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Can different kinds of dogs mate?
This was inspired by a show in which two different kinds of dogs, who were neighbors, "dated," in order to bring their human neighbors together. This is a theme seen in Disney's "101 Dalmations" or "The Lady and the Tramp."
Can dogs of similar sizes, say Rotweilers or pitbulls actually interbreed? Can any of them mate with say, wolves? And under what circumances?
(I am "encouraged" by the fact that horses and donkeys can produce mules, and lions and tigers can produce "liger" or "tigons." Also of note is that dogs are of the same species as wolves, and "domestic dogs" are actually a subspecies.)

You don't need to restrict this to similar sizes. As long as the female is not much smaller than the male (making the uterus too small for successful pregnancy), it is possible (although it might require help for the mating act or even artificial insemination).

Yes, the vast majority of dogs out there are not pure bred. They are therefore a cross between two breeds. Consider cockapoos for example. The offsprings of a Cocker Spaniel and a poodle is called a cockapoo.

Yes, and domestic dogs can interbreed with both wolves and coyotes.  Also wolves and coyotes interbreed, producing the "coywolf", which is apparently becoming a significant predator in eastern North America: https://en.wikipedia.org/wiki/Coywolf


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Can two half-cut potatoes fuse back together?
If I cut a potato in half, then I hold the two parts together, will the two halves fuse back into a single potato?

I'm voting to close this question as off-topic because it could easily be answered by running a very simple experiment.

I'm voting to close this question, it can be answered by a small practical. Also it's off-topic.

I do not agree. While the experiment can be done easily, it does not explain the underlying process. Will it hold together because it is glued by the starch, or do the cells regrow, or is there something that make it really impossible? As a novice in biology, I really thing this deserves a detailed answer.

A question does not become off topic simply because it can be easily answered using a simple experiment. It looks on topic (may be a bit funny but still related to biology) and can have a scientific answer.

source: Stack Exchange

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

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How does hydrophilic and/or hydrophobic components of polysaccharides influence their 3 dimensional conformation?
It is my understanding that polysaccharides are insoluble in water. Does this mean they are hydrophobic? Beyond being insoluble in water how does this affect their 3D structure?
Thanks!

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


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Hormones - biotic or abiotic
Are hormones biotic or abiotic? I have tried reading different articles, and  I've found that it is both, but can that be true?

Hormones occur inside organisms as signaling factors, and arise from biological activities, the development or homeostasis of the organism.
Thus, they are considered neither biotic nor abiotic factors in ecology.
(Terrible analogy warning!) It's a bit like asking whether the wheel of a car is petrol- or diesel-based. It makes no sense!
Here's a helpful, comprehensive website.
Biotic (living) factors are living organisms in an ecosystem, that must share common resources or compete in a habitat one way or another. Abiotic (non-living) factors are things like temperature, wind, salinity, etc. that affect individuals or the community of an ecosystem.
As you can see, hormones are just one of many components of a living organism. They aren't living themselves. It's a silly question to ask, as I hope you can see now.


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Why did a lot of common insects evolve such a thin waist?
Something that doesn't quite make sense to me is why lots of insects like ants, bees and wasps have a such a small petiole when it connects many major organs to the rest of their body from a suddenly much wider abdomen.
Normally from an engineering standpoint, you don't increase the width of a cantilever from a joint because the torque applied to a joint already increases with the length of an overhanging segment, so increasing the width would only multiply the torque that joint or opposing segment needs to balance.
It could have something to do with ants being so small that large  torque isn't an issue in proportion to their body size, but if it wasn't, then why do their legs also get thinner as they measure further in length from their body?

Human limbs also get thinner the further they go from the body, and it's not because they'd buckle under their own weight otherwise.

But it would be even harder for those limbs to move due to the extra torque that needs to be counteracted to move a specific direction. Joints are especially thicker than the shaft of a bone because they face more strain during locomotion and impact, and it makes sense bones would get thinner because if they were thicker, they would be that much harder to move at the same distance.

The normal engineering of cantilevers at the human scale can be relaxed at insect scales.  At the small sizes of ants and wasps, gravity is a very minor factor because of the gravitational force affecting small masses as compared to the electromagnetic forces within and between materials.  Not only does this mean insects can easily walk up walls and across ceilings, but also the extra weight of a wider, heavier cantilever (the abdomen) can be supported and moved by the material of a narrow supporting joint.(the petiole).  Similar consideration occurs for the inertial force due to mass.

This thin waist is called petiole (aka.  wasp‐waist).
How many times did the petiole evolve?

Why did a lot of common insects evolve such a thin waist?

Reading this question make it feel that you are assuming that several lineages evolved this petiole independently. It would be wrong. The petiole evolved once only and all the species that are having a petiole today (ants, bees, wasps, ...) are descendent of this lineage that evolved this petiole.
The taxon of all these species having a petiole is called Apocrita, which is a suborder of hymenoptera. You can learn much more about the phylogeny of these taxons in Rasnttsyn and Haichun (2010).
Why did it evolve?
The early lineage who evolved this trait where parasites (or even parasitoids at that time, I am not sure). This lineage was laying their eggs in tree trunk (or maybe already in other insects larvea if they were already parasitoids). The constriction that is the petiole allowed these individuals to have greater maneuverability for depositing their eggs accurately (Peters et al., 2017; Wilhelmsen et al., 2010).
The evolution of this petiole greatly affected the future evolution and diversification of Apocrita as things like stings and even maybe eusociality. From Peters et al., (2017)

The evolution of the wasp waist, a constriction between the first and the second abdominal segment greatly improving the maneuverability of the abdomen’s rear section, including the ovipositor, was a major innovation in the evolution of Hymenoptera that undoubtedly contributed to the rapid diversification of Apocrita

So if it was thicker, they wouldn't be able to maneuver their abdomen as well to use as a stinger or to lay eggs? But if their petiole was thicker, wouldn't there also be more muscle tissue that could move in a desired direction?

@VaneVoe Well, more muscles does not necessarily give you more flexibility. You need some room to make the movement. Just like if you take a cardboard cylinder and creat a "petiole" in the middle, the movement will be greatly increased. I am no good physiologist but it feels pretty intuitive to me that this thinner waist increase movement amplitude. Watch a video of a wasp using its sting and you'll see how much flexibility they have at their petiole compared to other, thicker, body parts.

Apocrita insects (i.e. the clade containing bee, wasps and ants) are supposed to have evolved a thin waist because it gives them more flexibility to manoeuvre their abdomen. Most Apocrita are parasitoids and they need this flexibility to parasitize theirs hosts. The others have evolved a stinger: the petiole can serve them as a lever to better defend themselves against their natural enemies.
So while it's true that this thin waist brings physiological constraits (e.g. for food transit or the torque needed to move the abdomen), these disavantages are very likely over-rode by the adaptive advantage brought by the increased maneveurability of the metasoma (which carries the ovipositor/the stinger).
You can find more information about the petiole's evolution here and here.

Specialized mechanical anchors join up arthropod exoskeletons to muscles and tendon cells. There's a complex network of interconnected matrix constituents, junctions and associated cytoskeletal elements. F-actin based fibres used as tendons fuse onto to myosin based structures which are used for muscle contraction.
The tendons can go through relatively thin areas of the insect with massive leverage. We think about robots and humans as using bones and metal joints with pivots and motors, when arthropods muscles move the exoskeleton rather than interior bones.
The exoskeleton constriction at the abdomen-thorax joint of arachnids and ants demonstrates the relative strength of insect exoskeletons, the exoskeleton material is so light and powerful relative to the size to permit the small form while conserving enough resistance.
The abdomen-thorax joints, which can be multiple segments, are bit it stronger than the legs. They are less likely to get damage there than on their legs. The abdomen and thorax are containers for all the internal organs, which is different than a mechanical limb, so they are bigger.
The slender waist allows for a lot of arthropod behaviour like weaving, stinging, burrowing, preening, symbioses, it's a complex field.
If humans can change the magnet based rotary muscles and use tendon based mechanics they can probably develop very cool machines for the future. here is the human designed comparison for arthropod locomtion:
https://www.youtube.com/watch?v=Vi1hwdWUHvU
https://www.youtube.com/watch?v=eYFYSYmv4v4
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2555930/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3335404/


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Why does inbreed produce a higher percentage of abnormal babies?
The babies of close (say, brother and sister, or cousin and niece) family members have a higher chance of being born with an abnormality than babies from non-family related men and women. Why?

Who says this is a homework question?

Please do not edit in content to questions that is not part of the question. The homework policy here doesn't only cover assignments specifically given as homework, it covers other types of school work as well as questions that need further research effort. "This isn't homework" does not make a question subject to different rules.

Many disease/abnormality causing alleles of a genes are maintained in populations through their recessive nature. That is to say, in order for the disease to manifest itself in offspring they must in have TWO copies of the disease causing allele - they must be homozygous for the disease causing allele. Inbreeding leads to a far greater chance of being homozygous at a disease locus if a recent common ancestor of the parents was affected or a carrier. The likelihood of this occurring is measured by the Inbreeding Coefficient.


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Confusion about the duration of different phases of the cell cycle such as G1, G2 & S
We all know that normally most of our cells (which are alive and have nuclei - except for cells such as "stem cells", "red blood cells", etc) spend most of their lives in interphase.
But the Interphase itself is also composed of other parts, other stages, including G1, S, and G2.
Is the staying duration of the most human cells in each stage(G1,G2 & S) is comparable to the other stage?
For example, is it true to say that:

"Most human cells, which have the ability to divide(passing the cell cycle), spend most of their lives on stage G1 than S phase or vice versa."?

