donate blood?
I was wondering whether it makes a difference when during the menstrual cycle a female is donating blood in terms of:

Blood quality (iron or hormones levels)
Her health/safety

I am aware that females can donate blood during menstruation as the blood they lose does not directly come from circulatory system and the amount is not that big after all. As for the hormones - their levels do change considerably during the cycle and can affect a whole range of things. Can they also affect the blood quality or are such fluctuations rather negligible?

1)
Hormones involved with Menstruation (FSH, LH, Estrogen, Progesterone, etc.) will vary depending in concentration depending on the time-frame:

You are correct in saying that not much blood is actually lost in the menstrual fluid: Less than 80mL (80cc), although the blood's origin is ultimately the circulatory system. Does it affect the quality of the blood? No. Usually not enough iron is lost during menstruation to make a difference between being able to donate blood and not donate. However, women who bleed heavier than the average can experience anemia (iron deficiency) - although anemia attributed to menstruation is often misdiagnosed gastrointestinal issues (up to 86% error rate).
One thing to consider is that common pain medications can affect blood content, and thus a woman taking aspirin cannot donate platelets for 5 days after she stops, and a woman taking NSAIDs (like Ibuprofen) cannot donate for 2 days after she stops.
2)

...the combination of blood loss from periods and donation will make iron deficiency anaemia more likely, particularly if the periods are heavy or prolonged. This effect can be minimised by taking supplemental iron.

In general, as long as the woman feels well or the pain is controlled, she is perfectly capable of donating as long as her iron levels reach the minimums. The blood makeup is not significantly different, although hormone and iron levels will minimally fluctuate.

As always, this response is based upon information during some light research. I am not a doctor, and the information presented in this response may be modified later to increase accuracy or remove errors upon the discovery of new information.


text:
copper vs aluminum, what's the safest for health?
I'm working on a mini project for a milk dispenser machine, using a peltier device to cool the milk down, I have to choose between a copper or aluminum cooling block (see pictures bellow).
But I'm worried about health issues in the long run, (oxidation and stuff), I have no idea what to choose.
What would you guys recommend me ?

What are the temperature and pressure conditions of the milk coming in and out?  With Cu oxidation could occur, and I would be less inclined go with it.  Al is already going to be oxidized, but Al2O3 is harder and on the outside of almost any Al product.  The only downside with Al are possible correlates with neurological disorders, and that would be over lots of exposure (probably not nearly the dose from deodorant).

Household water is typically run in copper pipes.

@AtlLED Pressure would be gravity based, not really high, and temperature around 0°C (~32°F). The neurological thing you mentioned is scary stuff, looks like maybe copper is safer based on kmm's comment ?

@kmm I think that copper piping is only a good solution so long as you have very clean and controlled water running through it (as is common in the US).  Just searching about copper pipe corrosion show examples of where that can go bad with just water, let alone milk (see my answer).

Assuming the answer can't be C) Stainless Steel I would go with Aluminum.
The USDA specifically mandates (1) stainless steel 300:

"Milk contact surfaces shall be made of stainless steel of the 300
  series, equally corrosion-resistant non-toxic metals or heat-resistant
  glass."

Is the copper tinned?  From what I can tell after reading some old sources (2) un-tinned copper will be corroded by milk.  You have the advantage of a cool temperature lowering contamination risk (3), but many states following the FDA specifically removed the allowance of tinned copper (Sec. 22-201).
While the effects of life long dosing of Al are becoming more and more clearly tied to Alzheimer's (4), the effects build up over time.  Copper has a tendency to be more acute (5) and pronounced (6, 7), and further it can tasted in low amounts  and discolor the food (8).  It can be said that water flows through Cu pipes, but soda is put in Al cans.
The research for this has been quite enjoyable, and led to things I didn't even think of.  A alternative cleaning site has even recommended using milk to clean Cu pans.
Again so my final recommendation is to follow USDA guidelines and use stainless steel, but my second choice would be Aluminum.
Citations:
(1) USDA. 2011, July. Milk for Manufacturing Purposes and its Production and Processing.
(2) US DOC. 1917, April. STRUCTURE OF THE COATING ON TINNED SHEET COPPER IN RELATION TO A SPECIFIC CASE OF CORROSION. Technologic Papers OF THE Bureau of Standards.
(3) COMMITTEE ON COPPER IN DRINKING WATER, NATIONAL RESEARCH COUNCIL. Copper in Drinking Water. NATIONAL ACADEMY PRESS. 2000.
(4) Walton, J.R. Aluminum Involvement in the Progression of Alzheimer's Disease. Journal of Alzheimer’s Disease 35 (2013) 7–43. DOI 10.3233/JAD-121909
(5) Reilly C. The dietary significance of adventitious iron, zinc, copper and lead in domestically prepared food. Food Addit Contam. 1985 Jul-Sep;2(3):209-15.
(6) Conor Reilly. Metal Contamination of Food:
Its Significance for Food Quality and Human Health. Pg 50. John Wiley & Sons, Apr 15, 2008
(8) ibid pg. 16
(7) Lee A. Price, et al. Chronic copper toxicosis presenting as liver failure in an Australian child. Pathology. 1996, Vol. 28, No. 4 , Pages 316-320 (doi:10.1080/00313029600169264)


text:
Axial skeletal system
I was curious about a fact given in my biology textbook as to why the Japanese have  3 pairs o floating ribs unlike the rest who have just two?

