text:
Why might dogs get sick less frequently than their owners?
An article I was reading cited this study result "A comparison of 2473 pairs of dogs and their owners found that dogs were about 50 per cent less likely to have had two or more acute illnesses in the previous year than their human family members (p < 0.01, preliminary data)." The article is here http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3189355/.
In the absence of any species specific reasons, we would not only expect rates of sickness to be similar, but in fact, owing to dogs' extremely poor hygiene standards relative to humans, we would expect them to be sick vastly more often.
I have read a number questions on the general subject of humans appearing to get sick more than animals, but most have ended with a presumption (but without any evidence cited) that animals do get sick as often but we just don't see it. This study is the first I've seen on the subject and seems to demonstrate that it is a real phenomenon after all.
The author's explanation seems entirely based on meat-eating, which seems plausible, but perhaps a bit narrow. I wonder if anyone could offer any alternative explanation?

The article is hypothetical. It's written as a discourse trying to explain why pets are sick less than their owners, while the foundation of that hypothesis is not founded: see section 4 of your linked paper:

A hypothesis put forth in this discourse is that humans get sick more often than animals and, correspondingly, typically engage in medical practices more frequently than animals. There is relatively little direct evidence that might firmly refute or confirm this hypothesis.

So your question why

humans appear [to] get sick more than animals

is more a question of if, rather than why.
I think the major problem with this article is that there is not a strict definition of 'sick'. What we may experience as being 'sick' may not be recognizable to us when an animal is in a physiological comparable state.

Thanks for your response, but I wasn't really asking for an review of the article itself, more a comment on the study it cites. The article might have been hypothetical in nature, but the study actually took place and got the results it did. It's these results I was interested in. I presume the uncertainty about observed 'sickness' is why the study chose dogs. It seems unlikely that such beloved pets were actually acutely ill without their owners knowing, and if they were that just means the question becomes 'why do humans exhibit more visible symptoms than animals?', hardly much different.

If your  question is on cited studies - cite those. The linked article is quite poor in its scope. What I mean is that the assumption of the article is iffy. I don't buy it.

Do women get "sick" more frequently than men? I bet a study would find that men do have fewer acute illnesses than women. But do they really? We know that men tend to go to the doctor much less than women for a number of reasons, ranging from laziness to stoicism to expense. Similar reasons apply to dogs and their owners, therefore I also strongly question the premise of this article.

Also, the population dynamics of pet dogs would be quite different from their human owners.

I agree with the above three comments. Dogs get sick, and probably on the same order of magnitude as humans. More than one human disease (like narcolepsy) has been solved because of canine conditions, and with genetic studies, more are certain to come. "...such beloved pets were actually acutely ill without their owners knowing..." How would their owners know? My dogs are quite beloved, but they just can't complain about certain illnesses. They get over it with time, or it becomes vet-worthy.

I don't mean to offend, but I originally asked about a study mentioned in a perfectly legitimate scientific journal. I was hoping someone might either offer an explanation or perhaps some evidence to the contrary. I'm not sure I see the sense, on a science site, of people adding comments that they 'reckon' it's probably not true. If anyone has any scientific, evidence based opinion, it would be good to hear. If you think dogs do get sick as much as humans then perhaps some studies showing this would be a useful contribution.

I hadn't realised I had come up against such a wall of preconception. According to Occam's Razor, if a study seems to show that dogs get sick less than humans, then we should presume that they do and then look for evidence to the contrary, not presume they don't because we don't like the conclusion and proceed to make up reasons why the study might be wrong. This is exactly the sort of confirmation bias that holds scientific investigation back, people decide on a world view and only accept evidence which supports it, anything that doesn't gets picked apart until it can be safely swept away.

I'm not quite sure where the vitriol is coming from, I did not say that any study proved it conclusively, but was careful to use 'might' in my question and 'seems to show' in my comments, please don't put words in my mouth. If mentioning an analytical axiom by name constitutes a 'lecture', then I'm not sure there is any value to continued discussion. I asked the question 'Why might dogs get sick more than their owners?' An answer would be a scientific reason why they do or a study showing they don't, I did not ask for a personal opinion about the value of the article.

Your question finishes with: "The author's explanation seems entirely based on meat-eating, which seems plausible, but perhaps a bit narrow. I wonder if anyone could offer any alternative explanation? It implies you take the finding for granted. The question you now pose in your comment is different than the one in your question body.

I presume you have deleted your previous comments? It looks like I'm having a conversation with myself which is misleading to anyone reading this. With regards to your remaining comments, I did indeed take the finding for granted, for the time-being, it was published in a reputable journal and I had no evidence to the contrary (and still don't), it seemed entirely the rational thing to do. All I did in my comment is flip it on it's head, it's the same question either way, what scientific, evidence based, explanation could there be for the results of this study?


text:
Is the bulbourethral (Cowper) gland turned on during puberty or is it on at birth?
I am trying to find information about the bulbourethral (Cowper) gland and if it gets turned on during puberty or not. I tried asking several other online sites and they said they couldn't help. I don't know where to ask or where I could look up the answer.

What does "on" mean in this context? To my knowledge, the exocrine function of the bulbourethral glands (it's a paired organ) is limited to ejaculation, so I'm not sure what you are expecting that they might be up to at birth.

@Susan On as in active. So basically, do the glands get activated during puberty? Thank you.

Yeah, because the bulbourethral glands are from accessory glands of the male reproductive system as the seminal vesicles and prostate gland. The male reproductive system starts working at puberty.

Can you please [edit] you answer to add some references that support it? Reliable sources include books, research articles/reviews and websites of reputed academic/research organizations.

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Was Darwin aware of the difficulties behind the concept of species?
Introduction
The concept of species is a very old concept that suffers from not being a natural category. There exists no single definition that would categorize living beings into groups and that would fit our intuitions of what a species should be.
Many of such problems in definitions are revealed in the field of evolutionary biology. For more information about the difficulties behind the definition of the concept of species, have a look at

How could humans have interbred with neanderthals if were a different species?
This post on ring species.

Question

Did Charles Darwin comment on this problem?
If yes, did Charles Darwin comment on the reason why he chose to keep using the term "species" instead of simply "lineage"?

On the contrary, species seems a fairly natural and obvious categorization.  The problem is with people who insist on rather too narrow a definition, e.g. deciding that Neandertals should be a different species from modern humans, when the evidence shows otherwise.

I did not think a debate on the question remained. I assumed it was given the overall agreement on the Sapiens and Neanderthals question. I don't think there is a subjective threshold for how low should the fitness of the hybrid (unless we chose sterility). There is also no objective way to solve ring species problems. Also the concept of species based on reproductive isolation fits only sexually reproducing lineages.

I don't think we can comment about whether Darwin was aware of this problem, unless he documented it.  Since we don't have a rigourous definition of species,  we can parsimoniously assume that he didn't. In that case the other two questions would have no meaning.

@WYSIWYG I slightly rephrased to ensure the questions are not opinion-based. Does it seems better to you?

Yep but still it is quite easy to assume that Darwin didn't comment. If he did, we would probably have known.

Sure.... "Not that I am aware of" could well be the best answer. As I never read through any of his books, I would not be confident enough to say such thing.

As this is not really a biology question I think it would be better suited for History of Science and Mathematics SE.

There is a history tag on Biology.SE though. But I agree that HS&M.SE could eventually be an even better place for this post. Thanks

The whole point of Darwin's theory was that transition from one species to another is extremely slow and gradual. There are plenty of quotes in "Origin of Species" stating this, and also affirming that there is no clear boundary between species and subspecies, or "races".
Quotes from Origin of Species > Variation under Nature (Chapter 2)
Quote 1

Nevertheless, no certain criterion can possibly be given by which variable forms, local forms, sub species and representative species can be recognised

Quote 2

Several experienced ornithologists consider our British red grouse as only a strongly marked race of a Norwegian species, whereas the greater number rank it as an undoubted species peculiar to Great Britain. A wide distance between the homes of two doubtful forms leads many naturalists to rank them as distinct species; but what distance, it has been well asked, will suffice if that between America and Europe is ample, will that between Europe and the Azores, or Madeira, or the Canaries, or between the several islets of these small archipelagos, be sufficient?

Quote 3
It is here the most definitive quote I managed to find and partially answers to your second question.

From these remarks it will be seen that I look at the term species as one arbitrarily given, for the sake of convenience, to a set of individuals closely resembling each other, and that it does not essentially differ from the term variety, which is given to less distinct and more fluctuating forms. The term variety, again, in comparison with mere individual differences, is also applied arbitrarily, for convenience sake.

Great answer. +1 Thanks. I edited the post to change the format. Feel free to roll back if you don't like it. It'd be great if you could add the book/chapter/paragraph/page at which these quotes were taken.

Thanks, your edits made the response easier to read. As for the quotes, I gave a link to the book available online. There are no pages as such, but anyone may search it by text. These quotes are the first relevant ones it took me literally a minute to find.

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Who are humans' closest relatives, after primates?
This question here addresses the controversy of whether humans are more closely related to bonobos or chimps.
My question is - which group of animals are are closest relatives, beyond primates? Or which group of animals are all primates most closely related to?

Short answer
It is a flying lemur (there exist only 2 species). Flying lemurs and primates are together a sister clade to treeshrews.
Easy source of information
Have a look at the post The best free and most up to date phylogenetic tree on the internet?.
In short, you can have a look at onezoom.org, tolweb.org or opentreeoflife.org by yourself!
Tree of life of placental mammals
Here is a screenshot coming from tolweb.org.