Usually, which stage is the longest or shortest?
It is quite clear that the G1 is normally longer that G2 and as far as I know the G2 is the shortest stage in interphase, but what about G1 and S?
Is stage S usually longer than G1?
Is there any information?

It depends on the conditions, cell type or state of the cell.
I don't think anyone here can do better justice to the question for a beginner than this web page.
To show you why your answer is not answerable, by way of example: some cells exit the cell cycle and enter a stage called G0. This can be a permanent state for some cells, or, for instance, others may return to the cycle if they receive (external) signals.
Here is a very loose approximation, circles are to scale with respect to cycle time. Notice, for instance, the human circle is for an immortalized cell line under laboratory conditions, rather than for cells in your body. A neuron (brain) or an enterocyte (gut) have vastly different cell cycle states, so it's impossible to give you a single straight answer without misleading you totally.

Bonus food for thought: notice that the fraction of time cells spend on G1, S, G2 and mitosis is also different between different cell types.
Bonus food for thought #2: In fruit fly embryos (pictured bottom right in the above picture), you have an extreme example of unconventional (non-textbook) cycling. Rather than synthesizing new cytoplasmic materials, the size of the developing embryo is constant except for the replication of the genetic material. This happens in the growing larva for ~10 cell divisions, in thousands of cells. One of these cycles takes about 8 minutes to complete fully. That's an impressive time to copy a genome; most* bacteria can't do it this quickly!
(*any that I am aware of)

Is it true to say "Most human cells, which have the ability to divide(passing the cell cycle), spend most of their lives on stage G1 than S phase or vice versa."? Is there any information?

I don't think this is known definitively. We can only guess. Most cells are in interphase (i.e. not mitosis+cytokinesis). There is an important cell-cycle checkpoint at the end of G1 which, when passed, means that the cell is preparing for eventual division (S or synthesis phase means it's duplicating its genome). I would hazard to guess most cells in the body, by sheer number, are in G1 or have entered (semi)permanently into the G0 phase. Even some adult stem cells await signals to enter the cell cycle again and divide, and these are the most proliferative cells. Don't quote me on this.

I wonder whether entering the G0 is only done through G1. Is it possible for the cell to go from stage S or G2 to step G0?

By definition G0 is prior to S phase. Cells can remain for a long time in G2 but if they are not 'actively readying for division', they are either in G1 or out of the cell cycle entirely, in G0.

@AmirhoseinRiazi also have a look at https://biology.stackexchange.com/q/13703/3340

A typical eukaryotic cell cycle is illustrated by human cells in culture. These cells divide once in approximately every 24 hours (Figure 10.1). However, this duration of cell cycle can vary from organism to organism and also from cell type to cell type. Yeast for example, can progress through the cell cycle in only about 90 minutes. The cell cycle is divided into two basic phases:
Interphase
M Phase (Mitosis phase)
The M Phase represents the phase when the actual cell division or mitosis occurs and the
interphase represents the phase between two successive M phases. It is significant to note that in the 24 hour average duration of cell cycle of a human cell, cell division proper lasts for only about an hour. The interphase lasts more than 95% of the duration of cell cycle. The M Phase starts with the nuclear division, corresponding to the separation of daughter chromosomes (karyokinesis) and usually ends with division of cytoplasm (cytokinesis). The interphase, though called the resting phase, is the time during which the cell is preparing for division by undergoing both cell growth and DNA replication in an orderly manner.
The interphase is divided into three further phases:
G1 phase (Gap 1)
S phase (Synthesis)
G2 phase (Gap 2)
G1 phase corresponds to the interval between mitosis and initiationof DNA replication. During G1 phase the cell is metabolically active and continuously grows but does not replicate its DNA. S or synthesis phase marks the period during which DNA synthesis or replication takes place.
During this time the amount of DNA per cell doubles. If the initial amount of DNA is denoted as 2C then it increases to 4C. However, there is no increase in the chromosome number; if the cell had diploid or 2n number of chromosomes at G1, even after S phase the number of chromosomes remains the same, i.e., 2n.
CELL CYCLE AND CELL DIVISION
In animal cells, during the S phase, DNA replication begins in the nucleus, and the centriole duplicates in the cytoplasm. During the G2 phase, proteins are synthesised in preparation for mitosis while cell growth continues.


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Help in identifying marine specimen?
I came across this specimen which I assume belongs toeither the phylum porifera or to the coelenterata.
Can someone please help me identify it?
The specimen was found in Ayodhya, India.

Please update your question by including where you found this specimen. Thanks

I am thinking it is the skeleton of a colonial large polyp stony coral. I am not certain, but I suspect a species of the Favia genus. Most likely one of these two species (see links for info and pictures):

Favia lizardensis
Favia rosaria

Looks quite similar. However, many stony corals appear rather similar when dead. Could you add additional information in support of your answer?


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What do the haploinsufficiency scores in the clinVar database represent?
I understand that haploinsufficiency occurs when one of the two copies of a gene is mutated to the point of being unusable, and the single copy remaining is unable to cope with the cell's demands for a given peptide, resulting in a phenotypic deficiency.
In the clinVar database, there is a "haploinsufficiency score" (example here) which seems to range from 0 to 3 (though that is anecdotal only; based on the genes that I've looked at).  I assume it refers to how phenotypic or how deficient the cell is.  However, I fail to find a place where this is clearly outlined...
Am I correct in this assumption, and if so, what does a score of 3 (for example) represent?

Okay, I finally found an official source outlining what the dosage sensitivity scores represent.
0 represents no evidence of dosage sensitivity: clinical interpretation is that dosage differences is "likely benign."
1 represents little evidence of dosage sensitivity: This can be marked if only secondary evidence shows dosage sensitivity; clinical interpretation is that dosage sensitivity is "uncertain."
2 represents "Emerging evidence," meaning that the evidence suggests fairly strongly that the gene is dosage sensitive, but that there is insufficient evidence to prove it.  The clinical interpretation is that dosage sensitivity is "Uncertain, likely pathogenic."
3 represents "Sufficient evidence," meaning that the evidence is sufficient to prove that the gene is dosage sensitive.  Clinical interpretation is "Pathogenic."

Source:

Riggs ER et al., Towards an evidence-based process for the clinical interpretation of copy number variation. Clin Genet. 81(5): 403–412.


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In plant photosynthesis, in the light dependent reactions, why is 3 ATP produced per 2 H2O?
I've been looking at the light-dependent reactions on Wikipedia and Khan Academy.
This is the net reaction:
$$2H_2O + 2NADP^+ + 3ADP + 3P_i \to O_2 + 2NADPH + 3ATP$$
So for every $2H_2O$ I expect $2NADPH$ and $3ATP$. I tried to count:

These are my assumptions:

Cytochrome b6 complex pumps $1H^+$ for each $1e^-$.
FNR makes $1NADPH$ for each $2e^-$.
ATP synthase makes $1ATP$ for each $1H^+$.

If we want to end up with $3ATP$, then $3H^+$ need to diffuse through. The thing is, there's too many $H^+$. $4H^+$ is contributed by the cytochrome b6 complex pumping alone, and another potential $4H^+$ is contributed by the water splitting.
Clearly I'm missing something here that would lead to the correct count.

I remember being confused by the numbers when I first studies it primarily because most sources seem to differ on the stoichiometry. I have tried to explain why is it difficult to comment upon such large equations, hope it helps!
Short Answer
There are two faults in your assumptions.

The plastoquinone-cytochrome cycle actually pumps $2H^+$ per electron (terms and conditions apply)
ATP-synthase requires $\approx 4$ protons per ATP produced

So, 12 protons per 2 water molecules is what is pumped, which makes 3 ATP.
Full Answer
As you might notice, the above scheme does not account for many things. For starters, since the 4$H^+$ from water splitting are produced and not pumped, only 2 of those need to be pumped back via ATP-Synthase to restore equilibrium. So even if you account for the $2H^+$ consumed by $2NADP^+$, there is still something that doesn't quite fit. Furthermore, some sources also try to account for the acidity of the inorganic $Pi$ in the ATP-synthesis which will further allow for changes in the $H^+/e^-$ ratio.
Why the confusion?
Most of what we know of the stoichiometry is based on a conglomerate of experiments, beginning with experiments on isolated chloroplasts. As a result, some experiments give us some parts of the stoichiometry (we know that the $NADPH/ATP$ ratio is around $2/3$) and others give us the reactions. Often times, many possible reactions are proposed, from which, the ones which can best be integrated with results from different experiments are thought to represent the actual truth. But this process is often mangled with complications, unexplained patches in the theory and the like. Furthermore, biological processes often are stochastic and do not have perfect stoichiometries. This is all overlooking the actual disagreements between experiments (the $H^+/ATP$ ratio for the synthase had significant variations in different experiments).
Okay, so now what?
Don't loose hope. We do know quite a bit about photosynthesis. What we currently understand about photosynthesis (light reactions) is thus:

There are three distinct processes that can produce a chemiosmotic gradient of $H^+$.
a. Non-cyclic Photophosphorylation is the main method. This constitutes the popular Z-scheme involving a linear electron transport from water to the final acceptor $NADPH$, and this process pumps about $12H^+$ per $2H_2O$
b. Pseudo-cyclic Photophosphorylation which is basically the same as above, but the final acceptor is an $O_2$ molecule, with similar ratios.
c. Cyclic Photophosphorylation which allows for recycling an electron, that is, proton pumping without there being a final acceptor of electron solely by internal shuffling of the electron between different states (primarily involved Plastoquinone (Q) cycle. This can pump $2H^+$ extra for 1 electron.
The ATP-synthase is slightly different from that found in animal mitochondria. The number of protons per ATP depends on the rotational symmetry of the synthase. (details in the references below). Basically, initially, it was thought to have 12-fold symmetry (needing $12H^+$ per rotation, in which $3ATP$ is produced, hence $4H^+$ per $ATP$) but was later found to have 14-fold symmetry actually needing $14H^+$ for the observed $3/2$ ratio of $ATP/NADPH$.
The number of Photosystem 1 units(where the cyclic version operates) is more than that of Photosystem 2 units. This means, that cyclic photophosphorylation goes on simultaneously at these centres, and will account for the extra $2H^+$ required to meet the experimentally observed ratio (1 in every 5 electron is "recycled").