Because your textbook is probably worded poorly.
It appears that the Japanese (and several other ethnic groups) apparently have a higher proclivity for the 10th rib to be a true floating rib, but every ethnic group has the chance of having a floating 10th rib.
With that said, the one McGraw-Hill book cited in the Wiki article is the only source I've seen for this higher morphology rate. I, personally, wouldn't trust just one source, and (if true) the rate may not be much higher.


text:
Is this some sort of fungus?
There is something strange growing straight out of the glass windows at work. They look like hairs, about half an inch long, and each have a white spot on the tip of them, slightly weighing them down. I first saw a few of them a week ago, and now there's about twice as many. They don't move, except when blown in the wind, etc.
Here's just a few of them, the first ones I discovered:

They haven't budged from this spot since I first discovered them, but more have appeared surrounding them. This is located in Louisville, KY, USA, and there has been some hot humid weather lately. This particular area where they're growing is in the shade and a partial roof, so these windows rarely ever get rained on.
A friend hinted that they might even be insect eggs.
What are these things? Fungus? If so, what kind?

Looks like a couple mold sporangia. I have no way of making an ID though.

@CMosychuk That makes sense (now that I look at pictures of them). Also since that area never gets any rain (but plenty of moisture in the air).

@CMosychuk But now that I look a bit more, I don't think so. A) None of these have any appearance of any sort of root or anything holding it on, and B) None of them are grouped together or growing two at once. They're all stand-alone.

I'm imagining some isolated spores blew in with the wind and attached. That would essentially illustrate how a colony gets started. Those fruiting bodies will eventually release spores of their own and you'll find more stalks over time (and eventually more features of a mold colony). I'd just use some bleach water and clean it off.

Now that I think about it, there is some field of fungus growing in the woodchips about 10 feet away. Those ones look a bit more developed, and look like light orange bubbles.

The ones growing a bit further away look like this: http://my.kwic.com/~pagodavista/schoolhouse/species/plants/pics/fungi3.jpg

This is definitely not fungus. See a related question here

These are lacewing eggs. Lacewings lay their eggs on stalks.
From wikipedia  :

can you add some sort of reference or other picture for confirmation? Thanks for your efforts.

From the linked article... "Eggs are deposited at night, singly or in small groups; one female produces some 100–200 eggs. Eggs are placed on plants, usually where aphids are present nearby in numbers. Each egg is hung on a slender stalk about 1 cm long, usually on the underside of a leaf."

Two differences - they weren't clustered like that, they were scattered - and also they were on windows, at least a few yards away from any vegetation.

this comment is a little late,but I read about this in a book,then another book,then Buggguide" i think


text:
Exactly what kind of spider is this in Louisville, KY?
I took this photo many years ago, but I guess the year doesn't really matter. It was here in Louisville KY, on the outside of a window, on a web it built. It was a couple hours after sunset in the summer. It was about the size of a silver dollar.

Some people said it's a Garden Orb at first, while recently others say it's a Wood spider. Either way, I'm not entirely sure.
What species of spider was this?

It is an Orb Weaver (Neoscona crucifera). It is found from Maine to Florida in the east, to Minnesota in the Midwest, to Arizona in the southwest, and in Mexico.

Females are about 9.5–19 millimeters (0.37–0.75 in) long, while males are somewhat smaller. The upper surface of the abdomen is brown and hairy. The legs display alternating light and dark brown bands. The undersurface of the abdomen is black, with two white spots.
This species is relatively variable in color and sometimes pattern, but is most commonly seen sporting a rusty-red or golden orange color. The orb-shaped web is very large and is often constructed on buildings and other man-made structures, especially near outdoor lights. This species is most conspicuous in late summer and early fall.

For many years, this kind of orb spider would build a very large web every night just outside the back door (near a light.) While fascinating to watch, if was a lot less fascinating to forget it was there in the morning and walk face first into it. But I prefer to live and let live, so... :)


text:
Can CRISPR knockout of a gene be referred gene inhibition?
Can gene knockout (e.g. by CRISPR) be referred to as gene inhibition? I am trying to use precise words for a manuscript. We first showed siRNA of a gene has effect X. We also found knockout of the gene has the same effect. For the MS, could I say:
Knockout of the gene showed effect X, confirming inhibition of the gene causes X.

This is really a question of English rather than science. Look up inhibition in a good dictionary, do a Google search for “inhibition of the gene” or search your electronic reprint collection to find that no reputable native speaker would ever use that phrase. That is how you check usage in a foreign language. You say you want to be precise. What precisely does knockout do? Remove the gene? inactivate it? Or what? Read a review to find what words are used.

Looking to a standard source of definitions, the Systems Biology Ontology definition of inhibition is "Negative modulation of the execution of a process."
As such, it doesn't really make sense to talk about inhibiting a gene per se. What people are actually doing when they say that is using a shorthand to describe inhibiting either the expression of the gene or the activity of its product.
siRNA fits this quite well, as there you are talking about inhibiting gene expression. Knockout, on the other hand, means the gene isn't there to have its expression inhibited.
I would thus recommend not referring to knockout as inhibition. A better phrasing of your sentence above might be: "Knockout of the gene showed effect X, consistent with the prior result in which siRNA inhibition of the gene also produced effect X."


text:
How could 45 milligrams of a substance equal 4,500 micrograms?
In this book, the author repeatedly states that 45 milligrams of vitamin K2 equals 4,500 micrograms.  I thought 1 mg = 1000 mcg.  How could this be?