In this tree, there are polytomies showing everything that is unknown. This tree was last updated in 1995 and there are also clades that we now know were misplaced including the bats (as commented by @NoahSnyder). It is not handy to make a good screenshot from onezoom.org or opentreeoflife.org so I just welcome you to explore the tree of life by yourself on onezoom.org or opentreeoflife.org to get a better representation of the reality.
Tree of Supraprimates
Supraprimates (=Euarchontoglires) include all primates and a few of the most related clades. Stealing the tree from @Gwenn's answer, here is the tree of Supraprimates
[
Here is the original tree from Janecka et al. (2007)

Here we see that flying lemurs (=Dermoptera) is a sister clade of primates (ignoring the extinct plesiadapiformes) and treeshrews (=Scandentia) are a sister clade of flying lemurs and primates together. Below I briefly talk about these three clades and about their position on the phylogenetic tree.
Flying lemurs
Flying lemurs is a small clade that contains only two extant species, both found in the family of colugos. Note that flying lemurs are not lemurs (which is confusing). Here is what a flying lemur look like

The position of flying lemurs on the phylogenetic tree has always been quite uncertain. In the tolweb.org screenshot above, flying lemurs (=Dermoptera) is a sister clade to bats (=Chiroptera) and together they are sister clade to treeshrews and primates. However, Janecka et al. (2007) placed flying lemurs as the sister clade to primates. Together flying lemurs and primates are a sister clade to tree shrews.
Tree shrews
Treeshrews is a clade of 20 species native from southeast Asia. Before, the era of phylogenetic comparisons, treeshrews were mistakenly thought to be part of the Insectivora.

Extinct clade of Plesiadapiforms
Although they are represented above as a sister clade of primates, it is possible that they the fossil we found are just individuals coming from the lineage giving rise to primates. As such, they would not be a clade aside from primates. Below is an artistic representation of what they may have looked like.

Introduction on phylogenetic trees
As the question is quite introductory, I presume you might want to improve your understanding of phylogenetic trees. You might want to make sure, you understand what a monophyletic group (=clade) is and understand why a chimpanzee and a human are both equally related to any species of treeshrews.
Here are two sources of information for you:

Understanding Evolution (UC Berkeley) > The history of life
This answer on Biology.SE

The most closely related animals to primates are colugos (order Dermoptera).
The next most closely related after colugos are tree shrews (order Scandentia).
The next most closely related after tree shrews are rodents (order Rodentia) and lagomorphs (order Lagomorpha) (rabbits, hares, and pikas).

Sources: Wikipedia's section on the evolutionary history of primates and onezoom.org.

Where did you see that Dermoptera is sister clade to primates? Do you have a reference for that? Note that colugo is a family made of two extant species only. This family is nested within Dermoptera and therefore a colugo is equally related to any primate than any other dermoptera

@Remi.b Just Wikipedia's section on the evolutionary history of primates. Wikipedia in turn cites this Science article from 2007 (which I sadly cannot read to verify because I don't have a subscription). And from what I understand, colugos are the only extant members of Dermoptera.

@Remi.b: The position of colugos (Dermoptera) in the evolutionary tree has traditionally been somewhat uncertain, but recent studies (such as the 2007 Science article by Janečka et al. mentioned by Gwenn, PDF here) do apparently support their position as the closest surviving sister clade to the primates.

Oh, I just realized that Dermoptera are also called flying lemur (which is a confusing term)! As a consequence, it is not so much an issue of definition as I suggested rather than an uncertainty about the position of flying lemurs on the tree. I will update my answer. Thanks for your help. +1 on answer and comments!


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What species of fox is this?
I found this picture of a fox in a news article about arctic foxes in Sweden (source), but I'm not sure whether it is actually an arctic fox.

On the one hand, it has white fur, which is the correct winter coat for an arctic fox. On the other hand, the fox's ears do not have the distinctive shape of arctic fox ears, but ears that look more like red fox ears.
The image credit given by the article is just "iStock", so I searched iStock to see if I could find more information about the photo. I found another photo of the same fox here, also labeled as an arctic fox, but not really any further information.

What species is this fox?

It tells you in the source!

@PichiWuana I have only the word of iStock's tags to go on, and that's not exactly trustworthy in an unclear case like this. I have seen images on that site be tagged with multiple species names before.

This is a white morph red fox, not an arctic fox.
As noted in the question, this fox has larger, more pointy ears than an arctic fox, and the second picture shows it to have a longer muzzle as well.
Another clue is that these pictures were taken in the springtime or early summer (which you can tell from the new growth on the plants in the picture), and that arctic foxes are only completely white during the winter. During the spring, an arctic fox should look like this:

You can also easily tell that the fox in the picture is not an albino, because of the dark pigment in the nose and eyes.
The red fox has quite a few different color morphs, and this fox looks to be a white color morph.

In that diagram, this fox would be labelled as leucistic (white).
Here are some other white morph red foxes:

I like how your profile picture matches the subject of the post. +1 for the good answer


text:
Is there a way to identify a species of tree?
My family has been passing down  seeds from a lemon tree for about 3 generations now, There is some controversy about its origin or species. The lemons look like tangerines and when cut the pulp is very orange but are sour just like lemons. People always think we dye the lemonade. We have asked family members where our family got the original seed from and some say it was from Vera Cruz, Mexico but other family members say it might have came from Hawaii. Regardless it appears to have been from a tropical region. Is there a way a seed or part of a tree can be tested? If so, how much can I expect it to cost and where could I get it done?

Images would be helpful. We can try to identify it here, asking where to get it tested is not really on topic here.

True, true...but I don't have the tree physically with me and I ate all then lemons, lol. Sending a seed to a lab maybe?

I don't think OP is asking us to identify the species. He is asking for a test that will confirm the species of the plant. @MrHons Genetic tests should tell you the species. You can do a 16S rRNA sequencing. The cost shouldn't be very high but if you have a friend working in a bio-lab then you can ask for a little favour.

@WYSIWYG You could make an answer out of your comment if you want especially if you extend it to add a link to who the OP could send the tissue sample to for sequencing and analysis


text:
Does a woman contain all the genes needed to make a man?
I know the answer of inverse is at here, but how about this question?
I also read this question, can I imply to human that a woman can also contain all the genes needed to make a man?

Edit:
I think everyone has  the ability of being a man or a woman in terms of their DNA, and that their gender is just determined by the presence of SRY.
Is my concept correct?

Male mammals require a Y chromosome because the genes needed to express masculine features are on that chromosome. Females don't carry a copy of the Y chromosome, so they don't carry those genes, and can't pass them on. A male could hypothetically provide all the genes needed to produce a female because you could copy his single X chromosome to produce two identical X chromosomes.

Your pseudocode is not necessary here. It actually oversimplifies the issue and is likely to generate unnecessary debate. You should verbally explain what you mean.

Human female cells contain most of the genetic information required to make a male, but they do not contain a critical component: The Y chromosome. This is a relatively small chromosome. Wikipedia claims we have identified around 200 genes on it to date, compared to estimates of 20,000 - 25,000 genes overall in the human genome.
Importantly for your question, only other males contain and make full copies of all the genes on the Y chromosome. The Y chromosome does not cross-over* with the X chromosome during meiosis when producing sperm cells, which keeps the Y genes isolated, except for rare exceptions (e.g. gene translocation). So those genes are passed down the male line only. The SRY gene is just one of the genes encoded uniquely on that chromosome, so something else is definitely missing - the question could be re-phrased "how important to being a functional male are the unique genes other than SRY unique to the Y chromosome?"
The linked question (an experiment on mice that produced XX "males" by finding an alternative trigger to the SRY gene to induce male development) demonstrates that in terms what we might consider a physical male specimen, the Y chromosome probably contains a minority of critical unique features. The mice developed into apparently complete physical males. That means genes outside of the Y chromosome cover most of the body development plan for both males and females.
However, such XX males will in most mammal species not be fully functioning males - the missing genes do make a difference. One outcome is infertility - biologically speaking, XX males do not possess a key male function, the ability to mate with a female to produce offspring. There are missing genes related to sperm production.
Human XX males - as in developmentally male - do occur naturally. This can be caused by gene translocation - specifically the SRY gene moves to the X chromosome in a sperm from the father (potentially other Y genes will move in the same event). The symptoms that present with the syndrome vary, but give some indication of which critical components are missing.

Not all animals have the same mechanism. Birds have W and Z chromosomes (with males being ZZ and females ZW). Yet other animals do not use genetic switches, but environmental ones. In those cases, the female does contain all the necessary genetic information to create a male. In cases where there is parthenogenesis (production of offspring without fertilization), then this can be fully demonstrated.
* Technically there are some small regions, about 5% of the Y chromosome, which do cross-over with X, called the pseudoautosomal regions. At the time of writing the linked article mentions 29 genes found in these regions.

You don't explicitly put it this way, but the reason the Y chromosome is critical, is that it couldn't be simulated just by removing part of an X chromosome. Recombination doesn't occur in all regions of the X/Y chromosome pair, and that's why there's stuff on the Y that really is unique to the Y as you describe. If there was recombination along the whole Y then everything there could appear also in an X somewhere, but there isn't so it can't.

Also worth noting the existence of pseudoautosomal regions - "the genes other than SRY on the Y chromosome" are not all unique to men.

Nope. A woman does not contain all the genes required to make a man. Humans are mammals and mammalian male gender is governed by the ~200 genes on the Y chromosome. However a man (XY) does have all the genes required to make a woman (XX).
In birds they have WZ sex determination system. So a hen, is the heterogametic sex,(WZ) does have all the to make a cockerel (ZZ)


text:
Is it possible to have multiple stop codons in one exon?
I would be very happy if someone can help me to find the answers for the following related questions.

Can one exon have many stop codons?
Can protein synthesis happen, if the stop codon is at the beginning of the exon?

An exon can have multiple stop codons but the first codon will terminate the ORF. The remainder of the exon will be a part of the 3'UTR.
However, there are some cases in which stop codon readthrough happens [1]. In these cases an internal stop codon does not terminate the translation and the ribosome reads through it. During this process an aminoacyl-tRNA successfully competes with the release factor. This is quite evident in the case of selenocysteine and pyrollysine- tRNAs which bind to the UAG (amber) stop codon in certain organisms [2,3] (this is also referred to as amber suppression). The exact mechanisms that affect stop codon readthrough are not elucidated but features in the mRNAs are likely to play a role in this. In case of amber suppression, the relative rarity of the UAG stop codon and lower concentrations of release factor-1, can be major factors.