References

A good overall paper addressing all the main issues. Photosynthesis of ATP—Electrons, Proton Pumps, Rotors, and Poise; John F.Alle; Cell Volume 110, Issue 3, 9 August 2002, Pages 273-276
General resources on these reactions. Here, here and here.
Studies on the $H^+/ATP$ ratio.
a. Petersen, Jan et al. “Comparison of the H+/ATP ratios of the H+-ATP synthases from yeast and from chloroplast” Proceedings of the National Academy of Sciences of the United States of America vol. 109,28 (2012): 11150-5.
b. Watt IN, Montgomery MG, Runswick MJ, Leslie AG, Walker JE. Bioenergetic cost of making an adenosine triphosphate molecule in animal mitochondria. Proc Natl Acad Sci U S A. 2010;107(39):16823-7.
Old studies to illustrate the difficulty of explaining the results of many studies:
a. Function of the Two Cytochrome Components in Chloroplasts: A Working Hypothesis; R. HILL & FAY BENDALL; Nature - volume 186, pages136–137 (1960)
b. Photosynthesis by Isolated Chloroplasts; DANIEL I. ARNON, M. B. ALLEN & F. R. WHATLEY; Nature - volume 174, pages394–396 (1954)


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How exactly do birds get drunk eating fruit? Fermentation should be anaerobic
The Washington Post article Drunk birds are causing havoc in a Minnesota town. Police say they’ll sober up soon. describes birds becoming intoxicated after eating berries:

“The Gilbert Police Department has received several reports of birds that appear to be ‘under the influence’ flying into windows, cars and acting confused,” Police Chief Ty Techar wrote in a statement Tuesday. An early frost meant that berries had fermented earlier than usual, he explained, and birds were eating them and getting drunk.
Incidents around town involving intoxicated birds appear to be more prevalent than in past years, Techar added, because many have not yet migrated south. “It appears that some birds are getting a little more ‘tipsy’ than normal,” he wrote. “Generally, younger birds’ livers cannot handle the toxins as efficiently as more mature birds.”

A few supporting videos:

ABC TV: Drunk birds are flying into windows, cars
TIME: Drunk Birds Are Flying High In Gilbert, Minnesota | TIME

Is the fermentation happening to the berries while on the tree or on the ground as the police suggest, or is it really after being ingested by the birds? How is an anaerobic environment produced for fermentation into alcohol but not subsequent conversion to vinegar?
Humans are a clever species, on par with some birds. They are known to collect the berries and ferment them first before ingesting, and will forage for a trap to let gas escape but keep the oxygen out. Have birds found a better way?
 Source

The insides of fruits are relatively anaerobic environments. Natural fermentation, as in berries that get birds intoxicated, is primarily from yeast, and it seems most likely that humans recognized this process before intentionally encouraging fermentation of anything. Natural fermentation reaching high ethanol concentrations occurs especially when berries high in sugar are frozen and then thawed.

Dudley, R. (2004). Ethanol, fruit ripening, and the historical origins of human alcoholism in primate frugivory. Integrative and comparative biology, 44(4), 315-323.
Fitzgerald, S. D., Sullivan, J. M., & Everson, R. J. (1990). Suspected ethanol toxicosis in two wild cedar waxwings. Avian Diseases, 488-490.

Interesting! I usually think of the inside of fruit as sterile, but maybe that's not exactly the case. Sounds like the basis of a new question!


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PBS or TBS, where cannot use each buffers?
As you know, Tris buffered saline and Phosphate buffered saline is multipurpose. For finding each buffer's use, there's so many use experiment for PBS and TBS. TBS uses for western blotting, and PBS uses for cell culture.
but some experiment never use PBS and some experiment never use TBS, I want to ask this situation which when you use TBE but never use PBS, and the opposite situation(use TBS but never use PBS), For example, When you western-blotting with alkaline phosphatase never use PBS and PBS-T. this case, phosphate inhibits AP, and amine-coupling with NHS-EDC, never use Tris buffer because it have primary amine.

I think you answered your own question.
The buffer used in a given experiment depends on the requirements and limitations of the experiment itself. You just have to look at the properties of the buffer, and if it is relevant to your experiment.
You just gave two great examples... are you just looking for more examples of experiments when one would not use phosphate buffer vs Tris buffer?
PBS is supposed to closely mimic/represent the osmolarity of a cell, and buffer from pH = 7.0 to 9.0. Tris also buffers around neutral pH. It is pretty cheap, but as you've stated, has primary amine groups that are nucleophilic and thus interfere with certain experiments like disuccinimidyl suberate crosslinking, etc.


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How to confirm secondary structure formation of Precursor miRNA on gel?
I want to fold precursor-miRNA into its secondary structure and then confirm it on gel. At first, I heat it in annealing buffer at 95°C for 5 minutes and cool down slowly. Then I run it on gel but the samples are at same position as the original dilution.

What kind of gel are you using? pre-miRNA will mostly from hairpin loops (I guess), which don't change the overall size of the RNA by much (it's still linear, now just a bit 'shorter' but therefore 'wider'). I'd guess you need a relatively high percentage gel (native and probably better poly-acrylamide), with custom markers for your size-range)

Your question looks incomplete. For e.g. you haven't mentioned how many minutes at 95°C. Please [edit] your question to all necessary details. I advise that you provide the full protocol that you are using.

My gel is 18 % polyacrylamide ( 40% acrylamide; 1M Tris, 1M Hepes, 1M EDTA, 1M MgCl2, TEMED and APS) in 1X Hepes (containing 1M Tris, 1 mMEDTA, 30mM MgCl2)

 Disclaimer: Although I have attempted northern blots for miRNA, I haven't actually done the kind of experiment you are talking about.
First of all you need controls.

A negative control: a same length RNA that will not fold (you can introduce some mutations in your pre-miRNA sequence to disrupt the base pairing). You can use the miRNA secondary structure prediction tools for rationally designing such controls.
A positive control: perhaps a folded pre-miRNA that is crosslinked. Frankly, I haven't come across anyone using such crosslinking agents to study RNA secondary structure. I had however, seen some old papers on this topic (Wagner and Garrett, 1978, Rabin and Crothers, 1979). You may also try some conditions (salt concentrations etc) under which the RNA will fold (studied using biophysical assays).

Now, you cannot run agarose gels. You would need long polyacrylamide gels ~15%. You also need to use the right buffers. 0.5-1x TBE supposedly works. You may want to run your sample in two conditions: denaturing (with 8M urea) or non-denaturing. You can refer to this protocol (Petrov et al. 2013).
Your positive control should migrate faster than the negative control. If your RNA is folded (fully or partially) it should migrate between the positive and negative controls in the non-denaturing gel. In the denaturing gel, your RNA should migrate at the same level as the negative control. Positive control (if it works) should not be affected by urea.
Also, the gel heats up during electrophoresis which in turn can dentature RNA. You may want to run the non-denaturing gel in the cold room.
Having said all this, I would advise that instead of putting in so much effort in gel based assay you can use more sensitive equipment to study RNA folding. There are many biophysical studies on in vitro RNA folding. You can check them out.


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Why do we use cRNA instead of initial extracted RNA in the microarray technique?
I am recapping for the exam in transcriptomics and stumbled into a question about microarray. So, our regular workflow is to

extract RNA from cells
generate cDNA from the initial RNA using reverse transcription
transcribe cRNA from cDNA
label cRNA with biotin
fragment biotin labeled cRNA
hybridize to a plate, scan and quantitate

So the question is - since we use RNA for the further quntification steps why should we perform reverse transcription+transcription to produce cRNA while we could just use the initial RNA?
Is the cRNA more stable than RNA? Or we already make labeled cRNA using labeled nucleotides?

Could you give a source or at least application for this workflow? It sounds pretty specialised, both the biotinylation and the in-vitro transcription (cRNA) are - as far as I know -  not standard procedures.

I don't know exactly the applications of this method, the scheme was shown, for example, in this lecture http://www.binf.gmu.edu/jafri/binf636/GMU-higgs.pdf in the section about Oligonucleotide Arrays.

I can't find any mention of biotinylation or in-vitro transcription/cRNA in the slides you linked, they don't seem to have anything to do with the workflow in your question.

It's slide #16 and you have a picture in dark blue.

Ah, only checked the text of the slides, not the figures as well. I tried to answer - but the figure looks like an example that isn't very well explained (the text next to it doesn't clearly correspond to it)

by @WYSIWYG
my guess is that the final cDNA after doing RT-PCR (not the first strand) which is double stranded is transcribed to make a ssRNA which can then be used as a probe. ssDNA would also work but the cDNA synthesis followed by PCR would not produce ssDNA. You can simply use the first strand after RT but the concentration would be less. With a cDNA library, you can produce a lot of RNA using IVT.