It's a typo. 1 mg = 1,000 mcg.

Conversion tool.

I'm voting to close this question as off-topic because it is a trivial question.

@AliceD, It's only trivial if you have a certain amount of experience.  With vitamins and "nutraceuticals", I've seen errors caused by conflating and mislabeling between "mg", "mcg", and "Mg" (where "Mg" was perversely meant to be convey micrograms!) .  This is so serious that the FDA has repeatedly warned about it

@BrockAdams - you may be right, but then again I doubt this is the right forum for these matters.

This is a typo.  In the text he states:

... only 0.120 milligrams (120 micrograms) of MK-4 ...

So, he knows the correct conversion.
Then:

... the "same" product is almost 40 times more potent in one country
  ...

40 times 120 micrograms is 4800 micrograms -- which is close to 4500.
So, that suggests that the (4,500 micrograms) in the table is correct and that the 45 milligrams is a typo.
It should read 4.5 milligrams.


text:
What is a "scutella of reindeer"?
In the film "The Perfect Human Diet" at 32:36, a scientist points to animal remains and states "we've got a scutella of reindeer there."  What is scutella in this context?

Scutella refers to shield or plate-like structure on animals (dictionary.com), such as the scutes of a turtle shell.  I have never seen reference to scutes or scutella or anything similar on any type of deer, including reindeer.
I have not seen the movie so I do not know the context of usage. My gut reaction is the person was trying to make something sound important or "scientific" when a much simpler (and perhaps more accurate) word would have sufficed.


text:
Gene APOA2 SNP rs5082 alleles are A or G, but papers describe it with CC and TT?
rs5082 is a SNP in the APOA2 gene. It is associated with obesity and heart disease risk.
According to this article the alleles can be A or G
https://www.ncbi.nlm.nih.gov/snp/rs5082#frequency_tab
Why does this article only discuss CC or TT?  Where is the A or G?
https://academic.oup.com/ajcn/article/108/1/188/5036568

It is probably a matter of strand. Check which DNA strand authors of both papers refer to - forward or reverse.

The rsID letters are assigned based on the genome being the default "forward" direction while the researchers on that gene think of the nucleotides of the context of the transcript, (or in this case the promotor sequence) which runs backwards.


text:
Are biological systems engineered? They are often reverse engineered at a molecular level!!
Understanding biological systems, molecular biologists need to “reverse  engineer” them. Is this evidence that the systems were engineered to begin with?

No.
So I looked up a definition of 'reverse engineering'. Wikipedia states:

Reverse engineering is the process of discovering the technological principles of a device, object, or system through analysis of its structure, function, and operation. It often involves taking apart something (a mechanical device, electronic component, computer program, or biological, chemical, or organic matter) and analyzing its workings in detail to be used in maintenance, or to try to make a new device or program that does the same thing without using or simply duplicating (without understanding) the original.

How else are you suppose to study something? Anything?
I dont want to answer a question with a question so I will continue. If you are working with a complex system, you will need to study the individual pieces. Although it is helpful to sometimes to look at the system of a whole, doing that introduces many variables that makes it impossible to tell what is really going on.
Some will say you need to do this because biological systems are so complex and that this is 'evidence' for a creator. That is silly. I can agree that biological systems are complex, but that is not evidence for a creator. Complexity is not a good thing. I think sometimes people have a naive view of a cell that it is organized and everything works perfectly and there is precision in everything (or even a lot of things). But thats not true. It is messy. Cells are chaotic. They are a freshman's dorm room. I study splicing, a very complex process.  And I just read a paper where they looked at highly conserved transcripts with no known alternative isoforms. And what did they find? They found that in small amounts every exon was being spliced incorrectly. Sure, most of the time it was spliced correctly. They even called it high fidelity. But the gene they looked at had 5 exons. Consider that the largest gene in humans has over 300 exons, and if all of those are being spliced incorrectly, it adds up. If an exon is misspliced 1/1000 times, and you have 300 exons, that means 1/3 of your transcripts are not what you want. It adds up to a lot of wasted effort by the cell, and it certainly would be better if there was no splicing (or at least less) for large genes.
Thats just one example but you could literally pick any component of the cell and find inefficiency. Sure, 1/1000th is good accuracy fot splicing, but lets have some context. Since we are talking about designers, does anyone here use a watch (designed by mere mortals) that stops working one minute out of every thousand? A computer that shuts down randomly one minute of every thousand? Me either.
Is 'reverse engineering' evidence of a designer? No, its evidence that cells are a mess and we need to separate the noise from whatever it is we want to study.

No. We can reverse-engineer diamonds, or oil, or waves, or the sound of leaves in the wind. Neither of these were engineered. Thus, whether or not we can reverse-engineer something does not tell anything about the origin of the thing.

