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Which chromosome of the two contained in a haploid cell goes into the diploid cell after fertilisation?
I am totally new to biology and I have a very stupid question. In the typical representation of meiosis, haploid cells contain two different chromosomes, resulting from the crossing-over process. But diploid cells have two homologous copies of each chromosome, usually one from the mother and one from the father. So, since there are two identical copies of the same chromosome for each parent, it means that each haploid cell brought only one out of two chromosomes into the zygote. My question is: how is this chromosome selected? Is it a combination of the chromosomes contained into the haploid cell? Is it one of the original two, while the other one is discarded in the fertilisation process?
I'm sorry if my question is not clear. Thanks.

Have you looked at Meiosis II, the second part of the process?

I am not sure about where is your confusion. Do you understand that homologous chromosomes are represented as having same size in the image? So the chromosomes in doughter niclei II are definitely not homologous?

Can you provide an image presenting what confuses you? "Haploid" by definition means only one chromosome, so I think there is something off here. Remember in meiosis (re: Bryan), 2n (diploid)-->4n -->2n (meiosis 1)-->1n (meiosis 2, haploid), e.g. https://en.wikipedia.org/wiki/File:Meiosis_Stages.svg. The terminology gets hairy because people don't like calling it 4n before meiosis 1, but that's still what it is.

@MaximilianPress I think a better way to put it would be 2n,2c(diploid)-->2n,4c(DNA replication)-->n,2c(meiosis 1)-->n,c(meiosis 2) since the 2 chromatids are still attached at the centromere after DNA replication.

Thank you guys. I think that my confusion about this representation arises from me thinking that the two same-color chromosomes in the first diploid cell were identical. I hadn't noticed the difference in size. So let us take the first haploid cell from above. The longer chromosome will be the homologous chromosome of the same-size one coming from the other gamete? (The same for the short one)

@Luigi Yes, I think that they usually include more than one non-homologous chromosome in the models to remind us that most (all?) organisms that do meiosis have >1 chromosome in their genome (e.g. humans have 23 chrs in the haploid state). So it's always super important to sort out homologous vs. non-homologous chromosomes before you do anything.

@trinitrotoluene I see the point, but I have always found that logic to be extremely confusing- it looks like the chromosomes come from nothing if you count that way! IMO much simpler to just say 4n, even if they take away my geneticist union card.

@MaximilianPress I guess it just depends on whether you count chromosomes by the number of centromeres or consider the number of chromatids instead

@Luigi Since you were also confused about the colors: The same colored chromosomes represent chromosomes coming from the same parent. So for example red chromosomes came originally from mother and gray from father. Thay do this to show that after crossover there are "mixed" chromosomes - patchwork from both parents.


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What does +60mm mean in MRI scans?
What do the -30 to +60mm markings mean in this MRI scan image?

Short Answer
They are marking distance from a reference plane.
Longer Answer
In the images you provided, you are looking at horizontal slices through a brain. The legends are indicating that each plane has that vertical distance from a reference point (if the subject were standing); the positive numbers are dorsal to that reference and the negative numbers are ventral.
A common reference point for MRI images (to define as [0,0,0]) is the midpoint of a line through the pre-auricular point, though ultimately it is an arbitrary distinction.
If the actual reference point is important to you, you will need to verify the reference coordinate system used in the study you are looking at. It's also possible you are looking at coordinates transformed to some reference brain rather than real-life coordinates for that particular subject, but again, whether that matters or not depends on why you care. If you are doing research across subjects, you probably want to know reference coordinates; if you are doing brain surgery on a particular patient you want real-life coordinates.

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What do the column labels in this table mean?
This table shows the effect of sound (song and tones) on female birds. However, I'm not sure what the labels (F1 22, P and η2) mean. I've seen the labels on other tables too.

(from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3508516/)
If anyone could help I'd be very grateful :)
thanks!

F(1,22) is the result of an F-test with degrees of freedom 1 and 22, in this context most likely this is an F-test in the context of ANOVA; for the meaning of those degrees of freedom I would suggest further reading on ANOVA. Specifically, in this table it looks like we have a 2x2 ANOVA: with stimulus songs or tones and treatment E2 or none, and the interaction between them.
P is the P-value associated with that F-test; it is the probability of observing a result as extreme or more extreme than the F-test gave in this circumstance, given the null hypothesis was true (typically the null hypothesis is something like "the groups don't differ"), and assuming all of the assumptions of the statistical test hold true.
η2 is read as "eta-squared" - it is a measure of effect size, meaning it describes the magnitude of an effect controlled for some other characteristics of the measure, typically the variance. Many statisticians prefer presentation of effect sizes rather than p-values. A large value of η2 means that lots of variance in the outcome variable is explained by the parameter of interest.

brilliant answer

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What is the point of inter-species specific quorum-sensing?
So apparently, according to this TED video, there is a kind of quorum sensing involving a universal, inter-species specific molecule that all bacteria secrete. Is there any evidence of bacteria being able to examine levels of other species-specific bacteria, rather than just any bacteria that can secrete that universal peptide? It just seems like its not enough to generally survey the amount of ANY bacteria in relation to that of your own species.