After clarification via the comments of the OPs question:
1) The procedure you describe is not for standard RNA microarray experiments, it for olgionucleotide microarray. This type of chip is special because it has multiple probes for each gene to allow detection of special features (i.e. mutations, alternative splicing, ...).
2) The reason for the generation of cDNA with subsequent reverse transcription and biotinylation is not explicitly stated in the source of the OP, but there are some possible advantages:

Amplification of material: cDNA can easily be amplified, which would make it easier to analyse samples whit low RNA yield, genes with low expression levels or to analyse the same sample on multiple chips.
Sensivity: oligonucleotide arrays may use very short (10-25 bases) probes, for which fluorescence readout may not be sensitive enough. Biotinylation of a given RNA base (by the use of pre-biotinylated NTPs during reverse transcription) can give multiple 'marks' on each fragment, which can be read with out streptavidin coupled signals. Additionally this would allow the signal strength to change in respond to certain SNPs/mutations.

Good intro to oligonucleotide microarray but still not clear why we would convert cDNA back to cRNA after biotinylation.

@PolinaNovikova my guess is that the final cDNA after doing RT-PCR (not the first strand) which is double stranded is transcribed to make a ssRNA which can then be used as a probe. ssDNA would also work but the cDNA synthesis followed by PCR would not produce ssDNA. You can simply use the first strand after RT but the concentration would be less. With a cDNA library, you can produce a lot of RNA using IVT.


text:
What is the most genetically complex organism?
I understand that new genomes are being sequenced ever day and these answers replace themselves often; although as of today, what has been proven to be the most genetically complex organism (Other than a human of course)? I keep getting a multitude of different answers like Daphnia pulex, Axolotl, Paris japonica or Adder’s Tongue all from different dates and sources so it becomes difficult to tell what is the right answer here if any. If this question is not specific enough I would be happy to revise.
Edit: I would define genetic complexity as either genome size or number of genes. Either answer  would work. If you would like give other information like chromosomes or isoforms from any other definition, that would be helpful. Whatever is the best of the best.

I think one of the biggest problem with this (type of) question is how you define 'genetically complex' - there a lot of different things one can consider (and weigh differently): genome size, number of genes, genome architecture, isoforms and/or copies per gene, (alternative) splicing, regulatory interactions of genes (at different levels). Additionally its worth to note that we know a lot more about the human (or also mouse genome) than most others - just because we haven't found things like cryptic transcripts or circular RNA's in other species (yet), doesn't mean they don't exist.

Complexity is not the length of a genome, but the amount of information encoded in it.  (See Information Theory.)  And even that isn't the whole story, since some "simplifications" like mammalian live birth & post-natal care can lead to a more complex result...

Edit: I would define genetic complexity as either genome size or number of genes. Either answer or information would work.

Largest genome: Paris japonica, a rare plant. Its genome is 149,000,000,000 base pairs large. Approximately 50 times larger than the human genome, by base pair count.
Higher number of genes in an organism: Daphnia pulex, a very common species of water flea. 31,000 protein-coding genes.
As already pointed out, the most genetically complex organism is an unclear question. Complexity can be interpreted in different ways, and I don't think we could agree on a satisfying measure (or definition, for that matter) of genetic complexity.


text:
What species of short plant is this in Iran?

Anyone knows the name of this Iranian local species?

Hi welcome to Bio.SE! Please see our guidelines for writing a good species ID question. After reading the guidelines, please update your post accordingly. Otherwise, unfortunately, it'll be downvoted or closed. Thanks.

it's a chalk area species which is very generic, without a bloom photo it looks similar to 100ds of other species. You therefore need a mountain plants book specific to iran and local chalk areas.


text:
What does common viruses found in the body weigh?
On NPR public radio news it was said that if the bacteria that is natural that assist in body function or just present in your body was put it into a ball it would weigh more or less 7 ounces (approximately 200 grams). I tried to find the exact quote but am still looking for it and will revise when I find it.
Can viruses assist in body function as in extending life in any way?
Can a body be 100% free of viruses of not how much would the total virus weigh if put in a ball?

It seems like after your edit you now have a bunch of questions rather than one.

Our analysis also updates the widely-cited 10:1 ratio, showing that the number of bacteria in the body is actually of the same order as the number of human cells, and their total mass is about 0.2 kg. (0.4 pounds) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4991899/

Possible duplicate of https://biology.stackexchange.com/q/74887/3340

Viruses, in general, are obligately pathogenic i.e. they don't usually co-exist (as commensals or symbionts) with our body cells. Their mechanism of survival involves usurping of the host cell machinery to produce their own proteins and genetic material. However, as pointed out in the comments, there are some viruses such as the GBV-C which can infect the host but seldom cause any disease. Moreover, this virus has been shown to have a positive effect on the innate immune response and inhibitory effect on HIV [1].
(Also, have a look at: Do beneficial viruses exist? If so, what examples are there?)
In our genome, here are some remnants of viruses that had infected our ancestors long back in past. A prominent example is that of retrotransposons. Retrotransposons are DNA sequences that constitute a significant part of our genome and they are structurally similar to the genome of retroviruses (like HIV). Retrotransposons had been considered junk DNA in the past but recent studies have shown that they do play some important roles in our body. For example, L1 retrotransposons cause somatic diversity (genetic diversity at the cellular level) of neurons and may possibly contribute to increasing the plasticity of our brain[2,3]. Retrotransposons can also regulate gene expression[4].
Other than that, there may be infectious viruses that are present in the body but are dormant. These may become active later (when the conditions are conducive) and cause the disease in that individual or spread to another person.
You can perhaps calculate the weight of these viral remnants (retrotransposons). It won't provide any great insight to anyone. You just have to calculate the percentage of genome these DNA sequences occupy and multiply it with molecular weight of the genomic DNA and total number of cells in the body. I'll leave that exercise to you.

Viruses are not obligately pathogenic. There are a number of free viruses (i.e., viruses that are not retrotransposons) that are beneficial. GBV-C, for example.

There are also many many viruses that do not appear to be associated with any disease, but have not been demonstrated to be beneficial. There is much still to be learned about the human virome.


text:
Is bi-allelic gene expression random?
Supposing we have the genotypes “Aa”, “AA”, and “aa”... which are not mono-allelic (not imprinted and not X-inactivated). Does the dominance of the “A” allele over “a” allele affect which gene is transcribed, or are both alleles transcribed and the allelic dominance only determines the observed phenotype?
I’m guessing it’s the latter, but that makes me confused as to what the concept of allelic dominance would mean for mono-allelic expression, where only one allele is always expressed and observed.

I guess this answer might help.


text:
Element of promoter responsible for expression power of gene
I know that there is a classification of promoters like: strong, medium and weak. This shows how a promoter affects gene expression levels. So my question is: what part of the promoter affects it?
For example I want to raise or lower the expression of some gene, so, what part of promoter I need to edit or maeby I can just replace it with another promoter?

Tldr; In an in vivo context the answer is going to be dependent on DNA sequence and context.
Simplistically, Eukaryotic genes promoters can be segmented in to several parts. The first, a core promoter region where RNA pol II will bind. This isn't capable of a robust transcriptional response on its own and relies on proximal promoter regions, or more specifically transcription factor binding to the proximal promoters. Proximal promoters are usually 100 or so base pairs upstream of the transcription start site and will bind proteins that will assist in Pol II binding and activation (or silencing). Enhancers (and Silencers) are conceptually similar to proximal promoter regions with the exception that they can be a looooooooooong way away from the transcription start site in sequence space. See here:1.
So, if you just wanted to drive expression of a transgene in a cell line in the lab there are plenty of established cloned promoters and enhancer regions known to work such as SV40 or Gal4. This would be an example of "replacing the promoter". That's exactly what it is and why these sequences were chosen to be cloned.
If you are asking which regions are specific to activate or repress a gene in vivo and/or in context then it will be, of course, context dependent and you'll have to find out yourself if someone hasn't already. Generally, these regions of effect will be binding sites for sequence specific transcription factors  which interact with the core transcriptional machinery (or bind other proteins that do) to effect the rate of transcription. So, if the sequence is what can induce an effect, how can you find it? You can search for these sequence specific sites by analyzing your sequence of interest with a slew of computational tools for potential binding sites and directly assess any hits ability to increase/decrease expression as isolated units when cloned upstream of an appropriate reporter construct. I guess you could even go as far to CRISPR single base pairs in or out to "edit" any hits. Alternately, you could use a purely wet bench technique such as promoter bashing to similar effect - performing serial deletions to find out which part of your promoter is important for strong/medium/weak effects or activation/repression.
The Stark Lab developed a cool genome-wide approach looking at the ability of DNA to drive expression. Although, something worth bearing in mind is that in a normal in vivo situation everything is context dependent - one piece of sequence may be reliant on another close by (like the core promoter requires proximal promoters) or it may require one or more pieces of DNA that are distant in sequence space to be close by in 3D space (like distal enhancers).
People have also taken completely synthetic approaches to making promoters .
This would be easier to answer if your question was more specific.
HTH.


text:
Does the renal vein have a greater glucose concentration than the renal artery?
My IGCSE markscheme says that the renal vein has a lower concentration of glucose? I would expect the renal artery to have lower glucose concentration as water is lost from the kidneys. Why is it so?

What is an "GCSE markscheme"? Can you add a quote of a few sentences to show the context?