I don't know what you mean by "beginning of the exon" but there are short ORFs (< 100 codons) which can code for small peptides [4]. Small peptide as small as 6 amino acid residues has been reported but most of the known small peptides are ~30-100 residues long.

References:
[1] Loughran, Gary, et al. "Evidence of efficient stop codon readthrough in four mammalian genes." Nucleic acids research 42.14 (2014): 8928-8938.
[2] Agafonov, Dmitry E., et al. "Efficient suppression of the amber codon in E. coli in vitro translation system." FEBS letters 579.10 (2005): 2156-2160.
[3] Wikipedia: Expanded genetic code
[4] Andrews, Shea J., and Joseph A. Rothnagel. "Emerging evidence for functional peptides encoded by short open reading frames." Nature Reviews Genetics 15.3 (2014): 193-204.

Thank you for your answer. I have one more clarification. In one of the human protein, i am getting three stop codons (UAG, UAA, UGA). However, i am getting more than 80% of UGA in my transcripts. I appreciate if any one educate me, which is the most frequently present stop codon in human transcripts.

@Krithi.S I have not checked but this is fairly easy to do. Just download all human mRNA sequences from RefSeq/GTF file with CDS annotations and find the stop codons.

I'm tempted to link articles from the sixties with me being so old. Amber is the most commonly read through stop codon throughout nature.  http://www.sciencedirect.com/science/article/pii/S0014579305003224 for a modern example of how it's used

Right that appears to be the mechanism, but it should be noted that it's specific to the Amber stop codon. In bacteria and viruses you can often see doubling or even tripling up of stop codons to prevent Amber readthrough

@AtlLED Is there readthrough in mammalian/human genes?

@MattDMo I certainly know of cases in cancers and viruses using host machinery. Off the top of my head I don't know of any endogenous examples in mammals, but one could look. I note the OP makes no mention in the question.

@AtlLED yeah, I haven't heard of any endogenous examples either, I was just wondering if recent work had come up with anything. Of course, anything goes with tumors/viruses, so that's not surprising.

@MattDMo Quiet true. But given that when it happens, it's normally only a small portion of actual translation, that I don't think anyone is looking closely enough in the absence of some pathology. I suppose if a bioinforamtics PhD student wants to tackle this, you could look for cases in the human genome where there is an amber followed by another stop codon and see if you find read through on that gene (with 2nd stop oblated). I think it would be hard to get funding on it though. Checking PubMed, I'm pretty sure nobody is looking.

@AtlLED something for me to do at home in my spare time. Minus the wet work, of course :)

@MattDMo the linked article (ref#1) talks about readthrough in human genes

@WYSIWYG My point was that wasn't endogenous. I was thinking a Crisper exp. would be more convincing than transient expression.

@AtlLED As long as the entire cDNA is cloned and expressed there should not be a great difference, unless the plasmid expresses too many mRNA copies in which case there might be concentration dependent effects. I agree that working on an endogenous system is better. By CRISPR experiment you mean mutate one of the stop codons?

@WYSIWYG That's exactly what I mean.  The transfection experiment was a good 1st step, but I have a hard time imagining that cDNA under CMV or PGK promotion will not confound studying read-through (over expression or lenti incorporation as done in ref 1).  I think oblating the second stop codon in the genome would be the ideal way to look at this.  Also, we should probably move to chat after this, because I think we're diverging from the question.

@MattDMo absolutely. Not only is there "abnormal" readthrough, you also have selenoproteins where the amber codon codes for a bona fide aminoacid, Sec.


text:
Do camels have nucleated RBCs or enucleated RBCs?
Most mammals have enucleated RBCs as an adaptation to facilitate the transport of oxygen. My text says that camels and llamas are exceptions to these.
I was wondering why they are exceptions, and the Google search results are confusing. Some sites say that camels have nucleated RBCs to facilitate cell division. Some others state that camels, like all other mammals possess enucleated but different shaped RBCs. So, which is correct?
The links:https://www.quora.com/Why-do-camels-have-nucleated-red-blood-cells
https://in.answers.yahoo.com/question/index?qid=20070702070352AAkfspZ

Could you maybe add some links to some of the sites you found? Then it is easier to track down, where they get their information from and figure out which is reliable.

You should probably write to the editors of your textbook and ask them to correct this. It is time for education boards to make it compulsory for textbooks to cite references except for very basic information.

Camel RBCs are anucleate [1, 2]. The dark structure seen in microscopic images is not nuclei but a network of microtubules called the marginal bands. Marginal bands cause these RBCs to adopt an ellipsoid shape. The unique shape of these RBCs possibly allows them to survive osmotic stress and is probably advantageous to a camel under extreme dehydration.

References:
[1] Cohen, William D., and N. Barclay Terwilliger. "Marginal bands in camel erythrocytes." Journal of cell science 36.1 (1979): 97-107.
[2] Long, Charles A. "Evolution of function and form in camelid erythrocytes." Actas de The 2007 WSEAS International Conference on Cellular & Molecular Biology, Biophysics & Bioengineering. 2007.

Camel erythrocytes are oval in shape and without nucleus. No intracellular organelles were observed with the occasional exception of a small number of mitochondria . are well-adapted to hot arid environment and .The red blood cells of the dromedary camel protect it from dehydration because the oval-shaped cells can circulate even in thick blood and can significantly expand during re hydration

Welcome to SE Biology. Please take the Tour and read about how to answer questions. The poster asked a question because he had found a disagreement or inconsistency in different accounts of camel red cells. To resolve this conflict it is not enough to state what you think the correct situation is, but to cite authoratitive evidence for your point of view. You may well be right, but how can the poster or anyone else (including me) tell?


text:
What happens when the parietal cells of gut epithelium becomes partially non-functional?
The options are
a) The pancreatic enzymes will not work properly
b) The pH of the stomach will fall abruptly
c) Steapsin will be more effective
d) Proteins will not be adequately hydrolysed by pepsin into proteoses and peptones.
The answer is D because pro enzyme pepsinogen gets converted to active pepsin in presence of HCl.
But, Why can't the answer be B ? Because if HCl is not secreted by perital cells then obviously pH of the stomach is going to fall down ?

If you think you got the answer that you wanted then please accept it by clicking on the "tick" mark near the top left corner of the answer (below the vote buttons). If you think the answer was helpful then you can upvote it as well.

Parietal cells are responsible for acid secretion (HCl) in the stomach.
pH is inversely correlated to H+ concentration; the higher the H+ concentration, the lower the pH.
If the stomach's parietal cells become partially non-functional, there will be less acid secreted into the stomach (a lower H+), and the pH will rise.
Answer (b)

(b) The pH of the stomach will fall abruptly

is the opposite of what would be expected to occur.
The correct answer is d), for the reason you listed.

Proteins will not be adequately hydrolysed by pepsin into proteoses and peptones.

Regulation of Acid Secretion


text:
How can neurons divide without centrioles?
I have read in my studies that neurons lack centrioles. If that is so, then how is it possible that new neurons are added to our brain? Does this have anything to do with memory loss?

Neurons do not divide.

@WYSIWYG: in certain places in the brain, neuronal stem cells do.

@Christiaan  yes but they are not neurons.

You talk about memory loss. The hippocampus is involved in the formation and storage of memories and indeed one of the few places in the brain where new neurons are formed. The formation of new neurons here is indeed linked to the formation of memories (Coras et al., 2010).
Hippocampal neurons do not lack centrioles (Dotti & Banker, 1991; Poppov & Tsygunova, 1996). In fact, centrioles may not be necessary for cell division to occur (source: BSCB), although the lack of centrioles in cell models may result in aberrant cell division (Rodrigues-Martins et al., 2008).
In the hippocampus, however, it is not the neurons themselves that regenerate, but rather the resident neural stem cells and progenitor cells (Kirby et al., 2014).
References
- Coras et al., Brain (2010); 133(11): 3359-72
- Dotti & Banker, J Cell Sci (1991); S15: 75-84
- Kirby et al., PNAS (2014); 112(13): 4128–33
- Poppov & Tsygunova, Neuroscience Letters; 203(2): 135–8
- Rodrigues-Martins et al., Cell Cycle (2008); 7(1): 11-6


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Is there a correlation between Animal Intelligence x Playing time?
I'm writing a small text for a blog about playing time and I wish to have more resources about the correlation between Intelligence and Playing time in animals. If not exactly that, maybe some indications leading to this conclusion or even going against it. Correlations between playing time and animals sociability are welcome too.
Thank you very much in advance.

Please explain what you mean by "playing time".

Great, thanks for the interest James. By playing time I mean the time dedicated to playing activities, as in small cubs playing together or with their mother, or chimps chasing one another with the intention of "having fun". I know the concept is very hard to define in behaviourism, but I wish to get some insights regarding to this. I wish to correlate this in order to show how playing is important to learning not only in humans but also in animals. Pardon for the innacuracy of the terms I use.

@FernandoTsukumo I am afraid, that the concept of (measurable) intelligence might be as hard to define (especially for animals), as is playing time. Are you looking to compare the same species of animals, but little ones play more or less or are you looking to generally compare animals that play a lot to animals that do not play as much?

Hi, thanks for the answer. Yeah, I am aware this wouldn't be an easy task, just decided to try a long shot... who knows? Actually, I am trying to find some evidence to something I feel, which is a link between the need of playing time and learning or maybe playing time and sociability among a good number of animal species or even just mammals. I saw that discussion about life expectancy x intelligence and then I got all hopeful about finding something similar regarding playing time. Maybe an impossible task: At least for now?


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What are golgi blobs?
From a general google search I have come to know that golgi 'blobs'(also referred to as "golgi haze") are tubular vesicles formed during the interphase of mitosis.
I would like to be reassured and also learn more about this topic. If possible please include a diagram in your answer.

What are golgi?