All bacteria is most certainly wrong.


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Why does cut grass cause allergies?
I know that cut grass from a lawn or field can cause allergies in some people.
I also know that most plant allergies are due to plant pollen.
However, most people do not allow their lawn grass to flower, and therefore, any allergy from cut grass is likely not due to pollen.
So, what exactly in the grass is causing the allergy?
I did a google search but only found evidence and info for grass-pollen allergies.
Does anyone know what's going on here?

www.allergicliving.com claims that the cause to such an allergy is not the grass but is actually mold:

Often patients will have allergy symptoms with fresh cut grass...That's not grass pollen allergy, that may be mold allergy from the molds being stirred up.

The site also mentions that simply having the physical presence of lawn mower "dust" in one's nose may cause symptoms.
Source: www.allergicliving.com/2010/07/02/outdoor-allergy-grass-allergy-attack


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Why do birds legs' not get frostbite?
In a nature documentary I watched a while ago, there was a scene where a flock of flamingos slept in a lake that froze overnight. Each morning they just had to wait until the lake defrosted sufficiently to release them so they could get on with their day.
How do they not get tissue damage etc doing this?

Birds have a few adaptations and behaviors to keep their legs warm in cold weather:

Blood vessels (veins and arteries) run very close together or are intertwined:

The arteries and veins intertwine in the legs, so heat can be transferred from arteries
back to veins before reaching the feet. Such a mechanism is called countercurrent exchange. Gulls can open a shunt between these vessels, turning back the bloodstream above the foot, and constrict the vessels in the foot. This reduces heat loss by more than 90 percent. (Wikipedia)

Birds have specialized scales on their feet and legs which act as an insulator.

Birds often alternately tuck their legs into their body feathers to minimize heat loss. (Audubon)

Other survival mechanisms such as shivering and torpor come into play with extreme cold.

Other sources: Mother Nature Network. I don't have my texts handy, but can highly recommend Manual of Ornithology: Avian Structure and Function by Noble S. Proctor and Patrick J. Lynch.

Left this open for a bit just in case of further answers with additional info, but marking this as the answer as it is perfect, thanks!

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What author citation and abbreviation does (would) a monarch or a crown prince get after publishing a new taxon name?
Even though taxonomic rules appear to be silent about this (I've checked ICN Art. 46 and ICZN Art. 51), author citations, as well as abbreviations, are usually based on a surname. However, monarchs and crown princes don't have surnames per se, at least in the Western culture. Even though they have dynasty names, they may only get referred to by their personal name and dynasty name used as (instead of) a surname after the monarchy was overthrown, and for our purpose let's assume otherwise.
Has there ever been a case when such a person, while practicing biology (either as a hobby or professionally) published a name for a new taxon and there was a need to make up an author citation/abbreviation? If yes, how was it (they) made? If no, what would be an author citation/abbreviation for someone like, e. g., British Prince William?

I know nothing about taxonomic nomenclature, but my gut feeling on this matter seems to be correct — the Christian or given name is used. The “List of organisms named after famous people” on Wikipedia includes:

Callicebus bernhardi — Prince Bernhard of Lippe-Biesterfeld
Megaselia mithridatesi — Mithridates VI of Pontus
Mitra kamehameha — King Kamehameha I
Ornithoptera alexandrae — Alexandra of Denmark
Paroxyna cleopatra — Cleopatra VII Philopator
Pinus montezumae — Moctezuma II
Victoria Lindl. — Queen Victoria

However this is not always unqualified — perhaps because he is not the monarch?:

Hyloscirtus princecharlesi — Charles, Prince of Wales

and there are exceptions:

Lepidoteuthis grimaldii — Albert I, Prince of Monaco (born Albert Grimaldi)

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Different Mutations Leading to Same Allele?
Can different mutations lead to the same allele? In my genetics books, I always see alleles referenced as, eg. Aa where A = dominant and a = recessive, but are these strictly binary phenotypes? Since there are an infinite number of mutations that could theoretically take place, wouldn't there be an infinite number of alleles? Eg (not an actual biological phenomenon but just as an example) A1C on chomosome 3 leads to allele a1, A1T leads to allele a2, etc.