No. If I wanted to study the sun, I might build a space ship to take me there. Does that mean the sun was put in place by a space ship? I can study your knee using X-rays, does that mean you knee was made by X-rays? The fact that you can use method X to analyze object Y in no way implies that object Y was created using method X.
To take another example, think of balancing rocks like these:

If I were to "study" them I could make the "intelligent" decision (I am using intelligent in the freest possible sense of the word) to poke the thing to see if it is really balancing or otherwise attached. If I were to do so, I would be acting, to use @Jason's terminology, "as an engineer making intelligent interventions and not as a gambler throwing dice". I would choose the place to poke carefully, near the top perhaps, so that it would return a maximum of useful information (fall), I would not just push them randomly. Does that imply that the rock was placed by an intelligent designer?
To go back to your basic question. First of all, we do not "need" to reverse engineer systems in order to understand them, in fact, with very few exceptions, we can't reverse engineer biological systems (which is also taken as "evidence" for intelligent design by the way, in a wonderful example of screwed if you do, screwed if you don't). Most analyses of biological systems consist of observing them.
Anyway, even if we were to reverse engineer that does not in any way imply that the systems were engineered in the first place. That is like saying that if I see you walking down the road today, that implies that yesterday you walked backwards up the same road. If we were to successfully reverse engineer a biological system, that could imply that we are intelligent, but it would imply nothing of the existence of a creator of these systems, let alone the intelligence of such a being.

In regular engineering one begins with a plan to construct a machine that serves a
given function and then builds the machine according to plan. In reverse
engineering, by contrast, one starts with a finished machine and tries to determine
what its purpose is and how it was constructed.
Scott Minnich, a University of
Idaho molecular biologist and prominent proponent of intelligent design, will
often remark in his public lectures that the only way for biologists to understand
the workings of the cell is to approach its various systems as a reverse engineer.
Thus the molecular biologist may take a functioning system in the cell, perturb it,
see how the cell behaves differently to infer the system’s function. Alternatively,
the molecular biologist may interfere at various points in the system’s self assembly to determine how the system is constructed.
In all such cases, the molecular biologist acts as an engineer making intelligent interventions and not as a gambler throwing dice. If we need the science of engineering to understand biological systems, then it wouldn't be a stupid bet that the systems are themselves designed.

With all due respect, this is really a ridiculous argument. An intelligent designer may or may not exist. The fact that we study systems by making intelligent choices however, only implies that we are intelligent, not their designer.


text:
Is the resting state of the forearm in the pronated or supinated position?
It seems to me that my forearm is naturally in a more pronated position than the anatomic (supinated) position and that it actually takes work to make it hold the supinated position. Anyone an expert in human anatomy/physiology here or know of any sources that could point towards a more scientific answer?

The main reason why the anatomic position is supinated is because the radius and ulna are crossed when the arm is pronated and parallel when the arm is supinated. It doesn't have anything to do with the resting state of the arm, it's just the easiest way to arrange the bones neatly for description and analysis.

I agree with the above answer. Also, we all tend to use our forearm more in the pronated form (holding, hand shake, driving, etc) so I guess it becomes second nature to us.


text:
Is lowered blood pressure a primary lethal symptom of an opiate overdose?
When someone has a opiate overdose, they can have no or almost no pulse and can  have shallow breathing or stop breathing. When you stop breathing (for example) by drowning, you can survive for a long time without breathing, so it seems that stopping breathing because of the overdose won't kill very easily.
Is the lack of (detectable) pulse due to the blood pressure going really low instead of the anecdotal explanation that the heart has stopped? Can the low blood pressure be more immediately dangerous than the reduced breathing because it makes the heart's pumping ineffective and cuts off oxygen from the brain?

This is an old question, and has an open bounty so can't be closed, but I would vote to close for lack of research if it didn't. And incidentally, without particular circumstances (e.g., hypothermia), you can NOT survive for a long time without breathing.

Yeah, this is quite a puzzling question the way it is framed, I'd like to vote to close it but can't because of the bounty so I'll just downvote. This shouldn't have been bumped.

Sorry for bump then. I came across this question, thought it was a decent one and wanted an answer.

If it is vote-to-closed as unclear, wouldn't a comment highlighting exactly why it is seen as unclear be useful. At the moment, the OP hasn't gotten any comments on the contents.


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What happens if an IV drip with a saline solution slips out of the vein, but keeps dripping into the body?
A patient has a saline solution IV drip into the vein. They have somehow moved around and the needle has fallen out of the vein, but remained in the body. Nobody has noticed and for a few hours water has accumulated like a balloon in the arm.
What happens? Is it dangerous? If untreated, would the body absorb the water, or would it remain as a balloon / pocket? If a pocket of water forms, what is the treatment?

Is this a question about a real case? Or are you possibly asking about a homework question? (It sounds kind of like that to me)

Real case. I've been sent home with a puppy and an IV. It is the middle of the night. Closest vet is 6 hours away, and only available in the morning.

@caseyr547 above where the needle was inserted. Between elbow and shoulder.

CALL YOUR VET ASAP. The following information is NOT from a medical or veterinary professional. It is based off of human physiology and doesn't necessarily apply to other mammals. I cannot guarantee the accuracy or effectiveness of any information that follows.

They have somehow moved around and the needle has fallen out of the vein, but remained in the body. Nobody has noticed and for a few hours water has accumulated like a balloon in the arm.

This is called "infiltration":

Is it dangerous?

It can be, depending on what was in the IV.

If untreated, would the body absorb the water, or would it remain as a balloon / pocket? If a pocket of water forms, what is the treatment?