The kidneys use glucose from the blood as a nutrient, so, this is the reasoning behind your source saying there is less glucose in the renal veins than in the arteries.
If the renal vein contains both less of water and glucose than the renal artery, the concentration of glucose in the renal vein still be lower. This agrees with Bioninja.com.au:

Blood in the renal vein (i.e. after the kidney) will have:

Less urea (large amounts of urea is removed via the nephrons to form urine)
Less water and solutes / ions (amount removed will depend on the hydration status of the individual)
Less glucose and oxygen (not eliminated, but used by the kidney to generate energy and fuel metabolic reactions)
More carbon dioxide (produced by the kidneys as a by-product of metabolic reactions)

On the other hand, an article in Scielo.br says:

Unlike the proximal nephron, cells in the distal nephron are fully
  capable of glucose utilization. In physiologic conditions, the amount
  of glucose utilized in the distal segments of the nephron equals that
  derived from the renal gluconeogenesis in proximal tubules. This is
  confirmed by the common finding that the arterial-renal vein blood
  glucose concentration difference in the post-absorptive state is near
  zero.

In conclusion, your source can still be right.


text:
What is this species of green frog found in store-bought flowers in France?
Today I found a frog in a big flower composition bought at a french shop (living in Grenoble, south of France).
It started snowing today, and I'd like to keep it until it's warmer outside.
So could someone tell me what species it is ? (To check what it eats and if it's legal to keep it)
Thanks !

(I'll edit with more pictures if it's needed and if she moves)
Edit :

Please update your post with the size of your frog. Thanks!

I think this is a type of green frog

This looks very much like a tree frog of which there are many similar looking species. Without knowing where your flowers came from or more characteristics about the specimen, it'll be difficult to provide an accurate answer*.
One possibility may be the European tree frog (Hyla arborea).
According to Wikipedia:

Members of the H. arborea species complex are the only representatives of the widespread tree frog family (Hylidae) indigenous to mainland Europe.

which is supported by genetic work by Stöck et al. 20081

Description [source]:

Small (3.2-5 cm in length)
Slender body shape with long legs and smooth dorsal skin+
Usually green (but variable) with dark brown lateral stripe across eye caudally to groin and whitish ventral skin surface.
Gripping discs on toes

The range of this species also includes much of France:

 Image Source
+ Although the description states this species has smooth dorsal skin (possibly like the OP's specimen -- I can't tell for sure), many of the pictures I've seen seem to suggest that the dorsal skin of this species is actually rather granular. For example, see here.
*Feel free to update your post with additional info and perhaps a better response will be added.

 Citations:
 1 Stöck, M., Dubey, S., Klütsch, C., Litvinchuk, S.N., Scheidt, U. and Perrin, N., 2008. Mitochondrial and nuclear phylogeny of circum-Mediterranean tree frogs from the Hyla arborea group. Molecular Phylogenetics and Evolution, 49(3), p.1019.

I think the European tree frog is more than a possibility. This looks exactly like one.

@RHA I agree it looks like a pretty good candidate. My concern came from the skin texture. Most images I've seen seem to suggest H. arborea actually has rather granular dorsal skin, whereas the OP's specimen looks to have smooth dorsal skin (which matches the description I quoted). This lack of clarity was the only reason I shied from giving a definitive response.

I think it looks smooth when the skin is wet. I've seen the Europeam tree frog a number of times in the wild and this looks like one. Besides, there is no realistic alternative in Europe.

@RHA Ok cool -- fair enough. My only thought was that perhaps some nonnative had been transported with the flowers. I appreciate the first-hand knowledge since its quite hard to catch a glimpse of one across the Atlantic :p


text:
How are fingerprints formed?
I know what influences the fingerprints to be unique always. But what actually process is taken to make these as we grow?

The question you are asking is very broad. One can dedicate an entire review if not a book chapter, on this topic. Can you please narrow your question down so that it could be answered in a few sentences (2-3 para at max)?

Fingerprints are called epidermal ridges in Biology. These are formed between the 3rd and 4th month of the fetus. The epidermal layer looses its strength, becomes like a cloth from a piece-board and falls on the underlying layer of skin cells, the dermal papillae. Now, you must realize that not all tissues are as smooth as the skin for evolutionary reasons. This tissue, although a part of the skin, is irregular and some its cells get little more swelled up. After falling, the epidermis begins to harden up and thus takes its shape.
This phenomenon has probably evolved from providing friction for traction and increase in surface area for sweat to come out.
Read more at:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1013024/


text:
Cis and trans linkage
Question:

Two dominant non-allelic genes are 50map units apart, the linkage is:
(A) Cis type
(B) Trans Type
(C) Complete
(D) Absent/Incomplete

My take:
After a lot of searching on the net I found that 50 map units =50% recombination frequency. And no recombination happens  when it is 50 map units or more than that.
But there is no information given about cis and trans linkage with that of map units.
Even though the answer for the above question is absent or incomplete (d),the options bugged me to ask this question
Is it possible to guess cis /trans linkage when map units are given? If i am wrong please correct me. Thanks in advance !

50cM ≠ 0.5 probability of recombination. See Difference between crossover rate and recombination rate?

Yep...i understood that ! Only genes  less than 50cM apart  can be recombined right?

It would be better if you post the question from your textbook (or exercise) as a text instead of an image.

As far as I know, cis and trans require the knowledge of which alleles of two traits are present and how they are linked. But based on the "two dominant" thing in the question, if there were linkage, it would have been cis type linkage. A random page on the first page of Google search, if it helps.


text:
Osmosis- basic questions

Hi there,
For the first picture: can someone please explain in simple terms (I started learning biology a few days ago), why the answer to this osmosis question is no?

For the second picture: The answer is left because "the tension of the balloon can resist osmosis". Can someone explain what this means?

Homework questions are off-topic on [biology.se] unless you have shown your attempt at an answer. For more information see our homework policy.

And not only is this a homework question, it is chemistry rather than biology.

Yeah, basic principles of osmosis there, but let me see if I can make it clear.  For illustration's sake, I'll take glucose as a solute and water as a solvent, but recall that the principles are true (though they can have added complexity) for other solutes and solvents (see this post on chem.SE).
Background
The basic principle behind osmosis is that conjoined systems tend toward equal concentrations.  In other words, if you have a more concentrated solution (more particles of glucose per amount of water) on one side of a membrane than the other, the solution "wants" to become equal on both sides of the membrane.
If the membrane is permeable, there's no problem: glucose can flow freely and equilibrate on both sides of the membrane.  So the solution just moves around "mixing" until there's the same concentration everywhere of solutes (ie., glucose) in the solvent (ie., water).
On the other hand, suppose that the membrane is semi-permeable, meaning that the the water can pass through but the glucose cannot.  The system still "wants" to get to equilibrium; a state of equal concentrations on either side of the membrane, but it cannot get the solute across.  What happens instead is that water starts moving from the side which is less concentrated to the side which is more concentrated.  This results in the concentration of particles on less concentrated side going up and the concentration on the more concentrated side going down, effectively equilibrating them.

Now look at Picture 1.  Intuition from all this would tell you that the concentrations would be equal.  However, there's a twist.  Osmosis can only exert so much pressure on a system, and if it has to resist a pressure, it eventually stops, even if the concentrations are not equal.
The assumption in the picture is that the balloons have the same elasticity, meaning that the balloon on the left is more stretched, and is exerting more pressure on the solution than the balloon on the right.  Therefore, it will counteract some of the osmotic pressure and push some water back onto the right side of the system.
Now look at Picture 2. Again, intuition would tell you that the balloons will have equal concentrations at the end of the scenario, but again, the pressure that the balloon on the left is exerting messes things up a bit.  Even though the balloon on the right is pushing water into the balloon on the left, it is unable to push as much as it would like to, because the pressure of the left balloon's elasticity counteracts the osmotic pressure.

Taking it to the next level
They're basically laying the foundation work for reverse osmosis in this question.  In the case of reverse osmosis, we would be artificially applying pressure to the balloon on the left, resulting in water flowing forcibly into the right container.  This can be an advantage if you want to increase the concentration of a liquid - which has hundreds of industrial usages, such as in concentrating maple syrup in Canada and the northern States.


text:
What is 'exhausted buffer' in gel electrophoresis?
For gel electrophoresis of DNA, we use TAE or TBE.
TAE buffer is cheaper than TBE but it has low buffering capacity; it exhausts faster than TBE buffer and there is a need to change the buffer during gel electrophoresis when electrophoresis longer.
but what is 'exhaused' in gel electrophoresis?

Do you have a source saying you need to change buffers during electrophoresis? I have never heard this and never seen any problems running gels longer.

Never heard of having to change the buffer during electrophoresis. When you turn down the voltage, you just throw it away. I would even think that replacing the buffer during the test, could produce errors and affect in a negative way the layers separated into the gel. Right now i do not have my labs notes under hand

OMG I heard about that where BRIC, Korean biologist community. ...I cannot believe there.

Then, what is 'exhausetd buffer' in gel electrophoresis?


text:
How are light sheet microscopy 3D images and their computed sections built up from stacks of 2D images?
The iBiology Techniques video Microscopy: Dual-View Inverted Selective Plane Illumination (diSPIM) (Hari Shroff) describes light sheet microscopy and the improvement in resolution by introducing dual-view (two cameras) capability.
What's happening is that the object is moving randomly in 3D, and so for each frame, the stacks are used to generate a 3D image, and then it is de-rotated to synthesize a view in a plane fixed to the object, rather than the microscope.
Is there a simple way to understand how these image stacks are processed to obtain a smooth 3D reconstruction that can then be sectioned computationally? Is there some kind of interpolation or modeling of structure at the limit of the depth resolution?
Rather than a complete explanation, which would likely be fairly mathematical and in depth, a simpler explanation plus a reference or link to a more in-depth description might be a better way to help me get on the right track.