Stacked array in the cisternae which are ought to connect vesicles and tubules
Made of >1000 different proteins
Has the ability to transform/alter in response to a cellular stimulation such as mitosis

Fragmentation of golgi during mitosis

During interphase, the Golgi receives secretory cargo from the ER via the COP II vesicle formation pathway. Depending on their nature, secretory cargo then travel through the Golgi apparatus by a combination of vesicular transport involving COP I vesicles and cisternal maturation. A retrograde COP I vesicle pathway connects Golgi cisternae and the ER to allow recycling of Golgi enzymes and integral membrane proteins of the transport machinery such as the SNAREs. Two models have been proposed to explain the fate of the Golgi in mitosis. The first is the direct fragmentation model, where Golgi cisternae are consumed by continued COP I vesicle budding in the absence of membrane fusion, which is blocked in mitosis. This generates a pool of tubules and vesicles (Golgi haze) containing Golgi enzymes and structural proteins. The second is the ER recycling model, where forward transport into the Golgi by COP II vesicles is blocked, but COP I recycling back to the ER continues until Golgi proteins are redistributed to this compartment. Some Golgi proteins may then exit the ER via the COP II pathway, but these vesicles are unable to fuse with a Golgi compartment during mitosis, and remain in equilibrium with the ER.

A more detailed outline of the process of fragmentation of golgi apparatus can be found here and here

As I know "golgi blobs" are also referred to as "golgi haze".
Sources:

http://www.clfs.umd.edu/classroom/mocb639/Hamza_Golgi_Apr5_2005.pdf
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2175146/
http://www.cbi.pku.edu.cn/chinese/documents/cell/xibaoshengwuxuecankaowenxian/cocb/15/15-4/15-462.pdf

@SanjuktaGhosh You're welcome. Let me know if you have any follow-up questions.

Golgi blobs are larger fragments and are resolvable by light microscope.  The golgi haze is not resolvable and just causes scattering of light in the microscope as if it were a fog.


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Relaxing Eyes when using Virtual-Reality-Glasses?
Accommodation is the process by which the vertebrate eye changes optical power to maintain a clear image or focus on an object as its distance varies (eye focusing). For distant vision, the ciliary muscle must relax and the eye’s crystalline lens is stretched out.
When using a Virtual Reality Device (Occulus Rift, Samsung VR, Sony VR, Google Cardboard etc.) the eye has to focus on the screen that is only a few centimeters away from the eyes. I am aware of the Vergence-Accommodation Conflict. Yet I ask myself,
Is the ciliary muscle relaxed or contracted when looking at a (virtually) far distant object projected on the LCD of the VR-Device?

The eyes cannot focus on something a few centimeters away. The average maximum distance where the eye can still focus is 14 Diopters in young people (Duane, 1922) (approximately 7 cm in 8-year olds). The distance to the eyes of the display in a head-mounted display (HMD) is often less than this and hence the eyes cannot possibly focus on this. Instead, with the use of lenses, a virtual image is created at a virtual distance approximately a meter away (Fig. 1). In the Oculus Rift DK1, for example, the virtual screens were infinitely far away; in the Oculus Rift DK2, they are about 4.5 feet (1.4m) away (source: Immersive Computer Graphics). One meters is a comfortable viewing distance with minimal accommodation needed and hence little eye strain (source: Immersive Computer Graphics). At around 6 meters the eye is unaccommodated.

Fig. 1. Virtual image in a HMD. Left: eye failing to focus on a very close real screen. Right: eye able to focus on the virtual image of the same real screen created by an interposed lens. source: Immersive Computer Graphics
Reference
- Duane, Trans Am Ophthalmol Soc (1922); 20: 132–57

Did you notice that the image you've posted gives an optical illusion when scrolling page up/down?! Or is it just me? ;)

@another'Homosapien' - wow! I hadn't noticed :D


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Calculating the human carrying capacity for turtle tours?
I am looking to calculate the human carrying capacity of a leatherback nesting beach in the Caribbean to inform conservation policy on the maximum number of people allowed on turtle tours; yet after an exhaustive search, I have found very little. Could anyone point me towards a research article that could be of assistance?

The carrying capacity of a species at a given location is the number of individuals of that species that can live at this location. I suppose what you are looking for is rather something like the maximum number of humans that can live at a given location while keeping a carrying capacity for leatherback above a certain level. You might want to rephrase the question


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Books about famous experiments in biology - 'methods of investigation'
I'll explain briefly what I need (hoping to find something) :
I wanted to know if someone knew about a book that in a way or another talked about the greatest experiments in biology (Griffith, Avery-MacLeod-MacCarty, Hershey-Chase) or methods normally used to study  certain phenomena  for example, and explaining or talking about the paradigm used in biology research in such cases.
I know it might sound too vague, but I will have a kind of 'exam' essay, in which in addition to the biologic phenomena asked in terms of "notions" one will also have to suggest a 'method of investigation' to study it.
And my main problem is that in school just the theory is normally taught and not the practical approach to such topics, so I really lack knowledge in this.
So what I'm asking is whether there is a certain book or even a suggested approach that I might start using that might help me in learning what I explained above.
Thank you for your help!

Honestly, someone needs to write this book.

Microbe hunters is an excellent book which will fulfill your requirements. You will get an insight into the working of some of the greatest minds....

Although it's not stricly about biology, A short history of nearly everything by Bill Bryson, especially chapter 5, is a good start to look for historical experiments.

The Eighth Day of Creation by Horace Freeland Judson is quite good, in the genre you're looking for. Also, Science as a way of Knowing may fit the bill.


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Can lactate be created in ketosis?
After looking at Cori Cycle (from wikipedia)

I have a question about how the lactate can be produced in ketosis. According to this article:

in a low-glucose state, where the body senses that dietary glucose might not be coming anytime soon, peripheral insulin resistance is triggered. This prevents the muscles from taking up “precious” glucose that the brain requires. The brain’s sensitivity to insulin is preserved, allowing it to grab what glucose it needs from the paltry – but sufficient – levels available to it.

it seems that the glucose is not even transfered into muscle cells. In spite of this fact, the lactate is still somehow created during hard exercise even in full ketosis when ketones are present in the bloodstream. How is it possible?

First, there are inaccuracies and misconceptions in the article you quote, which also relates to obese people with insulin-resistance (pre type II diabetics) rather than normal people. These are:

I’m not sure what a “low glucose state” is supposed to mean, but the tissues of the organism co-operate to ensure that the blood glucose concentration normally never falls below about 4 mM, with a range of approx. 4–8 mM. Thus, glucose is available in the blood for tissues that can take it up in a particular circumstance. These are not “paltry levels”, as quoted.
The body’s metabolism cannot predict the future. The scientific credentials of anyone who writes “the body senses that dietary glucose might not be coming anytime soon” are hardly to be trusted. (I don't think much of his literary style either.)
In short-term starvation, when the blood glucose concentration falls towards the lower end of its range, insulin resistance is not triggered. Insulin secretion from the pancreas stops (and glucagon secretion starts).
The brain is not sensitive to insulin (i.e. its glucose
transporter(s) is not), whereas the muscle is. This is what allows the brain continued access to glucose.

Some of this is elaborated in my answers to: “What is the purpose of gluconeogenesis?”,  “How do muscle cells synthesize glycogen?” and “During starvation, does the human body do anything to prioritize which organs receive nutrients?”. A section from Berg et al. may also be of interest.
Answer
Lactate can (and must) be generated by non-aerobic muscle metabolism (i.e. in muscle lacking mitochondria) during exercise because anaerobic glycolysis, with conversion of pyruvate to lactate, is the only way the muscle can obtain ATP to power its contraction. The source of this is the glycogen stores laid down in the muscle after a meal, and glucose taken up from the blood.
I don’t know anything about low-carb diets, but I assume they include protein, so that some of the amino acids from this can be converted to glucose by the liver (glucogenic amino acids) as well as those that cannot (the ketogenic ones that can give rise to ketone bodies). Even if the blood glucose is at the lower end of its range, in the non-starved state the muscle can take it up from the blood. (The blood glucose will be restored by the so-called Cori Cycle.) Even in starvation, if the muscle is working there will be a concentration difference between blood and muscle glucose that will allow uptake.
I think that this question is provoked by the feeling that the existence of ketosis means that glucose is not available to cells. This, as I hope I have explained, is a misconception, perhaps arising from confusion with the different situation of ketosis in long-term starvation.
Finally, there are other sources of lactate besides muscle, regardless of diet. One is the erythrocytes which lack mitochondria and therefore can only use anaerobic glycolysis to produce the ATP they need for active cation transport etc.

Thanks for clarification and links. It's the case for long-term ketosis - how is  the situation different?

Can you clarify a couple of things so that I know 'where you are coming from'. When you say 'long-term ketosis', do you mean as a result of following this low-carb diet for a long time? And what is this balance of carb/protein/fat in the diet that is producing this ketosis? Also, why are you so concerned about lactate — do you have figures for it or is it just a general concern?

80% fat, 20% protein and trying to avoid carbs for 3 months. I have no figures about lactate, it is just curiosity - I was not sure which articles should I trust.

In the circumstances I wouldn't expect any difference from what I have in my answer (although I'm not a nutritionist). If you are feeling well then you obviously don't have low blood sugar. I presume that the ketone bodies produced from fat and ketogenic amino acids are helping offset the brain's need for glucose and the glucogenic amino acids and any carb is keeping the blood glucose normal and allowing the muscle (and brain etc.) to replenish glycogen stores when needed. Assuming that you are an athlete, your usage will depend on which muscles you use for sport.


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Directed evolution: Point mutation vs Insertion-Deletion vs Shuffling
When attempting enzyme function improvement via Directed Evolution I can see three different strategies to generating variation for the gene sequence:

Point mutations
Insertion / Deletions
Shuffling

Is there a systematic difference between how successful each of these approaches are likely to be for a particular gene or in general? Does one choose one over the other approaches in any specific project based on any characteristics / goal differences?
A related question: On a methodological front, I know one can use error prone PCR to get #1 i.e. point mutations.
What are similar techniques for #2 & #3? i.e. How does one execute gene shuffling or Insertion / Deletions in practice?