Taken from here:
"If the infiltration is severe, you may consider the application of a compress in addition to elevating the affected limb. Check your institution’s policy regarding which type of compress (warm or cold) should be applied. Generally speaking, if the infiltration solution was isotonic, a warm compress is used to alleviate discomfort and help absorb the infiltration by increasing circulation to the affected area. However, sloughing can occur from the application of a warm compress to an area infiltrated with certain medications such as potassium chloride. In certain situations, a cold compress is recommended."

Thanks for this answer. Unfortunately the vet was not available to call, but by morning, the water pocket had been sloughed into the body. I think we dodged a bullet.

It seems like this was 'infiltration' as you say.

When we told the vet in the morning, they didn't even seem the slightest concerned this happened. I dont know - but I think that is weird. If we had of been asleep, this would have continued for another 6 hours. I am surprised they sent us home with an IV in the first place without telling us all the possible issues, such as blood clotting in the tubes (which happened earlier) due to poor circulation.

Well, I simply do not know how dangerous it is. My intuition says it's not particularly dangerous since the extra fluid is, eventually, absorbed. However, I'm not a medical professional and don't know the circumstances that dictates when it becomes dangerous. Thus, the big warning at the beginning. Better safe than sorry. :-)

The most common IV drip that would be sent home with a pet owner is Ringer's solution. This fluid is also commonly injected as a subcutaneous (between muscle and skin) bolus into both cats and dogs. Although IV administration is more efficient, this fluid is completely harmless if an IV catheter were dislodged allowing it to accumulate in the surrounding tissue.


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Taxonomy of viruses
There is a distinction drawn in the ICTV code between  "valid names" and "accepted names".
Valid names are those that are published and comply with the rules outlined in the code, while accepted names are those valid names that have been added to the Index.
My question is what is the correct way of introducing new names in a publication for them to be considered valid. Should they be introduced e.g. as simply new genus Xxxxxvirus or should they be supplied with an explicit "tax.nov.": Xxxxxvirus gen. nov.. Are quotation marks needed around names indicating that they are not yet accepted? Should there be any other indication that they are not yet accepted?


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Where can I get yeast mutants?
I want to use some yeast mutants to conduct gene functional analysis, and the gene was isolated from plants. Can anybody give me some information regarding the websites or agencies from which I can purchase the yeast mutants?

see this answer http://biology.stackexchange.com/questions/10917/sources-for-common-laboratory-saccharomyces-strains

as an addition to the above I'd add: the yeast deletion collection at Stanford http://www-sequence.stanford.edu/group/yeast_deletion_project/downloads.html#strainsavail  and this list of brewer's yeasts just for completeness: http://byo.com/resources/yeast


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Are there any differences between qRT-PCR and GEO (microarray data from NCBI) regarding dealing with internal control genes?
As we know, when we do qRT-PCR, the two most commonly used methods are absolute quantification and relative quantification, both the methods are involved in dealing with normalization of house-keeping genes or internal control genes (like GAPDH, Actin). In the microarray experiments, the similar normalization should also be adopted (I did not have any experimence with this kind of experiment). But I do know that someone obtained GEO file from NCBI, and simply did t-test analysis to find differenced expressed genes without any operation with the internal control genes. So I wander whether this is the right way, if not, what should we do with internal control genes to normalize data?

did you find an answer to your question? If you did, it would be great if you could post it here for people having similar questions in future


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Question about production of CFTR protein
How do organelles such as ribosomes, ER, Golgi and vesicles produce CFTR protein and mucus?

Can you provide more context? Also can you unpack CFTR?

Also, what is your background knowledge and where are you stuck?

CFTR (cystic fibrosis transmembrane conductance regulator) is an integral glycoprotein of the plasma membrane, and mucous is rich in secreted glycoproteins. All proteins are made on ribosomes: CFTR will be cotranslationally inserted into the ER membrane while secretory glycoproteins are cotranslationally sent across the same membrane into the lumen of the ER. In the ER the initial glycans are added to specific amino acid residues. The folding of all proteins is carefully monitored by chaperones in the ER to avoid misfolded proteins reaching the cell surface. Various folding factors also come into play, including peptidyl proline isomerase and protein disulphide isomerase.
Proteins destined for the cell surface leave the ER in COPII-coated vesicles (CFTR will be in the vesicle membrane, secretory glycoproteins in the vesicle lumen) and are targetted to the Golgi where the glycosylation process is completed. Another round of vesicle transport gets the proteins to the cell surface - when these vesicles fuse with the inner surface of the plasma membrane the vesicle content is secreted into the surroundings, while the vesicle membrane proteins enter the plasma membrane.
The classic example of a CFTR defect, resulting in cystic fibrosis, is due to the ΔF508 mutation - the loss of a single amino acid results in misfolding, and the defective protein is held in the ER resulting in loss of CFTR function at the cell surface. Overcoming this retention is one of the targets for CFTR therapy, because if the ΔF508 protein does manage to pass through the secretory pathway to the cell surface it provides sufficient channel function to abolish cystic fibrosis symptoms.
I haven't cited any references here because this is all standard biochemistry/molecular cell biology textbook stuff, so should be easy to confirm.

There are a couple nice videos here: https://synbiota.com/projects/325/
You can also check out some DNA sequences and some protein structures (PDB files) if you want to learn more.