According to their website dispim.org they are using registration software like the ImageJ Multiview-Reconstruction Plugin. Judging from the descriptions, this plugin uses the alignment of multiple points in the different angle images (like fluorescent beads that have been introduced to the medium or the cell nuclei) by rigid transformation and then deconvolves the 3D information using the point spread functions.
Knowing your optical system (microscope lenses etc.) you can calculate how the image of a point light source would look like in the image. This can be used to reversely calculate the actual position of your light source from the image and reconstruct an image without the distortions.
From that they get a volumetric image that can be projected into any coordinate system. I recommend watching the videos on the plugin page to get an idea how this works.

Oh this looks really interesting, thank you! I'll have a look now...


text:
Why do obese people heal more slowly?
I recall an obese patient who was referred to a transplant clinic as his stitch wounds hadn't healed after a year. While there's a myriad of side effects caused by immunosuppressive medication after transplants, the usual healing process for patients that underwent the same procedure is around one to two months1.
It's not an isolated example, as patients with very high BMIs can be considered ineligible for transplantation because of the post-surgical complications that follow, namely, delayed wound healing and increased chance of infection. It does not seem to be dependent on diabetes or merely low metabolism rates caused by a sedentary lifestyle (some of the patients perform well in exercise tests and monitor and control their blood glucose levels) and as such, BMI tends to remain the only (imperfect?) factor.
Why does a large percentage of body fat or a high BMI delay or impair healing?
It seems counter-intuitive to me because, as I understand it, the two major parts of the healing process involve 1) a great range of proteins for the creation of new vessels, tissue etc., and 2) The energy needed for the different processes, such as the mitosis of the cells. If blood glucose levels are close to normal and there isn't much of an insulin resistance, then surely it's not a problem of availability for either of the parts to play their role?
Clarification: I restrict the scope of the examples to transplant surgical procedures as what I state is more likely to be factually correct due to  personal experience. I would expect wounds other surgical operations to follow the same patterns, but I could be wrong.

[1]: That is an extreme case, especially considering the possibility of effects of diabetes, obesity and steroids compounding. However, there's a general trend.

It's well known that obese patients have slower wound healing, but the specific cause isn't known; most likely there are multiple causes acting together.

The correlation between obesity and deficient wound healing has long been established. ... Substantial evidence exists demonstrating that obesity is associated with a number of postoperative complications. Specifically in relation to wound healing, explanations include inherent anatomic features of adipose tissue, vascular insufficiencies, cellular and composition modifications, oxidative stress, alterations in immune mediators, and nutritional deficiencies.

--Obesity and Surgical Wound Healing: A Current Review  (This is an open-access article that nicely summarizes the open questions)

Obesity has been shown in a number of studies to impair wound healing, and chronic nonhealing wounds in obesity and diabetes are a major cause of limb amputations in the United States. ... Recent evidence indicates that aberrant wound site inflammation may be an underlying cause for delayed healing. Obesity, diabetes, and other conditions such as stress and aging can result in a chronic low-level inflammatory state, thereby potentially affecting wound healing negatively.

--Exercise, Obesity, and Cutaneous Wound Healing: Evidence from Rodent and Human Studies (Also open-access, a little more recent but less wide-ranging)


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Are there known life expectancy differences in non human mammals by sex?
In humans either for biological or cultural reasons there are life expectancy differences by sex. But how about non human mammals? Are there known life expectancy differences in non human mammals by sex?

Are there known life expectancy differences in non human mammals by sex?

Yes, there are. It is not well studied in general, but for certain species it is. Here is a relevant excerpt (Austad, Fischer, 2016):

Females live longer than males in humans and all Old World monkeys and apes for which we have the best data. . . This appears to be true in both wild and captive populations. . .  Yet whether there is a general mammalian pattern of greater female longevity under protected, captive conditions where intrinsic physiological aging dominates mortality patterns, is not known because so few species have been rigorously investigated. What is known about the best described species indicates that all show a substantially different pattern from humans.

See the linked study for more information. There is a whole section on sex differences in lifespan in mammals.
In general, in any species where males fight fiercely amongst each other for status, I would also consider it likely that males have shorter lifespan on average than females. Although I don't have a good citation for this at the moment.
In a more recent review, Lemaître et al (2020) confirmed the tendency for females to outlive males across many mammalian species:

In human populations, women consistently outlive men, which suggests profound biological foundations for sex differences in survival. Quantifying whether such sex differences are also pervasive in wild mammals is a crucial challenge in both evolutionary biology and biogerontology. Here, we compile demographic data from 134 mammal populations, encompassing 101 species, to show that the female’s median lifespan is on average 18.6% longer than that of conspecific males, whereas in humans the female advantage is on average 7.8%. On the contrary, we do not find any consistent sex differences in aging rates. In addition, sex differences in median adult lifespan and aging rates are both highly variable across species. Our analyses suggest that the magnitude of sex differences in mammalian mortality patterns is likely shaped by local environmental conditions in interaction with the sex-specific costs of sexual selection.


text:
How do I determine this logistic growth model formula?
The Question

Two yeast cells were placed into a special container to which food was
  continually added, to keep it at a constant concentration. All other
  factors were set for optimal yeast growth (for example, temperature,
  oxygen, and pH). The population was sampled every hour for 21 hours
  and the results of the estimated population size were recorded in the
  table below.
Time (hour), Number of yeast cells
(0, 2) (1, 10) (2, 15) (3, 20) (4, 40) (5, 60) (6,
  100) (7, 190) (8, 260) (9, 350) (10, 450) (11, 530)
  (12, 580) (13, 600) (14, 600) (15, 600) (16, 600) (17,
  600) (18, 600) (19, 600) (20, 600)
What population growth model does the population appear to follow?
  Write out the mathematical equation it follows.

The Attempt
Looking at the values, I recognize the carrying capacity is reached at hour $13$ with $600$ cells, signifying a logistic growth model. The formula given to me for logistic growth is:
$\frac{dN}{dt} = rN[\frac{(K - N)}{K}]$
From what I have researched:
$dN$ = population size change
$dt$ = time interval
$r$ = (max) growth rate
$N$ = starting population size
$K$ = carrying capacity
So:
$dN = 600 - 2 = 598$?
$dt = 21$ hours
$r = $?
$N = 2$
$K = 600$
Plugging the values in gives me:
$598/21$ = $r2[(600 - 2)/600]$
Update 25/01/19
With some help, I have discovered how to determine the r/rmax value and have the following formula:
$r = (90+100)/2$
$r = 95/hour$
$dN/dt = 95N[(K - N)/K]$
With $N= 2$
$dN/dt=95(2)[(K-2)/K]$
and if $K$ value is carrying capacity, $K = 600$
$dN/dt=95(2)[(600-2)/600]$
$dN/dt=190(598/600)$
$dN/dt=190(0.997)$
$dN/dt=189?$
However, the question asks me to "Write out the mathematical equation it follows." So am I supposed to leave a value unknown?

The coefficients of the solution to this differential equation are usually derived by regression.

@Roland I was able to make some progress with help. Am I on the right track?

Can you tell how you got the $r$ value, or rather the $r/rmax$ you refer to?

@SatwikPasani From what I understood, the r value refers to the maximum growth rate value, which happens around the 9th hour. So I was directed to average out the growth rate between hours 8 and 9 (90) and 9 and 10 (100) so (90+100)/2 = 95

I think your problem arises from misunderstanding the $r$ coefficient. I've tried to explain it below, let me know if you need more clarification.
Instantaneous vs Average Growth
Differential equations (like the logistic equation you write) talk about the instantaneous drowth, $dt$ is infinitesimally small, as opposed to your working where you are subtracting the population at two distinct time points and dividing to find $r$, which will only be an average $r$ for that time period. If we were to plot population vs time, we can understand $\frac{dN}{dt}$ as the slope of the equation, and it is apparent that it is changing with time. So, you cannot use distinct time points to find out R, since that will only give you an average $r$.

Logistic Curve Fitting
You can solve the differential equation to get $N$ as a function of time. The ideal way to do this is to try and fit a logistic curve to the data. This way, we already know $K$, $N_0$, and out job is to fit a curve to our data by trying different $r$ values to see which $r$ fits our data the best.
$$N(t) = \frac{KN_0e^{rt}}{K + N_0(e^{rt}-1)}$$
There is a formal way to do this cure fitting. Have a look here, here and here. There will definitely be better resources than these, but I could find these on a cursory google search.

Actually, for intervals of time where the slope remains approximately constant (i.e. the central part or exponential part of the growth), you can use the finite approximation of the derivative, taking two pints and dividing by the time interval between them. That will be an approx. of the exponential growth rate in that interval.