You are looking at high school biology books. if that.  I'd be shocked if a high school text didn't mention blood group genes, for instance.
The simple genetics that Mendel elucidated only applies to a very small number of situations.
In real life, very few situations are explained by the interactions of only two different alleles, one of which is classically dominant to the other, within a single gene.
So sure, you could have many alleles which break a gene, but where the presence of one working allele is enough to be functionally indistinguishable from having two working copies.  You could also have slight sequence differences that are functionally identical.
Here's a random example; all the variants ensembl knows about for a random gene.  Note that these are only variants which have been found, obviously private individuals and families might have their own variants that are not documented
http://uswest.ensembl.org/Homo_sapiens/Gene/Variation_Gene/Table?db=core;g=ENSG00000280165;r=13:61409685-61415522;t=ENST00000409204
Most of these are in the 3' UnTranslated Region, and likely have no functional significance.


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Which amino acids can be phosphorylated?
Definitely serine, tyrosine, and threonine. What about aspartate and glutamate? I thought the O- on the carboxylic acid side group could be phosphorylated but am getting mixed responses to this. Any thoughts / any other amino acids I'm missing?

Also check out the relevant wikipedia page. For "homework" questions, you are required to show your attempt to answer the question and to use the "homework" tag. (Note that "homework" can apply to questions even if they are not assigned as homework — for example those that are trivial to biology professionals and thus easily answered by searching.) ——— Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

I don’t see why it is suggested that this is a homework question. Most readers will not know the answer, and if there happens to be a resource that has all that information it may not be obvious to the poster. If either of those who have commented are able to provide a comprehensive answer which puts the topic into perspective, they should do so. The question is not posed in a very academic manner, but it can always be improved upon. A mere list is clearly of little interest.

There's a Wikinome page called Phosphorylation of unusual amino acids describing phosphorylation of histidine, aspartate, cysteine, lysine, and arginine. Lysine and arginine are apparently phosphorylated on the nitrogens. I was a little surprised to see histidine and aspartate on the list, as histidine kinases seem to come up often in my area of research.
I'm also aware of at least one non-proteinogenic amino acid, creatine, which is phosphorylated by a dedicated creatine kinase. It functions as a sort of phosphate shuttle for rapid regeneration of cellular ATP from ADP in situations of high metabolic demand.
References:
Phosphorylation on unusual amino acids. (http://kinase.com/wiki/index.php/Phosphorylation_on_unusual_amino_acids)
PubMed Abstracts: https://pubmed.ncbi.nlm.nih.gov/?term=18558627%2C10772951%2C10698688%2C1654322%2C9553104%2C8577821%2C19498169%5Buid%5D
Guimarães-Ferreira L. Role of the phosphocreatine system on energetic homeostasis in skeletal and cardiac muscles. Einstein (Sao Paulo). 2014;12(1):126-131. doi:10.1590/s1679-45082014rb2741


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Steroid hormones: how do they travel through the cytoplasm (not just the blood plasma) if they're hydrophobic?
I get that steroid hormones need hydrophilic plasma protein carriers (eg albumin, TBG) to travel in the plasma because they're not soluble in the plasma. However, I don't see any sources talking about how these hormones can then traverse through the (presumably also hydrophilic) cytoplasm to get to their receptors either in the cytoplasm or nucleoplasm. Anyone have any clarifications on this?

Firstly not all steroid hormones travel inside the cell and regulate the gene expression.
Basically there are two pathways- direct and indirect.
Steroid hormones are lipid-soluble, which allows them to cross the extracellular membrane to the inside of the cell.

Classical models of steroid action suggest that steroid hormones bind to specific nuclear receptor proteins once inside the cell. Reference

Once inside the cell, a steroid hormone binds with receptor proteins in the cytoplasm. The steroid hormone and its receptor form a complex, called a steroid complex, which moves into the nucleus where it influences the expression of genes.
Reference

In the indirect pathway,

The traditional nuclear steroid receptors can also indirectly regulate gene transcription by serving as signal transduction proteins that interact with various signaling pathways in the cytoplasm of a cell. In particular, ER can activate kinases, enzymes that phosphorylate and thereby activate other proteins. This sets in motion a signaling cascade that eventually ends in the nucleus with the induction of gene transcription.
Reference

I am not an expert in this area, but found a summary of and illustration from a textbook — Karen Lounsbury, Pharmacology, 2009 — on a Science Direct summary page.
Apparently for the glucocorticoid hormones there is a cytoplasmic glucocorticoid receptor protein (GR in the diagram) they bind to, presumably keeping them soluble in the aqueous environment. This causes heat-shock proteins (HSP90 in the diagram) associated with the receptor to be released from it, which allows the complex to be translocated to the nucleus where it binds to a glucocorticoid response element (GRE in the diagram), triggering transcription of appropriate genes.