In general, point mutations are introduced in the proteins of interest during directed evolution. These can be specific mutations in the active site of an enzyme if you would like to change its specificity towards a new substrate, for example. The point mutations can be introduced with primers when you amplify your gene of interest. However, if you don't know specifically what changes to make, then yes, a way to generate mutations is by error prone PCR or by Quick change PCR. If you'd like to see if a certain amino acid change abolishes activity/stability/etc, you would do Alanine scanning (https://en.wikipedia.org/wiki/Alanine_scanning).
I haven't heard much about introducing deletions or insertions for directed evolution. First of all, they have to be in-frame, so that the overall coding sequence does not change. People are usually introducing epitope tags on the N- or C-terminus for two reasons: 1) to purify the proteins; 2) to increase its solubility. But in general, the introduction of deletion will lead to unpredictable changes to the 3D structure of the protein of interest.
The DNA shuffling is very often used for directed evolution. Here is a figure from a Nature paper [1] describing DNA shuffling. The way it is usually performed is by using sequence homologs of the protein of interest. The different fragments can be obtained by PCR-amplification and introducing short overlaps with the neighboring fragments. The fragments can be then assembled by various methods, including Gibson assembly and homologous yeast recombination.  The advantage of DNA shuffling over introducing single mutations is that you have to screen fewer mutants and the activity/stability of the protein could be improved several hundred fold more.

DNA shuffling figure from [1]
Interestingly, a DNA shuffling using a method called SCHEMA [2] was developed in Chris Voigt lab. Shortly, SHEMA is a computational algorithm used to identify the fragments of proteins, or schemas, that can be recombined without disturbing the integrity of the three dimensional structure. It is based on the 3D structure (of one of the parents) and an alignment of the parental sequences. It calculates the interactions between residues and determines the number of interactions that are disrupted in the creation of a hybrid protein. A window of residues w is defined and the number of internal interactions within this window is counted. The window is slid and the schema profile is created. For example. in the figure below, the number of interactions that are broken in the possible chimeras are 0 on the right chimera and 3 on the left chimera. The right chimera will be used in the screening.

SHEMA method from [2]

Thanks @Gergana. I have posted a follow up question. Would love your comments if you can! http://biology.stackexchange.com/questions/45572/why-is-dna-shuffling-more-efficient-than-point-mutation


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How does consumption of vinegar affect food chemistry?
For example: does consumption of vinegar somehow change digestion of flour (bread, cakes, pasta, puffs) ? May be there are some benefits to eat flour meal with vinegar ?

How much vinegar are you talking about? 50ml? 500? 2L? What sort of "benefits" are you expecting? And could you define "dough" - do you mean uncooked bread dough, or something else?

@MattDMo I mean bread, cakes, pasta... quantity to taste.

In the case you're talking about (just using vinegar to taste), there should be no effect whatsoever on a healthy stomach. The stomach already contains a significant amount of acid, and a little bit more from the acetic acid in vinegar won't change much, just like eating some citrus fruit with a meal (oranges, lemons, and whatnot) won't change much. Acid-mediated hydrolysis of chewed food is only the first of many steps in digestion - a significant portion is performed by enzymes and commensal microorganisms in the gut. Changing the type or amount of acid by a small amount won't affect anything significantly in the long run.
The only exception I can think of is for people suffering from peptic ulcers, whether from over-use of NSAIDs (Non-Steroidal Anti-Inflammatory Drugs such as aspirin, ibuprofen, naproxen, etc.), infection with H. pylori, or possible genetic/developmental issues (most often seen in young children). In these cases, consuming an overly-acidic meal may aggravate the symptoms of peptic ulceration.


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What's the highest glucose concentration (in mM) anywhere in the human body (tissue, capillaries, tumor microenvironment, etc.)?
Glucose blood levels are around 5mM, or 10mM after meals. In capillaries these levels can rise by about 40 %. I haven't found measurements of glucose concentration in tissues, or in extracellular spaces. I'm wondering what's the highest glucose concentration, anywhere in the human body?

Fasting or prandial state?

@VanceLAlbaugh Highest, any state.

I would guess that the highest glucose concentration would be during the active absorption of a high carbohydrate meal - the carbs would be digested and broken down to glucose. The glucose concentration in the GI capillary beds - which would include both circulating glucose and glucose absorbed from the GI tract would be the highest concentration - not sure if there are any good estimates of the actual concentration

@VanceLAlbaugh I just need an order of magnitude.

Glucose concentration in the blood is a highly regulated biologic variable. From personal laboratory experience, it is very difficult to raise a healthy, non-diabetic individual's blood glucose over about 6.5-7 mM (i.e. 120-130 mg/dl). My best guess at where the highest glucose concentration might be in the body is within the hepatic portal vein that drains the intestines after a high carbohydrate meal. The glucose concentration is probably highest in the prandial state or, in other words, when carbohydrates (i.e. food) is being digested and absorbed by the gastrointestinal tract. Many simple and/or complex carbohydrates are digested to glucose and absorbed through the gastrointestinal tract. Once absorbed the glucose enters the venous mesenteric circulation and then drains into the hepatic portal circulation. This allows high concentrations of glucose and other compounds like amino acids from dietary nutrients to be "buffered" by the liver.
I don't have hard evidence to demonstrate that this is the highest glucose, but I think it's probably a good guess. It is inherently difficult to measure the blood glucose concentration in the portal vein - mostly because it's so difficult to get to that place anatomically during a meal. The dog is probably the most used animal for these types of metabolic studies, because catheters can be placed in the peripheral venous and arterial circulation, as well as in the portal vein and hepatic veins, to measure nutrient uptake by the intestine and nutrient extraction by the liver.
A number of previous studies by Cherrington and colleagues, who have done some of the most comprehensive work in this field, frequently measure glucose concentration and blood flow rates across the liver. In one such paper that is freely available from the American Journal of Physiology by Abumrad et al (1982) entitled, "Absorption and disposition of a glucose load in the conscious dog" you can see from Figure 1 the average plasma glucose concentration in the portal vein from a group of dogs given an oral glucose load of ~40 grams is somewhere in the 250 mg/dl region (i.e. ~14mM). These were otherwise healthy dogs, and similar to healthy humans I would bet the glucose concentration doesn't rise too much further. As you could imagine though, in a diabetic individual who has high peripheral glucose concentrations to start, the portal vein concentration might be expected to be higher. How much higher is another educated guess - maybe 100-200 mg/dl higher on an extreme end (obviously pathologic).
In a healthy human (i.e. non-diabetic) who undergoes a 75-gram oral glucose tolerance test I can't imagine that the portal glucose would go any higher than 300-400 mg/dl (or, 16.5 to 18 mM). But again - these numbers are just educated guesses. This is probably the highest glucose concentration anywhere in the body. Additionally, in diabetic patients the glucose concentrations would be expected to be slightly higher because circulating glucose may be slightly higher, but probably not by too much (definitely not an order of magnitude).

Thanks, these sort of estimates is kind of what I was looking for to get started.

happy to help @becko - in diabetic patients the numbers might be a little higher, but not that much higher (definitely not an order of magnitude)

@becko if this answer is sufficient to answer your question... think about accepting it officially - thanks!


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How can I accurately measure glucose concentration in culture media?
I am trying to identify the best way to measure glucose concentration in culture media with E. coli. Now, I imagine I can use those glucose meters that diabetic people use, but unfortunately can't find any papers as background.
Any ideas would be appreciated.

you definitely cannot measure media glucose concentration with a blood glucose analyzer - see this link for more information on that... http://biology.stackexchange.com/q/20325/16299

there are a number of colorimetric assays that are commercially available - we routinely measure plasma and other fluid glucose concentrations using a single reagent method and a standard curve - you just need a UV/Vis reader and some reagent which is inexpensive

Thank you Vance for taking the time to reply. As you can probably tell, it's my first day here!

@VanceLAlbaugh,  It think it's possible to measure glucose concentrations in pretty much any solution with a blood glucose analyzer. But you need to recalibrate the signal since the typical assumption of the instrument are no longer valid. Just do a standard curve of known glucose concentrations in medium. We have done this before with blood glucose analyzer and I think it works well. These analyzer are just a glucose oxidase kit in miniature, they are no better or worse than other enzymatic methods in my experience.

The most common method of measuring glucose concentrations (in pretty much any sample) is an enzymatic assay based on the glucose oxidase enzyme. This method is reliable because the enzyme is known to be quite specific for glucose; it does not oxidize fructose, galactose, or any of the other common hexose sugars which can contaminate many other measurement methods. The enzyme can be coupled to other reactions so that the amount of glucose oxidized can be read out by a standard spectrophotometer. There are many kits commercially available based on this principle, like this one. A review of glucose oxidase from the glucose measurement perspective is found here.
Blood glucose analyzers are also based on glucose oxidase. Typically, they have disposable slips that contain glucose oxidase along with some electron-carrying chemicals that convert enzyme activity into an electrical current sensed by the device. It is possible to measure glucose in pretty much any solution with such insruments, but as mentioned in comments, you need to make a calibration curve for glucose in your solution of interest (culture medium, or whatever), as you cannot trust the readings from the instrument directly when measuring under different conditions. We have previously used this approach to measure glucose in mammalian cell culture medium, and it works fine in our hands.
It is also possible to quantify glucose by mass spectrometry or nucleic magnetic resonance methods, but unless you have such a facility and expert help, I guess that is not an option in this case.


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Optimizing Gel Electrophoresis: Ampere, Volts and Buffer concentrations
I am a master student in biochemistry, and I have used gel electrophoresis many times before. What I want to know is how one should adjust the mA (mAmpere) compared to the voltage and the buffer one uses.
Normally I used 1xTAE buffer (run at 90V) or 1x sodium borate buffer (run at 110V). I know that if I adjust the voltage up, the buffer heats up faster, the samples travel faster, but the "picture" of the gel becomes more blurry. This is however all I know about adjust the parameter.
So my questions can be summarized as the following:

How should I adjust the ampere, is there a range I should be in
compared to the buffer or sample I am running?
Does the ampere effect the travel speed if adjusted up or down?
Can I adjust the concentration of the buffer to run sample at a
higher voltage, what effects will this have (to increase or decrease
concentration)?
Is there a relationship between the ampere and the voltage which I
can manipulate, in this case: how and why?