The growth of the yeast can be studied with a Logistic model (i.e. differential equation) as follows:
$$
\frac{dX}{dt}=\mu X \left(1 - \frac{X}{X_{max}} \right)
$$
This is an ordinary differential equation that tells you how the population of yeast is changing with time (in fact is telling you how the concentration of Yeast $X$ changes with time).
The two parameters in the equation are the specific growth rate $\mu$ and $X_{max}$ the carrying capacity following the Verlhust model.
We could also write the equation following your notation:
$$
\frac{dN}{dt}=r N \left(1 - \frac{N}{K} \right)
$$
where $r (\mu)$ is the specific growth rate, $K (X_{max})$ is the carrying capacity, and $N$ is the number of elements in the population.
Note that this is a dynamic model that you need to solve (i.e. integrate the differential equation) to be able to compare with your experimental data. This model tells you how any population of this time behaves not only your Yeast in the mentioned experiment.
The solution of this model is the following Logistic equation:
$$
N(t) = \frac{K}{1+\frac{K-N_0}{N_0}e^{-rt}}
$$
Where $N_0$ is the initial number of Yeast cells.
If you fit this equation (i.e. with least-squares) you get the following values for your experiment (with their 95% confidence intervals):
K =       603.6  (594.3, 612.9)
N0 =      2.108  (1.179, 3.036)
r =      0.6729  (0.6196, 0.7262)
And the following curve.

$r$ is the growth rate (in $hr^{-1}$) that is related with the doubling time by the following formula:
$$
t_d = \frac{ln 2}{r} = 1.0301 hr
$$
Check also this answer about growth models


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More general term than "adaptation"
The Wikipedia article about adaptation states:

Adaptation differs from flexibility, acclimatization, and learning.

What is a more general term than adaptation? For example, is there an umbrella term for adaptation and learning (and optionally other phenomena)?
Edit: Some examples of possible definitions of terms that I'm looking for:

mechanisms that change/improve fitness over time [over lifetime (learning) or generations (adaptation)] by matching the environment
how the phenotype changes [over lifetime (learning) or over generations (adaptation)] to match the environment
properties of anything that is alive that change [for example in the gene pool (adaptation) or in the brain (learning)] to improve chances of survival

Do you want a word in English or scientific/biological terminology? If the former, adaptation is fine. If the latter, I see little biological reason to group those terms since they are fundamentally different, and in the right context 'adapt'/'adaptation' can be applied to the other concepts: the article you link is only talking about adaptation as an evolutionary term (as is clear in the Wiki heading) - Wikipedia notes these other scientific uses also at https://en.wikipedia.org/wiki/Adaptation_(disambiguation)

@BryanKrause I'm looking for a word that is scientific/biological terminology or at least wouldn't contradict scientific/biological terminology. The umbrella term can for example have the meaning "properties of a population that change [for example in the gene pool (adaptation) or in the brain (learning)] to improve chances of survival".

Adaptation would be the term for changes in the population. Flexibility, acclimatization, and learning are all ways that individuals change.

@root It is a good question +1. That being said asking for an umbrella term for adaptation and learning is a bit like asking for an umbrella term for airplane and candy bar. I am going a little extreme but the point is there is not much interest for having a term for these two very different concepts. You can maybe go by with something like "how well the phenotype match the environment" or why not maybe just use the concept of "fitness".

@BryanKrause A population consists of individuals. Flexibility, acclimatization, and learning affect individuals, so they affect the population. That's what I meant. If you prefer: "properties of anything that is alive that change [for example in the gene pool (adaptation) or in the brain (learning)] to improve chances of survival". Or see my next comment.

@Remi.b I mean "how the phenotype changes [over lifetime (learning) or over generations (adaptation)] to match the environment". Or "mechanisms that change/improve fitness over time [over lifetime (learning) or generations (adaptation)] by matching the environment". (If changes acquired by learning are considered part of phenotype and fitness.) Question edited accordingly.

Adjustment = a small alteration or movement made to achieve a desired fit, appearance, or result; the process of adapting or becoming used to a new situation (Google Dictionary).
Adjustment is a very general term; it doesn't mean anything specific in biology or other sciences and it can cover all the terms you've mentioned: adaptation, acclimatization and even learning.
If you check in Thesaurus.com, you can see that synonyms for adjustment include acclimation, acclimatization, modification and improvement, and that one of the synonyms for adaptation is adjustment.

Factors or variable
Variable is probably your best bet, since it literally can cover anything that varies or can vary.
Factors can also be used but has specific meaning when dealing with experimental design so it may not be as good, on the other hand it is used less outside that so if you preface its usage with a description it is less likely to get confusing.


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Why are spinal nerves considered a part of PNS while the spinal cord is a part of CNS?
So from my common understanding, CNS consists of brain and spinal cord, and PNS consists of everything else. But the spinal nerves - the nerves connected to the spinal cord - why are those considered part of the PNS? And another clarification - spinal nerves are COMPLETELY DIFFERENT than the preganglionic neurons of the sympathetic nervous system?
Thanks for all your help.

I recommend that you stick to one question per post unless the different questions are interconnected to a great extent.

CNS consists of brain and spinal cord, and PNS consists of everything else

That's really it. The distinction is slightly arbitrary, I'd think of them as the central (nervous system) and the peripheral (nervous system): that is, the most important part is that together they are parts of the nervous system, rather than being distinct systems; the central/peripheral difference is fairly minor, especially if you are thinking primarily of the somatic part of the peripheral nervous system (that is, not the autonomic part) relative to the associated part of the CNS.
The peripheral part of the nervous system is not protected by the bones of the skull and spine, does not have the protection of the blood-brain barrier (specialized endothelial cells and astrocytes that limit transmission of molecules between CNS and the blood circulation moreso than in other tissues), and myelination is mediated by cells with a different morphology: Schwann cells in the periphery vs. oligodendrocytes in the central. That's about it.


text:
Is there a measure for degree of reticulation in a phylogenetic network?
When working with phylogenetic networks, how does one talk about reticulate (i.e., web-like) the branches are? Is there a standard measure of this?

biostars.org may have some phd students that deal with that alot.


text:
Does natural selection select for randomness in development?
In a podcast with Sean Carroll and Liv Boeree they discuss a result from game theory that the optimal strategy in the face of incomplete information can require random decision making. For example, without more information (e.g. the robot that uses high frame rate video and fast movement to see what the human is picking and quickly pick what beats it), the strategy in rock-paper-scissors that cannot be dominated is to choose which one your going to do randomly with equal probability.
We know that situations where there is not one optimal strategy exist in biology. Examples: male vs. female, side blotched lizards, E. Coli (produce toxins and defense vs. just defense vs. neither).
Now, in most of the examples above the source of the randomness is entirely from sexual reproduction (meiosis). The only example I can think off the top of my head of where this isn't the case is for crocodiles (maybe only some) where the sex is fixed by the temperature the egg is at during a certain stage of its development. In a sense, for them, sex selection is completely non-genetic but is done as a response to a stimulus.
My question is this: are there examples of genes that control development in a non-deterministic way (i.e. are there genes that by their presence will produce a trait with some probability greater than zero and less than nearly 1)?
I think genes that can be switched on and off in response to relevant environmental stimuli shouldn't count (e.g. the development into a queen for a honey bee). I'm just interested in whether there are genes that function in a highly random fashion and if natural selection has lead to such genes being produced (something like the presence of gene X causes trait Y with 30% probability, all other genes being equal). I add the qualifier "highly" to the randomness because these processes are ultimately always going to have some randomness from thermodynamics, and our cells go to a lot of effort to mitigate that randomness in most situations.

X-chromosome silencing/inactivation is inherently random (in all mammals), but can only lead to a phenotype in the case of heterozygous genes on the X-chromosome. Would that fit what you're looking for?

@Nicolai I don't know. Isn't that random on a cell by cell basis, leading to a mosaic expression? Although, you raise an excellent concern: how would the gene's activation be coordinated across the body? Maybe if the activation only lead to a particular trait if it was activated in a particular tissue, then yes, that would work.

Yes, you're right that the randomness is cell-based and leads to mosaic expression and that happens so early that it afaik affects almost all cell types, so I'm not sure if it would be possible (or at least probable) to have a specific phenotype in a given tissue.

@Nicolai It is. See: calico cats. https://en.wikipedia.org/wiki/Calico_cat It's just a question of if an entire organ or tissue (e.g. the adrenal glands) can express one or the other, that I don't know.


text:
How much of human's behaviors and preference can be explained by evolution?
I'm talking about things like the tendency to feel sleepy after eating, avoidance of excrements, general preference for sweet foods, etc. Do all those characteristics have biological or evolutionary basis?

Your question is super broad. The "evolutionary explanation" for single traits itself is quite difficult and you are asking about many complex traits.

What is heritability?
First of, please read about the concept of heritability. See for example the post Why is a heritability coefficient not an index of how “genetic” something is? You should be able to understand why all else being equal, why if environmental variance for a given phenotype increase it results in a decrease in heritability and why directional selection in a population decreases heritability.
Do you now know what heritability is and is not?... Good!
Your question is very broad...
As you now understand, heritability is a concept define for a given population in a given environment and most importantly for a given trait. There is no way to give a single answer for all traits one might want to consider.
By experience, it seems that, in humans, most behavioural traits that we decided to investigate has heritability estimates in the order of 0.05 - 0.6.
One example
I will consider just one of the trait you list, "preference for sweet foods". Sweet taste preferences appears to have a high heritability in humans with estimates of the order of 0.41-0.66 (Keskitalo et al., 2007). For heritablities about other food preferences, you might want to have a look at Reed et al. (1997; there are probably more recent papers that make better reviews though).
Preference for sweet foods

What I think is not immediately clear in this answer in response to a question like the OP is that heritability in the contexts you are presenting refers to variation in the population. If you look at the heritability of, say, height, that coefficient completely misses that evolution led to human-sized humans and not ant-sized humans, which is definitely genetically encoded.