More detail is given in a paper by Bledsoe et al. (2002) in which the structure of the dimeric GR bound to a steroid analogue was determined. To quote from the introduction to that paper:

Like most nuclear receptors, GR is a modular protein that is organized into three major domains: an N-terminal activation function-1 domain (AF-1), a central DNA binding domain (DBD), and a C-terminal ligand binding domain (LBD).
…
Within the context of the full-length receptor, both the AF-1 function
and the DNA binding activity of GR are dependent on hormone binding.
In the absence of ligand, GR is retained in the cytoplasm by
association with chaperone proteins such as hsp90 and p23, which bind
to the LBD (ref). The chaperone activity of the hsp90
complex has been shown to be critical for hormone binding by GR
(refs). Hormone binding
initiates the release of chaperone proteins from GR, allowing
dimerization and translocation of the receptor into the nucleus. In
the nucleus, GR binds to DNA promoter elements…

A image of their structure is shown below:

I suspect the issue is mainly one of diffusion distance. Steroid hormones are not that insoluble as they are compact and have multiple oxygen functional groups. Checking predicted log octanol/water partition coefficients on PubChem gives 3-4ish for steroid hormones compared to 6+ for a typical fatty acid, despite the latter having an ionizable headgroup.
These hormones are present in the body at nanomolar concentrations or even lower, and at that concentration, almost anything is soluble. The problem with them being in the plasma at any concentration, though, is that as soon as a molecule would collide with the lipid membrane of a cell in the wall of the vessel, it would tend to stick, and therefore the vessels would act sort of like a chromatography column that drastically reduces the apparent diffusion coefficient and generates steep gradients. While this might actually be desirable for a local mediator like a prostaglandin that has a range of a few cell diameters, it is very undesirable for something like steroid hormones that travel to completely different organs from where they are produced. Therefore, a hydrophilic carrier is essential.
On the scale of the cytoplasm of a single cell, this is not likely to be an issue, especially since there are receptors inside that act as a "sponge" or "sink" to catch and trap molecules that diffuse in.


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Suspensory ligaments: why are they ligaments?
Don't ligaments connect bone to bone? In the eye for example, the suspensory ligaments connect the ciliary muscle to the lens, which obviously aren't bones. Is this just one of those instances where the terminology isn't that precise and you just have to memorize the exception?

you are thinking of articular ligaments, those connect bone to bone there are a lot of other types of ligaments. suspensory ligaments support many different organs.

"...The suspensory ligaments connect the ciliary muscle to the lens..."

You must be referring to the Zonule of Zinn (Such a great name).
You are absolutely correct, the definition of Ligament varies across texts which can create confusion.
For example:
Merriam-webster:
A tough fibrous band of tissue connecting the articular extremities of bones or supporting an organ in place.
Wikipedia:
A ligament is the fibrous connective tissue that connects bones to other bones.


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Diarrhea / constipation: why are they associated with failure of the large intestine (and not the small intestine) to reabsorb water?
When I see reference to diarrhea or constipation, it's almost always in reference to the under- or over-reabsorption of water, respectively, in the large intestine. However, if the large intestine plays a much smaller role in water reabsorption than the small intestine (80% vs 20%), why is the small intestine rarely implicated in these disorders? Is it because the small intestine usually doesn't malfunction in this way and malfunctions are much more common in the large intestine?

Suppose, small intestinal pathology occur, fat absorption won't take place, osmotic load will be delivered to colon and then osmotic diarrhoea occurs. Eg of such small intestinal pathology: celiac, Whipple, tropical sprue, chron, TB etc

Well, a lot of diarrhoeal diseases are because of small intestinal disorders too. (See https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3621726 for a detailed discussion.) Something similar holds for constipation: https://www.msdmanuals.com/home/digestive-disorders/symptoms-of-digestive-disorders/constipation-in-adults.