This page by Thermofisher also gives a lot of tips for optimization: https://www.thermofisher.com/se/en/home/life-science/pcr/elevate-pcr-research/agarose-content-with-tips-and-tricks.html

As far as I know you can either adjust the ampere or the voltage as
both is dependent of the resistance from the buffer. Which means that
I would suggest you to let the voltage as it is.
As the ampere = voltage / resistance and voltage = resistance *
ampere and as you can see that the voltage has to get higher if the
ampere is increased and the ampere has to get higher if the voltage
is increased (at least if I understand it correctly) the travel speed
should be increased the higher the ampere is set.
I would neither decrease nor increase the concentration of the buffer. Maybe easily using another kind of buffer would help you. But this depends on the different samples you are running. Maybe that could help you:
Brody, J.R., and Kern, S.E. (2004). History and principles of conductive media for standard DNA electrophoresis. Analytical Biochemistry 333, 1–13.
The resistance is more or less given. Therefore as far as I know: No.


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Does the creation of memory involve mRNAs crossing the synaptic gap?
There is a diagram from a book titled "Teaching with the brain in mind". The diagram shows
The diagram appears to show that the "creation of memory" involves "messages coded by RNA" moving through an axon and being released into the synaptic gap, whereupon they presumably bind to the receptors on the other side of the synapse.
Unfortunately the book does not seem to provide any sources for this and I have not been able to find any sources corroborating this claim. Can anyone provide any references?

The diagram is garbage.  The book's author, Jensen, has a degree in English, not science, and the book is part of the promotion of his workshops on how to teach.

That mystifies me. He could have shown the usual cholinergic signaling.

I have never heard of this pathway. Memory is usually assoiciated with synaptic plasticity by ‘Long-term potentiation’ (LTP), which has glutamate as a neurotransmitter. Neuroscience Exploring the brain (Bear, et al,. 2007), has a pretty good explanation of this process, if you're interrested. Motor patterns have more mechanisms than LTP, and are not as well understood.

Neurons have been shown to secrete exosomes (extracellular vesicles containing RNA) which may regulate neighbouring cells. However, this is mechanistically different from synaptic signalling by neurotransmitters. Moreover, I am not sure if exosome secretion is linked with synaptic activity and whether it plays a role in memory formation. Even if exosomal RNAs do have a role, their contribution is likely to be minor, compared to other pathways (such as NMDAR, mGluR, neuropeptides etc) involved in memory formation.

References:

Bahrini, Insaf, et al. "Neuronal exosomes facilitate synaptic pruning by up-regulating complement factors in microglia." Scientific reports 5 (2015).
Bellingham, Shayne A., Bradley M. Coleman, and Andrew F. Hill. "Small RNA deep sequencing reveals a distinct miRNA signature released in exosomes from prion-infected neuronal cells." Nucleic acids research (2012): gks832.
Chivet, Mathilde, et al. "Emerging role of neuronal exosomes in the central nervous system." Front. Physiol. 3 (2012): 145.


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How are chemical reactions organized in prokaryotic and eukaryotic cells?
I realized I only have a vague understanding based on what remember from high school and I don't know if they ever really broke it down for us but:
In general how do both prokaryotic and eukaryotic cells organize their chemical reactions? In prokaryotic cells I thought there were no organelles so does that mean that every reaction depends on the diffusion of the reactants throughout the cell and that any reaction could happen anywhere in the cell? And in eukaryotic cells, are organelles always used to compartmentalize stages in chemical synthesis?
What I'm getting at is that if everything is just floating around freely within a cell, wouldn't a lot of reactions interfere with each other? I'm wondering how these two types of cells approach this problem.

Okay, this is my first post on this site so please bear with me when it comes to the format of my response!
To begin with I'm going to try and answer your question by clarifying some things.

In prokaryotic cells I thought there were no
  organelles so does that mean that every reaction depends on the
  diffusion of the reactants throughout the cell and that any reaction
  could happen anywhere in the cell?

Yes and no, the fact that there are no membrane bound organelles in prokaryotic cells means a majority of the reactions occur in the cell's cytoplasm via diffusion but something to keep in mind is the selectiveness of the cell's membrane will regulate the substances entering the cell in turn controlling that reactions that occur within it.

What I'm getting at is that if everything is just floating around
  freely within a cell, wouldn't a lot of reactions interfere with each
  other?

When it comes to  eukaryotic cells structures do not float around freely like soup, there is cytoskeleton composed tubules and filaments that is used for  intracellular transport, this skeleton acts like a road system to move substances between static organelles. Prokaryotic cells do not require this since they do not have membrane bound organelles and the diffusion of substances into the cell is controlled by the cellular membrane.

in eukaryotic cells, are organelles always used to compartmentalize
  stages in chemical synthesis?

Not always, you can look at things like cellular respiration to see glycolysis occurring in the cytoplasm.
I hope this helped out some!

Please add references to your post for the sake of those who might want to read further  :-)

Organization of reactions occurs in both prokaryotic and eukaryotic cells. A very basic example of this would be that of multiprotein complexes such as fatty acid synthases and polyketide synthases. Organization of such complexes allows the substrate to be passed from one module to the other; in other words free diffusion of substrate is prevented. This kind of organization can also be seen in case of cell signalling receptors; there are scaffolding proteins that bind different components of signalling cascade together (for example the Grb2 protein).
Regarding organelles:
Prokaryotes do have organelles (in a way); they don't have the membrane bound organelles like ER, mitochondria etc. However, if you consider organelle to be a subcellular structural complex that is dedicated towards a certain function, then prokaryotes do have ribosomes, thylakoids, vacuoles (in some species) etc. All these structures have an organized structure that allows reactions to happen at a faster rate compared to a free-diffusion situation.
In eukaryotic cells, the organelles perform different kinds of function. Organization is one of the molecular aspects; they also can have different chemical (such as redox and ionic) environments which facilitate certain reaction. So their role they play in different metabolic reactions is a composite of all those molecular properties.

One more point to make that wasn't covered in the other answers - in some cases, free diffusion of reactants is desired in order to regulate cellular processes. For example, take amino acid synthesis. At least one of the enzymes in the synthesis pathways of the various amino acids is reversibly inhibited by the presence of the AA itself. Therefore, if AA levels in the cell are high (above a certain threshold concentration) then the pathway is inhibited, and no more of that particular AA is made. However, later on the cell could be in a starved state, AA levels would drop, and the enzyme machinery would start up again to make up the shortfall.
This is a very general example, of course, but there are specific instances of it all over the place - generation of ATP, glucose metabolism, fatty acid synthesis, etc.


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How is receptor production (recycling) regulated?
My understanding of receptor downregulation is that when activated, a receptor then gets absorbed into its cell, as shown in this weird video. It then gets either recycled or degraded. Tolerance presents when more degradation than usual happens.

Receptor activated (ligand binds to receptor)
Receptor-ligand complex internalized to cell
Some complexes recycled, others degraded
Tolerance = more degradation than usual, resulting in lower
receptor density at cell surface (called downregulation)

So, what is causing the higher degradation than usual? Is it the lack of the materials required to produce the receptor? If so, can this be compensated for via diet or supplementation (i.e. eating more dopamine precursors if you're trying to avoid dopamine receptor downregulation, for example?)

So, what is causing the higher degradation than usual? Is it the lack of the materials required to produce the receptor?

Lack of materials is almost never the reason. Receptor turnover is actively controlled by different mechanisms. Ubiquitylation is one of the common mechanisms. Ubiquitylated receptors are internalized; these internalized receptors can later on be sent back to the membrane (recycled) or be degraded depending on the conditions.
Receptor downregulation can also happen by stopping their production either at the level of transcription or translation (For an example see this).


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What physical traits are derived from the Neanderthal DNA in human DNA?
Some researches had found that Human DNA has a bit of Neanderthal DNA. So they suggested there would have been crossing between Homo sapiens and Neanderthals.
Now the Neanderthal looked a bit different from Homo sapiens, so is there something in human that has some neanderthal looks?
And is it only found in European people or also in Asian or African people. Could it be be possible that a larger hairiness of European man is due to Neanderthal DNA?

There was a very readable piece on this topic by Chris Stringer in Nature in 2012. At that time his general conclusion was:

It is not yet clear whether the archaic DNA many of us carry is tied to any visible traits.

Although he added:

More controversially, some of the known differences in coding DNA
  between Neanderthals and recent humans are associated with brain
  development and function

quoting the paper in Science (2010) in which the Neanderthal sequence was published. There may be more recent information of which I am not aware.
As to your question about Neanderthal DNA in different populations, it is not present in people of African origin, but is present in those of Europeans and Asian origin.

Some more recent work has also linked Neanderthal-derived alleles with a plethora of phenotypes. See Sankararaman et al. Nature 2014, Vernot and Akey. Science 2016, and Simonti et al. Science 20160. Also a nice summary: Our hidden Neandertal DNA may increase risk of allergies, depression

Thanks. I suspected there was more recent stuff. You should add it as your own  answer.

Adding to @David's answer, there has been some recent work looking at Neanderthal DNA in the context of Denisovan and modern human populations.
David Reich's group [Sankararaman et al. Nature 2014] found Neanderthal-derived alleles in genes that affect skin and hair (specifically keratin filaments), as well as some that confer risk of disease. Another cool finding:

... there is an approximately fivefold reduction of Neanderthal ancestry
  on the X chromosome, which is known from studies of diverse species to
  be especially dense in male hybrid sterility genes. These
  results suggest that part of the explanation for genomic regions of
  reduced Neanderthal ancestry is Neanderthal alleles that caused
  decreased fertility in males when moved to a modern human genetic
  background.