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Is cell membrane living
We say cell wall is dead but nobody says cell membrane is dead.
Is cell membrane living or dead ? If it is not dead then why is it not included in protoplasm :

Protoplasm is the living contents of a cell that is surrounded by a
  plasma membrane.

(Source : Wikipedia)

neither the cell wall is living nor is the membrane. It is not dead either. Being a vital part of the cell it is essential for life but the concept of life doesn't apply to it.

In addition to the comment from @WYSIWYG, you must also define what aspects of the cell membrane you are talking about - only the lipid bilayer or also the embedded proteins? The latter are most definately "alive".

Also, you question seems to imply that plasma membrane is something distinct from cell membrane, when they are actually alternative names for the same thing.

Woah, @fileunderwater how are proteins living?

@terdon Which is why I wrote "alive" and not living... What I was getting at was that membrane proteins are essential for cell function and are dynamically synthesized, while the lipid molecules are more of a passive component. But I agree the comment was probably confusing.

@fileunderwater membrane lipids are also quite essential (if anything, more so than membrane prots since there is no membrane and no cell without them) and dynamically synthesized, it's just that they are not coded for by genes. Nevertheless, the enzymes needed for their production are, so lipid production is as dynamic as anything else. The cell can produce more when needed. I don't really see any difference in 'aliveness' between lipids and proteins.

It is neither living nor dead. It is simply not alive the way that any other collection of chemicals is not alive. Is salt alive or dead?
A cell's membrane consists of a collection of chemicals (mainly lipids and proteins). Individual chemicals can never be considered living or dead, any more than rocks or water can be living or dead. While the actual definition of life is tricky, everyone agrees that in order to be alive you need to (at the very least)

Somehow interact with your environment
Be able to make more copies of yourself

Therefore, the cells themselves are alive but the individual parts of the cells are not since they cannot make copies of themselves (this gets complicated when considering some organelles but never mind that here). Similarly, you are alive but your teeth are not. While you can make more of you (you can have children) your teeth cannot make more teeth.

While I agree with the basic message in your answer, I also feel that this is a bit restrictive, especially when comparing to natural language. Earlier I was also considering e.g. teeth, and wouldn't you agree that the pulp can be labeled "living tissue" while the enamel is "dead"? Along the same lines, in plants (which can reproduce clonally, so living cannot be defined at the level of the whole organism), some cells are dead (but their cell walls might still provide a function), while others are living....

[cnd:] What about the cell walls around the living cells - are those living or dead, if they have exactly the same structure as the cell walls surrounding dead cells? I realize that this is bordering on questions concerning language and philosophy, but I feel that the possibility to talk about components of organsisms as living or dead is useful. Or do you have any other terms as suggestions?

@fileunderwater I can appreciate what you are saying but I think using the term 'alive' and 'dead' is confusing since we are talking about life. I think what you are mentioning is more related to whether or not something is capable of changing or being replenished. I would suggest the terms 'static' and 'dynamic'

@vonMises I honestly think that these terms are even more confusing. Good luck trying to convince people that enamel and hair is 'static' while pulp and hair sacks are 'dynamic' - I don't see how this would improve communication, especially with laymen.

@fileunderwater it comes down to semantics. Living is not the same as alive and the opposite of living tissue is not dead tissue. Teeth are not dead and neither are rocks, they are simply not living. The point is that life needs metabolism and reproduction, things that cannot do both are not alive. The cell's membrane is not alive, the cell itself is. Your hand is not alive, despite being made of "living tissue", you are. "Living" tissue consists of cells, each of which is indeed alive, the tissue itself is not.


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Does the eye image interval refresh?
It's known the human eye takes 24 images per second. But does this refresh?
For example after sleeping.
Or will it always be the same interval?
I talk about when the eye takes the images. So it are 24 images in the second, but this second is not defined. It can start at 09:00:00.00 or 09:00:00.50. Will this change after taking a sleep?
Hope it is clear what I'm talking about.

The human eye does not take 24 images per second - this is only (approximately) what is needed for a film to look fluid - and the image we see is continuously updated and interpreted by the brain. Saturation of human perception is another thing, that is, the maximum frame rate that we can perceive, and this depends for instance on light conditions.

Related question: What is the equivalent of shutter-speed in Human eye?

Human eyes do not take 24 images per second. Refresh done in parallel, each pixel separately, and the rate depends on the rate of color changing.
So, the work of eye is closer to MPEG encoding than to uncompressed AVI.


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Are sulfates or nitrates common ions in biochemistry (specifically of the body)?
It's a rather broad question but something I'm curious about.
I know sulfates tend to be very soluble ions and so don't know nitrates.
I also know that phosphates are extremely common in biochemistry (e.g. ADP) but they're not very soluble unless they involve group 1 elements, same goes for carbonates.
I think Carbonates tend to be more common in crustacea, or chicken egg shells. I can't remember if it's found in the Krebb's cycle (don't think so, but maybe in other vitamins?).
Solubility isn't apart of this question, it was just one of the ways I was just trying to pursue an answer. I'm more of a chemist than a biologist...