@BryanKrause Yes, this is why I insisted that the OP looks for what heritability means and I highlighted that directional selection actually reduces heritability. But I agree with you, when rereading the question, that the question should probably be be closed as it is not asking so much about heritability but more whether "it is explained by evolution", which does not mean anything.

I actually voted to close. Then removed my close vote when starting to write a comment that was too long, so I made an answer. Maybe, I should have just kept with my close vote. Anyway, I can't vote to close anymore!

Yeah, I know that and you know that but I don't think your answer here or the linked one conveys that message in easily, quickly digestible format. I do think the right thing in the end will be to close this question.


text:
The Hawk-Dove game: why is the average payoff half of the difference between reward and cost?
My question is about the well known Hawk-Dove model used in game theory. It concerns two strategies: the Hawk, which always fights the opponent, and the Dove, which does not fight and will either retreat or share. The payoffs for each of the possible encounters are presented in a matrix. Now, say that the reward (R) is 10 units and the cost of fighting (C) is 5 units. When a Dove meets a Hawk, it will retreat: Dove gets 0 and Hawk gets R=10. Vice versa, when a Hawk meets a Dove, Hawk gets R=10 and Dove gets 0 because it retreats. When two Doves meet, they will share the benefits; both Doves get R/2, in this case 5. These three, I have no problem understanding.
My issue is with the payoff when two Hawks meet. I understand that, under the assumptions of the model, both Hawks have a 50% probability of winning. I also understand that the winner gets R and loser pays C. But I'm completely stuck at why the average payoff is given as (R-C)/2. When you input the numbers above, it gives you a value of 2.5. How is the average payoff in an encounter between two Hawks 2.5 if one receives 10 and the other loses 5?

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

$\frac{(+10)+(-5)}{2}$, isn't that how an average is calculated?

It's about evolutionary game theory and it is considered a part of evolutionary biology. It cannot be considered off-topic.

One hawks gains 10, the other loses 5. So together, they gain only 5 (=10-5). On average, they gain 5 / 2 hawks = 2,5


text:
How does mineral oil kill a cockroach?
A recent post at a sister site Best field remedy for small cockroach in the ear has an answer that says

A few drops of baby oil (light nontoxic mineral oil) to suffocate the cockroach then tweezers to carefully remove it once dead and motionless.

This seemed unlikely to me, in the given scenario I suspected the baby oil had an additive. Per this link "some roaches can go up to 40 minutes without breathing" further suggesting suffocation was not the cause of roaches lack of motion.
I have done some more research and it appears this does actually work as described.

Doctors Settle Cockroach-In-The-Ear Controversy
The proper way to remove a cockroach from someone’s ear, it seems, has been the subject of little-publicized disagreement. The time-honored method is to drop some mineral oil in the ear, then try to pull the little critter out. A newer, competing technology is to squirt it with lidocaine, an anesthetic, to make it bug out on its own. Source

Both solutions above were ultimately successful. They found the lidocaine more effective.
Lidocaine does have draw backs as outlined in this article

Cantrell removed the dead roach with a set of alligator forceps, but the patient complained of dizziness for five hours after leaving the hospital.
"It is known that topical anesthetic agents entering the middle-ear cavity can be absorbed by the oval and round windows and cause vertigo," he said. The oval and round windows are parts of the middle ear used to transmit sound. Source

Putting aside which is the more appropriate choice. I just want to know how the mineral oil kills a roach quickly when it normally takes up to 40 minutes to sufficat one.
NOTE: Roach toxicity of Mint Oil is a completely different subject. (PDF)

Are you sure the cockroach died from the oil?

@StrongBad the references i read suggest they die from the oil.  There seems little question that at least they are rendered immobile within a few seconds to minutes of oil application.  If they come back to life like fleas do after drowning is not mentioned in anything I read. An answer supplying the mechanism of how the oil works on the roach should provide they answer to your question.


text:
Does reversion of resistant strains to wild-type only occur when no more drug pressure is exerted
We always read that wild-type reversion of a resistant strain occurs when no more drug pressure is exerted. Could resistance reversion also occur under drug pressure, but from a drug other  than the one to which the virus is resistant.
To illustrate my question, let’s assume an HIV strain resistant to a specific anti-retroviral drug class (e.g. NNRTI drugs). Would NNRTI-resistance reversion to wild-type HIV occur under the pressure of another drug regimen (e.g. PI drugs) or does resistance reversion only occur when no more drug pressure at all is exerted?

Welcome to SE Biology. Your question is good, but could be improved with a reference to support your initial assertion. Your "reputation" indicates you have not yet completed the Tour. We recommend new users do so, and perhaps view the Help on asking questions. And it is a good idea to check your title carefully. One with a spelling mistake and a word missing does not create the best impression. (I've fixed it).

I am not an expert on HIV but I am answering based on general principles.
This is a typical example of selection of individuals/populations with different fitness.
Reversion to wild-type (WT) would happen if the WT has higher fitness in that environment. Assuming that WT is the fittest under drug-free conditions, it is not difficult to understand that the WT population will outgrow other mutants.
For your question — "would a drug resistant HIV population revert to WT under treatment with other drugs", the simple answer would be no.

Explanation
HIV generally acquires resistance against different drugs quickly because it has a high mutation rate. In your example case, the HIV population that is resistant to the new drug will outgrow other populations if we assume that the selection is strong. There would not be any reversal to WT because WT would also be unfit in the new environment. If the selection is weak then the population genetic diversity would depend on the relative fitness of different genotypes.
There may also be pleiotropic effects: mutations that provide resistance against one drug can also possibly provide resistance against other drugs. This is well known in case of bacteria and there are many reports for HIV too (Rhee et al, 2010, Other Google Scholar Hits).


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How to distinguish the Ct of the target gene from the Ct of the housekeeping gene? (very basic qPCR question)
I will do a qPCR experiment for the first time, and I have a bottom-level question to ask. I know that for normalizing the quantity of your target gene you have to add an endogenous control, like a housekeeping gene, in your qPCR sample, and then you subtract the Ct of the housekeeping gene from the Ct of your target gene. However, since the same SYBR green fluorophore is used to quantify both the target gene and the housekeeping gene in the same sample, how do you know which Ct is from the target gene and which one is from the housekeeping gene?

You do not take readings from the same reaction, you split the sample. You would run each primer pair in their own reaction. You also want to run each reaction in triplicate so you can get some idea of the error.
So, a general plate set up might look something like this:
A1: Control sample, housekeeping primers; A2: Control sample, target gene primers
B1: Control sample, housekeeping primers; B2: Control sample, target gene primers
C1: Control sample, housekeeping primers; C2: Control sample, target gene primers

D1: Treatment sample, housekeeping primers; D2: Treatment sample, target gene primers
E1: Treatment sample, housekeeping primers; E2: Treatment sample, target gene primers
F1: Treatment sample, housekeeping primers; F2: Treatment sample, target gene primers

So in this scenario, the delta-delta Ct value comes from the following:
delta-delta Ct = ( Ct(treatment, target) - Ct(treatment, housekeeping) ) - ( (Ct(ctrl, target) - Ct(ctrl, housekeeping) )

If the PCR machine does not offer to do the delta-delta Ct analysis for you I recommend this blog which both explains it well and provides and excel spreadsheet so you can just drop you Ct values in.
HTH.

That makes more sense, I got that information wrong. Thanks for the clarification.

No problem. As much as possible, make master mixes and decant them in down in to the single reactions to keep things as homogeneous as possible. Good luck.


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Why does the peak magnitude of the cardiac pacemaker action potential not increase to levels closer to the Ca++ equilibrium potential?
it does for K+ and Na+ but not calcium? why?

The equilibrium potential at any point in time is determined by the relative permeability of ions and the reversal potentials for those ions, according to the Goldman equation/GHK equation. The voltage of the cell moves towards that equilibrium potential at a rate that depends on the membrane time constant (determined by the capacitance and resistance/conductance of the membrane).
In a typical neuron, during the rising phase of an action potential, the conductance of sodium compared to other ions is very large, large enough that you can almost ignore the other ions, so the peak of the action potential gets fairly close to the sodium reversal potential. Often there is also permeability to calcium, which pushes it even closer to sodium reversal.
However, in cardiac pacemaker cells (and in cardiac myocytes), although there is a big increase in calcium permeability, the relative permeability to other ions isn't quite as big, so the "weighted average" of ion conductances and their reversal potentials gives an equilibrium potential somewhere in the middle.


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For allele frequency determination, is it good to take samples from a college/school or a hospital or any other technique?
I am trying to determine allele frequency of a hla allele. Preliminary analysis shows the prevalence of the allele (homo or heterozygous both) is 3%. The allele is related to a disease (After exposure to risk factor). Taking samples from college or university can help reduce time and money. Taking samples from hospital may take time (the hospital I have contact to, has small sample size?). Though both ways may have ethnic diversity, college students are of a given generation only. What to do. Please suggest with references to read.

I suggest this as a starting point.
Basically, if your aim is to determine the population frequency of the alleles, then you should sample from the population.
A possible problem with the university is the age stratification, but also possible different proportion of ethnic groups compared to general population. Also hospital might be biased, because you will have a higher prevalence of people with health issues.
The best thing is to randomly collect samples from the population (but I know it is very hard, especially because you can sample randomly, but the ratio of people willing to give you their blood will be biased!).
One thing that is commonly accepted is to retrieve data from healthy blood donors (which is not unbiased, but is accepted!).
You can give a look at a paper I published a lot of time ago. In that case, the estimation of haplotype frequency was performed on the bone marrow donors registry, and it was considered perfectly fine.
Good luck!