A pair of papers from the groups of Joshua Akey [Vernot and Akey. Science 2016] and Tony Capra [Simonti et al. Science 2016] found associations between Neanderthal alleles and various phenotypes including depression, hypercoagulation, and tobacco use. These results are nicely summarized here.


text:
Which of the following lacks DNA?
a) An Enucleated ovum
b) Mature RBC
c) A mature spermatozoan
d) Hair root
According to me, there can be 2 answers, a and b because an ovum whose nucleus has been removed lacks DNA. And also, initially RBC has a nucleus but as it matures it's nucleus disappears. So, mature RBC should also lack DNA. Then which one will be a more appropriate answer ?

If it's a mild trick question, then note that it doesn't say "genomic DNA" but "DNA". Enucleated ova would still have mitochondrial DNA, while mature RBC would not.

This should not be closed - OP has clearly attempted to answer and justified it!

@layork - nice  one - write it up as an answer - +1 from me :-)

@iayork Thank You. I understood it. You can post this as an answer.

It should be closed! It's not a question about biology it's a stupid MCQ. it's no use to anyone else than the questioner to have it here. It's the sort of rubbish that demeans this SE.

Further to my last, I have posted a proposal on the Meta site to automatically disallow MCQs. Those who find this acceptable are asked to argue their case at: http://meta.biology.stackexchange.com/questions/3369/change-homework-policy-to-disallow-multiple-choice-questions-mcqs

One last comment. How could the moderators react constructively to an MCQ under my proposed ban? In this case they could rephrase the question as something like "Are there any cells in the human body that lack DNA? I can think of two..." This would transform a specific a, b, c or d MCQ into a general biological discussion.

its a tricky one but the answer of mitochondrial genes may help us to eliminate the option of enucleated ovum and we can go for rbc

I agree with @David. Although, the asker has attempted to find an answer, questions like this are not useful. They are not straightforward questions about biological facts and are primarily intended to confuse the students (or test their ability to read the question carefully instead of actually testing the knowledge).

There are two answers if the question refers to genomic DNA (neither enucleated ova nor mature RBCs have genomic DNA).  However, since the question doesn't specify genomic DNA, we can exclude enucleated ova, which would still have mitochondria and therefore mitochondrial genomic DNA.  Mature RBCS (at least in most mammals) do not have mitochondria, so the safest answer is probably b) Mature RBC.

First of all, 2) mature human RBCs don't have DNA. With the maturation of human red blood cells, the nucleus disappear. DNA is located in the nucleus so mature human RBCs don't have DNA.
However, your question didn't say "human RBC". Bird RBC have nucleus thus have DNA.
Then, both ovum and sperm cells have nucleus, thus have DNA, no matter which stage they are in.
I would say the possible answer be 4) hair root. The question didn't make it clear whether it's referring to the hair root cells or something else. But I would say that hair root is not made of body cells. No cell, no nucleus, no DNA.

the answer will be mature DNA.
We know that except for nucleus other organelle such as mitochondria also have ability to replicate an as mentioned in the question the enucleated ovum (ovum lacking its nucleus) do have the other cell organelles, whereas for the mature erythrocytes, they lack nucleus as well as other cell organelles such as mitochondria and golgi bodies; and hence RBC can't divide on its.
hope it helps!

You are repeating the point made by an existing answer. If you have a new point to add then please [edit] your answer accordingly.


text:
Standard cycles for virus detection
I would like to know if there is a Standard number of cycles for Virues and Bacterial PCR single and multiple targets

No, there isn't. It's completely dependent on the sample, how it was prepared, the quality of the template, and the viral or bacterial load in the sample. Try something, if there's no signal run more cycles, if the signal is overwhelming run less. That's science.

Or, run qPCR and study the amplification curves...

No, there isn't.
Quantitative PCR (qPCR) uses a specific (e.g. TaqMan) or non-specific (e.g. SYBR Green) dye to detect the point at which the quantity of dsDNA (or a specific template) exceeds a threshold during thermocycling. Assuming you have an appropriate primer, the quantity of target doubles (at most) during each thermal cycle, so the cycle at which the signal exceeds the threshold (the cycle threshold, or Ct value) gives you information about the amount of target initially present.
However, the amount of accessible target in a sample depends on many factors including sample processing, extraction efficiency, sample storage, or the presence of RNases/DNases. The PCR efficiency during cycling also varies depending on conditions. There are also many other sources of variation in qPCR results, for example the platform you're using, the risk of contamination, the cycling program.
In theory, you can keep running a qPCR until you get a signal, but in practice you would stop after about 40 cycles at most unless you were specifically designing an assay to detect extremely low copy numbers since after that the most likely explanation for a positive result is sample contamination. 40 cycles should be enough to detect a template that was only present at 1/1,000,000,000,000 of your detection threshold to begin with. When designing qPCR experiments purely for detection (as opposed to quantification) it is best to include a negative control which helps rule out sample contamination etc. I recommend reading the answer to this previous question to help understand why we stop after a certain number of samples, and see this paper as an example of the risks of not using an appropriate control.
There is some guidance on designing good qPCR experiments at http://www.rdml.org/miqe.php along with a checklist for best practice (although this is specifically aimed at quantitative qPCR studies so not everything on their checklist will be relevant if you are simply thinking about presence/absence).


text:
Does night sleep provide more energy-regain than sleep during the day?
After reading this, I know that sleeping is an universal function, and that basically everything with a brain has the need to sleep.
However, I am still confused to what extent it is necessary to sleep at night to regain energy, or if some rest during the day provides a sufficient energy-regain?

The circadian clock is entrained to sleep-wake patterns. (Sun)Light has a strong capability of adjusting and resetting that clock. Hormonal balance and other functions in the body, in turn, are synced to it. Hence, your question will depend much on whether you are aksing what happens after acute reversal of the sleep/wake cycle, or whether you mean what happens when you revert it for prolonged periods of time. Also, what do you mean with 'some rest'? Of course powernaps during the day can help. I vote to close because it is unclear what you are after.

I think the reason is primarily, that it is more quiet (the chance is very low that other people are disturbing your sleep) in the night as well as it is also dark. Keeping in mind, that the brain "gets tired" due to some proteins (melatonin) and in contrast, being more awake during the day, it seems to be just logical that the sleep in the night is healthier, thus providing more energy.

And isn't the production of melatonin controlable by outter conditions such as illumination and noiseness? Or do you think the biological clocks can keep going in the time undependent environment?

Of course, but it needs some time until it can rise high enough, sufficient for deep sleep at night, where your immune system can regenerate. Some people get health problems such as high blood pressure or weight gain when their sleep at night is insufficient. Found e.g. with shift workers. However, a "quick nap" (about 20 min) at daytime will provide you new energy, as you just rest quickly and don't get to relaxed, where your muscles feel weak, such as after a longer sleep.

i would like to know what happens exactly when you sleep? if you can answer me! (thanks by the way, your answer was a logical and brief one)

A couple of quick google searches would tell you that the important part of sleep is the REM (Rapid Eye Movement) sleep.
REM stands for rapid eye movement. During REM sleep, your eyes move quickly in different directions. That doesn't happen during non-REM sleep.
Usually, REM sleep happens 90 minutes after you fall asleep. The first period of REM typically lasts 10 minutes. Each of your later REM stages gets longer, and the final one may last up to an hour. Your heart rate and breathing quickens.You can have intense dreams during REM sleep, since your brain is more active.(1)
During an eight-hour sleep pattern, the average adult only spends approximately 1.5 hours (or 20% of total sleep time) in rapid eye movement (REM) sleep. REM sleep is important because it is the restorative part of our sleep cycle. Typically, you begin the sleep cycle with a period of non-REM sleep followed by a very short period of REM sleep. The period of non-REM sleep is made up of stages 1 to 4. Each stage can last from 5 to 15 minutes. A completed cycle of sleep consists of a progression from stages 1 to 4 before REM sleep is attained, then the cycle starts over again.
However, if your REM sleep is disrupted even one night, your body won’t follow its normal circadian sleep cycle (“inner clock”) progression. Instead, you will slip directly into REM sleep as a result of not getting the right amount of sleep the night before. You will also go through extended periods of REM sleep until you “catch up” on this stage of sleep. Poor sleep cycles can cause grogginess, a lack of concentration and more.(2)
During day, brain might not get enough time to restore itself as one can hardly sleep for 2-3 hours during day. Though your body might get refreshed after this, your brain might not. Also, as @TheGreenOne says, there are lot more chances of day sleep getting disturbed than night sleep. Another thing is that the brain is habitual to sleep at its normal time (night) (see SCN), so it won't be very easy to get in/out of the habit to sleep during day.
References:

http://www.webmd.com/sleep-disorders/guide/sleep-101
https://www.azumio.com/blog/health/rem-sleep

there's some great information up there, thanks


text:
Is tolerance unavoidable?
Do all psychoactive substances induce tolerance eventually?
For that matter, do all receptor-binding substances induce tolerance eventually?
It seems certain that different substances take different amounts of time to produce tolerance. Is there a pattern here? Do all receptor antagonists take similar amounts of time, or does it vary by receptor type?
(How do we know medications are not a zero-sum game?)

It also depends on concentration. If you're not over-stimulating the cell, tolerance won't be induced. Many patients do quite well on the same dosage of psychoactive drugs for years. Remember, the goal with drug therapy is to make up for the brain's imbalance in neurotransmitters, not to flood the system with them. That's what addicts do.

In general receptor-binding substances cause an "overflow" of your own already produced neurotransmitter. Your brain reacts by reducing the receptors. Also your own neurotransmitter production may be down-regulated by negative feedback. When you take away the "medication" afterwards, there are less receptors together with less neurotransmitter, causing withdrawal symptoms.
When you put in more substance in a control loop, there will always be some sort of "adaption" in order to reinstate a new balance (1). If you take in just enough drugs to balance the neurotransmitter-receptor system in a way, that the signal transduction in terms of nerve pulses remain the same, you have reached a tolerance stage, but not an effect stage. Still, medication is not "useless", since not all receptors will be dissipated. It is a matter of dose rate to increase the nerve pulses; once there is relatively more neurotransmitter (2) available than before medication, one should obtain a constant effect or an effectively altered control loop balance.
(1) https://books.google.at/books?id=z9TUch7m144C&pg=PA34&lpg=PA34&dq=receptor+regulation+up+down+neurotransmitter+drugs&source=bl&ots=2-4GRChqBi&sig=6e0YM-UrfgnMlw6e-rXR2Or7Qxc&hl=de&sa=X&ved=0ahUKEwixr_D25ZDMAhWB7RQKHcF9DqYQ6AEIHzAA#v=onepage&q=receptor%20regulation%20up%20down%20neurotransmitter%20drugs&f=false
(2) http://www.merckmanuals.com/professional/clinical-pharmacology/pharmacodynamics/drug-receptor-interactions

Please add some references to support your claims. Unsourced answers may be challenged and removed.