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Why does beta-2-Thienylalanine inhibit bacterial growth?
I'm trying to obtain a better understanding of the Guthrie Test, which checks whether people have a disease called PKU.
The Guthrie test uses bacteria to check for Phenylalanine (the amino acid) in blood samples. If both Phe and B-2-thienylalanine are available on the medium, the bacteria will grow. However, if only B-2-thienylalanine is available the bacteria will not grow.
In all of the articles I can find, I have seen no explanation, just a link to a paper that I can't find on the internet.:
" A standard culture of Bacillus subtilis was incubated on agar in the presence of an antagonist of phenylalanine (B-2-thienylalanine), which prevents the bacteria from growing.3 " Link
The reference they mention here is:
"The inhibition assay: Its use in screening urinary specimens for metabolic differences associated with mental retardation" by R. Guthrie from 1960.
Do we know what mechanism this protein is inhibiting?
Any help would be greatly appreciated.

β-2-thienylalanine is an analogue of phenylalanine. It is incorporated into proteins in place of phenylalanine, and the resulting proteins are inactive because of the substitution. Consequently growth medium supplemented with β-2-thienylalanine will not support bacterial growth.
Addition of phenylalanine to a medium containing β-2-thienylalanine will result in a competition between the two compounds - if there is an excess of phenylalanine then this will out-compete the analogue and incorporation of the analogue will be minimised, allowing growth. Blood from a patient with PKU contains phenylalanine, so the addition of this to the growth medium will relieve inhibition of growth.
Here is a link to a patent application in which a screen for E. coli strains overproducing phenylalanine was based upon the same principle.

Thanks Dr. Boyd! I greatly, greatly appreciate your help!


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What is the genetic distance where linkage can be ignored?
I heard several times that two SNPs, that have at least 1'000 nucleotides between them, can be seen as 'unlinked' due to frequent recombination events. I also once saw a paper showing a graph "degree of linkage vs. genetic distance". Unfortunately I can't remember which paper it was. Does anyone know where this number (1000) comes from?
PS: I'm aware that this topic is much more complex, especially if you are interested selective sweeps.

I think you must have misremembered what you heard.
The cut-off distance for genetic linkage is 50 centimorgans which corresponds to 50% recombination. In the human genome 1 centimorgan is approximately 106 base pairs, so the 'unlinked distance' is 5 * 107 base pairs.

Do you have a citation for that?

Well, you could start at the Wikipedia page for centimorgan - that's where I got the 1,000,000 base pairs from. The table at http://www.nature.com/nature/journal/v409/n6822/fig_tab/409951a0_T1.html gives some real values, which illustrate how it varies. If "unlinked" equated to 1,000 base pairs, classic genetic mapping which relied upon measuring linkage between genes would have been impossible - everything would have been unlinked.

I totally agree with @AlanBoyd. One cannot ask whether an approximation is reasonable or not without specifying the model of interest. Depending on the model of consideration some level of recombination might be enough so that you could consider two loci to be unlinked. I have never seen this kind of approximation though!


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How many recombination events are there per generation in humans?
I'm looking for a reference that tells me how many recombenation events occur in humans from one generation to the next.
Assuming that the human genome is a 3.3 GigaBases long DNA sequence, how many recombination events do you find, and what is he amount of DNA exchanged?
Is it in the order of 0.1%, 1% oder 10%?

"On average, between two and three crossover events occur on each pair of human chromosomes during meiotic division I" according to Molecular Biology of the Cell. 4th edition by Alberts B, Johnson A, Lewis J, et al. For simplicity we will call that 2.5 events per pair.
Each of those pairs ultimately forms 4 gametes. Each event connects one chromosome to another, so each individual event will leave 2 chromosomes with a location where an event has occurred. That means that in the 4 chromosomes in 4 different gametes that are produced from any single pair, there will be (on average) a total of 5 locations where a recombination event has occurred. On average then, each chromosome will have 5/4 or 1.2 locations where a crossover event has occurred.
Each human gamete has 23 chromosomes. Two gametes (1 egg, 1 sperm) unite to form an embryo. That embryo has 23 PAIRS of chromosomes, or a total of 46 (except in cases of certain chromosome abnormality). Therefore a first estimate would be that across a given set of 46 chromosomes, there would be 1.2 times 46, or 55.2 sites where recombination occurred on average.
It is important to note that the question cites 3.3 Giga-basepairs in the human genome. While that may be a reasonable estimate for the size of one complete human genome, each human has two copies of each chromosome and therefore two complete copies of the human genome. Wikipedia states that this is currently estimated to be 6.5 billion basepairs (6.5 Giga-basepairs). This distinction is significant because recombination during gamete formation in females is significantly more frequent than in males, so the genome found in a human egg cell will have many more recombination events than a sperm cell genome, therefore the average is only applicable to the entire 6.5 Giga-basepair genome.
The question about the "amount of DNA exchanged" through recombination is not really valid since total quantity of DNA in each of the four gametes produced in meiosis is exactly the same as the amount that had been contained in the original parent cell after DNA replication (but before meiosis I has produced two daughter cells). No base pair can be said to have been exchanged through recombination or not.

"Each human has two copies of each chromosome and therefore two complete copies of the human genome" - I believe that the term "human genome" refers to both sets of chromosomes together, so that each human only has one human genome.

Back-of-the-envelope calculation
The definition of the centimorgan is that it is the length of DNA in a chromosome corresponding to a 1% chance of crossover occurring.
In human chromosomes 1 cM  = approx. 1Mbp.
Your value for the length of DNA in the genome = 3.3 Gbp = 3300 MBp
Ignoring complications like the Poisson distribution:
1 cM corresponds to a probability of 1% chance of a detectable crossover. Detectable, because only an odd number of crossing over events between 2 genetic markers can be observed as a recombination, but even numbers instead go unrecognised. Therefore the actual chance of crossing over is doubled relative to the cM value.
If 1 cM = 2% actual chance of crossover, there will be on average 1 crossover per 50 cM or per 50Mbp
Therefore crossovers per human genome = 3300/50 = 66  or approx 2-4 per chromosome
This guess comes near empiric data:
Actual data

This Table, taken from here shows the number of chiasmata by chromosome for 8 human cells. (Note that it believed that there has to be at least one chiasma per chromatid pair since they have a structural role.)
The average chiasmata per chromosome for each chromosome can be estimated by dividing the number in the final column by 8. These vary from (rounding aggressively) 3.5 for Chr 1 and Chr 2, to 1 for Chr 20. So my back-of-the-envelope calculation seems to have produced a reasonable answer.
What is the amount of DNA exchanged? I'm not sure this question matches well with the picture that emerges from these numbers.

This is not easy to answer, since it depends on a number of factors. For example it is dependent on the region of the genome (there are hotspots). I found a PhD thesis, which goes into the details here and which also has a ton of interesting references:

The Estimation of Recombination Rates from Population Genetic Data


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How can we distinguish blended flavors?
As far as I know, humans can distinguish between 5 basic tastes based on various molecules in food and their interactions. There's a level to all 5 so there can be an endless variety of tastes, and we can recognize them with some precision. What surprises me is that we can often distinguish the original flavors in a mix - for example in a salad or even more so in a blended juice. Shouldn't we perceive an entirely new flavor having the average of each basic taste?
Not entirely sure this belongs on a biology forum, but I hope someone can explain :)

We can distinguish these five tastes, but smell many more. The nose takes a big part in the tasting process, this is why lemon tastes like lemon, and not just sour.

You're talking about the difference between "taste" and "flavor." In common speech we use these words synonymously, but they actually mean different things.
Taste refers to the five sensations your tongue can detect -- sweet, sour, salty, bitter and umami. There's growing evidence for a sixth taste, "fat."
Flavor refers to the combination of several factors:
1) taste, as just described,
2) the aromas of esters, flavinoids, ketones, and other compounds in your food, detected by the nose. This happens a) before you take a bite, and b) as you chew and swallow, releasing different compounds and higher concentrations into your nose through your retronasal passage,
3) physical sensations such as texture, heat and cold, visual appearance and even sound (for example, the crunch of celery or potato chips)
4) chemesthetic effects, like the astringency of tannins or the "artificial" heat of chili peppers. (The compound responsible for chili heat actually down-regulates physical heat receptors so they're more sensitive. Menthol up-regulates them to create a cooling sensation.)
5) Emotional and social factors, like the memory of your grandmother's homebaked bread, or many people's aversion to raw fish.
All of this put together is why blackberries and strawberries are both sweet and tart, yet blackberries taste like blackberries and strawberries taste like strawberries.
Hope that helps!
References:
-- The collected works of Karen Page & Andrew Dornenburg
-- "Tastebuds And Molecules," Francois Chartier
-- LOTS of personal empirical evidence (I'm a chef)


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probability of having normal daughter

If  father has hemophilia, mother is a carrier of the disease, then
  what is the probability of having a normal daughter ?

My question: Should the probability of having a daughter be also multiplied ? Should the answer be 0.5 or should it be 0.25 ?

Unfortunately, the question is ambiguous.

@ChinmayKanchi umm..I am not able to understand how this is ambiguous.Could you please elaborate ?

I can't understand what you mean by "Should the probability of having a daughter be multiplied?" But yes, the probability of having a normal daughter is 0.25, but she will be a carrier like her mother.
Let H represent normal allele for blood clotting (dominant); h represent allele for hemophilia, XY represent the male chromosomes and XX represent the female chromosomes.
Parental Phenotypes :
   Normal female(carrier) x Hemophiliac male

Parental Genotypes (2n) :
   X(H)X(h)         x     X(h)Y

Gametes (n) :
   X(H)     X(h)    x   X(h)     Y

Possible Outcomes :
XHXh - A normal female, carrier.
XHY    - A normal male.
XhXh - A hemophiliac female.
XhY    - A hemophiliac male.
So the probability of having a normal daughter, that is XHXh is 0.25.


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Hibernation in ectotherm and endotherm

Both snake and weasel hibernate. Which of the following is correct?
A. They will die when temperature decreases below the critical
  temperature.
B. Weasel will die when temperature decreases below the critical
  temperature.
C. Snake will die and weasel will wake up when the temperature
  decreases below the critical temperature.
D. Weasel keeps low body temperature and slow heart rate during the
  entire period of hibernation.

I don't think any of them should die, they would have some adaptation to prevent that. So,is the answer (D) ?
What is the snake's adaptation in this situation ?

A relevant article

Weasels don't hibernate.  See http://icwdm.org/handbook/carnivor/Weasels.asp
Both will die when the temperature falls below a certain level.  The difference between snakes (ectotherms) and weasels (endotherms) is that the snake's body temperature will fluctuate more, depending on the surrounding temperature.