So, in other words:
"No, medications are not a zero-sum game, as long as the dosage is such than an effect stage is reached, rather than a tolerance stage."


text:
What's the difference between evolution fitness and reproductive success?
What's the difference biological fitness and reproductive success in the biological terminology?

There is the term "evolution" in you title who is not found in the post. But this term is used in an unclear way. did you "evolution, fitness and reproductive success" or do you think that "evolution fitness" is a concept by itself?

The concepts are very similar but there are a few differences.
Firstly, fitness is usually applied to alleles or genotypes, reproductive success to individuals.
Secondly (and partially as a consequence of this), fitness is an average or idealised/expected property across a population; but actual reproductive success per individual is stochastic. Individuals possessing an allele with a relative fitness of "2" will on average have twice as many offpsring as their competitors, all else being equal, but individual reproductive success will vary as a consequence of other factors such as predation, parasitism, starvation etc.
Finally, absolute fitness relates to the proportional representation of a genotype in a population. Reproductive success relates to offspring per individual. For example, in a growing population a genotype could be simultaneously declining in proportion while it is increasing in absolute number, if other genotypes are increasing in number more rapidly.


text:
Are there insects who can or try to avoid colliding with raindrops?
Some insects are very fast. Does this mean that they are capable of finding a way through falling raindrops without getting wet?
Probably they don't do that at all, because riding on a bike or in a car they don't avoid colliding eather?!

In the case of mosquitoes, raindrop collisions aren't that serious, apparently: http://www.pnas.org/content/109/25/9822 (and related commentary at http://www.nature.com/news/mosquitoes-don-t-let-the-rain-get-them-down-1.10775)
It's out of my field somewhat but I'd suggest looking at dragonflies as they're big enough to be affected by a 'hit' and they're very agile.

@arboviral almost all dragonflies seek shelter when it rains. I think i read about one exception in the neotropics once.


text:
Why do Hot/Cold drinks taste sweeter once returning to room temperature?
Now, I know this is a very bizarre question, and I tried to find a correct exchange for this, but it might relate to biology/science as it being our taste buds and everything.
I am so sorry if there is a better exchange for this, but (I hate using this excuse) I'm new to StackExchange, so please be gentle and point me in the right direction.
Now, to meat and bones (Unintended pun; meat...bones...biology hehe), over the last few days I have noticed that after my drink returning to room temperature, it is so much sweeter than it originally tasted.
Drinks

Hot Tea - I normally only add 1-2 teaspoons of sugar into my tea and it tastes just right, though after taking a sip when it had returned to room temperature, it tastes about 3 or 4 times sweeter than when it was hot/warm. (Milk)
Iced Tea (Bubble Tea) - Just today I had a bubble tea with the smallest amount of sugar possible, it was still too sweet but I stuck with it, and again when it reached room temperature, it was almost unbearably sweet. (No milk)
Slurpee - Again, after returning to room temperature, it is extremely sweet, with it being much lighter with respect to sweetness.
Hot Coffee - Come to think of it, I have also had the same experience with sugared coffee.
Coke - Also, when coke (or any other soft drink) is flat and room temperature, it also produces the same super sweet taste.

So, I tried to think of possible reasons why this happens but, I cannot think of any possible explaination other than magic.
If anyone knows why this might happen, it would be greatly appreciated since I am tripping out trying to figure out why this happens!

This doesn't address all your issues, but with 1,2, and 4 - I would bet that the sugar is simply sinking (e.g. coming out of solution) to the bottom of the cup. If you drink your beverage as it comes to room temperature, a substantial portion of the sweetener has descended to the bottom of the cup where you are now drinking from. Regarding 3 - ice is less dense than water, so as your drink turns to liquid, there is more sugar per cubic centimeter than before. In neither case is the temperature making the beverage taste sweeter, it is just a coincidence with the sugar concentrations.

Generally, cold suppresses sweetness. As an example, consider soft drinks that are usually served cold: they taste sweeter when warm (like you said with your examples of drinks).
Our taste receptors send a stronger signal to the brain when activated by warmer substances and so the perception of sweetness, in this case, is lessened when we consume cold food or drinks.
There are taste receptors on the surface of our tongue which refer to the proteins TAS1R2 and TAS1R3 which, which bind to the “sweet-tasting” molecules.
When the molecules bind to the receptors, they trigger a series of actions which increase the number of positively charged potassium ions (K+) in the cell to which the receptor is attached. In order for the signal to continue along to the brain, the cumulative positive charge of the potassium ions must be high enough to activate a TRPM5 channel into the cell, so that calcium ions (Ca2+) can pass through. The Ca2+ ions are required for the release of neurotransmitters which send the signal. This channel requires a much lower positive charge for activation when it is warm than when it is cold.
Now if you were to put, e.g., a cold coke into your mouth, it decreases the temperature of the entire tongue and consequently the TAS1R2 and TAS1R3 proteins, and the TRPM5 channel. This will result in it requiring a greater positive charge in order for the signals to travel to the brain. This means overall also less signals are even received by the brain, thus resulting in us perceiving less sweetness.
Sources:

http://www.ncbi.nlm.nih.gov/pubmed/25963040
http://www.ncbi.nlm.nih.gov/books/NBK236241/
http://www.foodnavigator.com/Science/Food-temperature-affects-taste-reveal-scientists
http://www.ncbi.nlm.nih.gov/pubmed/17180301

What about hot drinks?

@moonman239 Upvoted your comment, because the answer really does not answer that. Yet, my guess only could be that is due to the damage caused by hot. Even if you drink something sweet and not hot (only room temperature) right after drinking hot drink, it still will not be as sweet as usual.

I found an article (1) which may help you understand what happened on your tongue:
Light cooling from 37 to 21°C of beverages increases your sweet taste adaption, but not actual sweetness of your drink!
Another article (2) states, that a certain receptor for sweet taste perception is heat-activated.
So I guess there is no universal rule for any drink, you must look into further detail what the sweeteners are and which receptors would detect the taste.
(1) http://www.ncbi.nlm.nih.gov/pubmed/25963040
(2) http://www.ncbi.nlm.nih.gov/pubmed/17180301


text:
Is there a difference between macroevolution and group selection?
I encountered two different attitudes towards macroevolution:

The first one included long-term microevolution such as the evolution of Cetacea.
The second one included only macroevolution in terms of group-selection - that is for example the evolution of altruistic behaviour (the groups - families or tribes survived more likely if they were altruistic and shared the resources).

What about for example evolution of the parental instinct? Would it be considered a macroevolutionary (because it is about the evolution of families) or a microevolutionary trait?
And in general, am I getting macroevolution right with the second attitude?

Your first definition of macroevolution is correct. Macroevolution is really not specific to group selection but included any evolutionary process (including neutral  processes).

Can you please link to where did you encounter the term macroevolution that excluded any process that was not group-selection? I suppose it was a paper talking about long term consequence of group selection but while focusing on that, they probably did not want to exclude other processes from the definition of macroevolution.

Is there a difference?
Yes, they are quite different things.
What is group selection?
Group selection is an view of evolution where selection acts at the level of the group, rather than the individual. It suggests that selection is mediated by fitness of the population, and leads to conclusions of things occurring for "the good of the species". It is generally excepted that group selection arguments can rarely be invoked (but see haplodiploid social insects and kin selection). There is a long and controversial history to group selection and it's well worth reading about in further detail if you are interested in the history of science!
What is macroevolution?
Macroevolution is the evolution which occurs at larger scales, things like speciation, extinction, and the history of life. It often involves comparing species or lineages for example.

"Macroevolution generally refers to evolution above the species level."

Microevolution on the other hand is, generally considered, evolution which occurs within lineages, or (more often) within populations. Researchers of microevolution would consider problems of adaptation for example.

"Microevolution is evolution on a small scale — within a single population."

Macro- or microevolutionary trait?
I've never heard anyone refer to something in this way, traits can be studied in both micro- and macroevolutionary contexts.


text:
How do stem cells produce 200 billion new blood cells every day? Does 1 stem cell division result in production of just 1 blood cell or many?
It is given on wikipedia that everyday 200 billion new blood cells are produced in the bone marrow. I want to understand how this is achieved. Does one hematopoietic stem cell's single division result in just one blood cell produced, or many so as to meet the demands of trillions of cells? For example, does single myeloid progenitor (refer to the image) produced from one stem cell further divides into several other identical progenitors before further differentiating into specialized cell, so multiple blood cells are created with the involvement of just one stem cell so that work load is shifted from stem cells towards the progenitors? Also, does the fact that RBC lacks nucleus help in producing trillions of them, making the entire process cost effective.

The hematopoietic stem cells are quite rare, and each progenitor cell produced by a stem cell gives rise to a large number of red blood cells (and other blood cell types).
I'm not sure if the precise number of offspring for the earliest progenitor cells is known in vivo, but recent cell culture models indicate that early progenitors can give rise to as many as 70,000 mature red cells. We also know that the erythrocyte burst-forming cell, a later stage cell in the erythroid lineage, gives rise to around 5,000 mature erythrocytes.
Red blood cells eject their nucleus in the final stages of maturation, and cannot divide thereafter. The ejected nucleus is consumed by a bone marrow macrophage, so it cannot be "reused" in any way. Hence, loss of the nucleus is probably not an advantage in terms of "production economy" --- a nucleus must be generated for each single red cell anyway.