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How do platelets produce proteins (if they do)?
I'm aware that platelets don't contain a nucleus, but do contain mitochondria (so have mtDNA) and rough endoplasmic reticulum / Golgi. Since platelets require many important cell surface proteins (such as aIIb b3 for ECM binding), are these proteins (1) synthesized de novo in the mitochondria using mtDNA, and then somehow shuttled to the ER / Golgi for secretion, (2) remnants from proteins that were synthesized in their megakaryocyte precursors and not actually created anew, or (3) synthesized via some other mechanism I'm not aware of? Online sources weren't clear on this question. Thanks!

it seems that megakaryocytes, while nucleated, create a large dormant reserve of mRNA and ribosomes, which can be used by platelets later, upon their activation. So platelets can synthesize only certain proteins already transcribed by their megakaryocyte predecessors. The reserve of mRNA decline with the platelet age.

Specific references would really improve this answer.

Please include references; even the best of answers are useless without resources to allow other users to background-read on your topics


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RT-PCR: Not seeing how it can measure mRNA expression levels
From my understanding, in RT-PCR we start off with an mRNA molecule, use the enzyme reverse transcriptase to create a cDNA copy (hence creating a double-stranded mRNA / cDNA hybrid), degrade the mRNA, and finally create a complementary strand to the cDNA with a DNA polymerase. If we're ultimately creating DNA and it's being duplicated at each cycle, how are we able to deduce the original quantity of mRNA in our sample? It seems like we would need to combine it with some other method, but a lot of sources I'm seeing seem to imply that RT-PCR alone is enough to "quantify" the amount of mRNA in a sample. Any thoughts on this are welcome

There might be a confusion of terminology. There is real-time quantitative PCR, which can sometimes be called RT-PCR. There is also reverse-transcriptase PCR, which is also confusingly called RT-PCR. To try to reduce confusion, real-time quantitative PCR is also called RT-qPCR or qPCR.
What you describe in your question is the reverse-transcriptase type of PCR. This is used for amplification, not quantification, of starting material.
QPCR or quantitative PCR, on the other hand, uses fluorescent dyes to measure the amount of amplified gene product. Standards provide a baseline measure of how much genetic material you should expect to see over time, at each PCR cycle, for a given amount of measured fluorescence. Measuring fluorescence of your own sample over time, and comparing it against the standard, gives you an estimate of what you started with, initially.

I just wanted to elaborate on the previous answer regarding the confusion between real-time (quantitative) and reverse-transcription(RT) PCR. RT-qPCR refers to real-time quantitative PCR, but some organizations refrain from any reference to quantitation (because it's really only semi-quantitative), instead using the nomenclature rRT-PCR (reverse transcription real-time PCR, I guess). In either case, this technique is theoretically capable of quantification of mRNA copies using the appropriate assay design and standards.
The general principle is that, after the cDNA is reverse transcribed from RNA, it is amplified similar to a normal PCR reaction. This can be accomplished in a single reaction with master mix containing both the reverse transcription and qPCR reagents, or in two separate reactions, by first performing an RT first, and then a standard qPCR on the resulting cDNA. The all in one method requires fewer reagents and less hands on time, but it can be difficult to optimize both reactions at the same time.
Here's a good primer on qPCR assay design. As stated in the previous answer, the quantification comes from some measure of fluorescence related to the amount of amplification product present. In an optimized reaction, the number of amplicons should double with each cycle, allowing for quantification based on how many cycles it occur before a specified fluorescence threshold is reached by each reaction well. Intercalating dyes like SyberGreen quantify total DNA present, whereas fluorescent probes are more specific to your gene of interest. Because it's only semi-quantitative, a standard dilution series of known concentration is included on each plate and used for quantification. The standards should be of the same material and sequence as your gene of interest (DNA or RNA) and should be diluted into a range of concentrations that will likely include the concentration in your experimental samples. You also need to be careful about the possibility of degredation of your standards, as the quality of your quantification is entirely dependent on the quality of your standards.
An alternative approach is to quantify a gene of interest relative to some reference gene that is constituatively expressed at the same level regardless of the experimental sample. This method (sometimes called the delta-delta Ct method) eliminates the need for running a standard curve, but requires additional reactions or multiplexing, in addition to identifying a stable reference gene with primers and possibly probes that will work under the same thermocycling conditions as your gene of interest.
A third option is absolute quantification via digital PCR (dPCR). One issue with qPCR in general is that, even when running samples in duplicate or triplicate, it can be hard to confidently resolve differences in quantification smaller than about 3-fold. Enter absolute quantification. dPCR works by dividing up the reaction into tens of thousands of nano-liter sized compartments, such that each compartment may or may not contain an actual copy of your gene of interest. Fluorescence is only used at the end of the reaction to determine whether each compartment has amplified or not (hence digital, each compartment is a 1 or a 0). Quantification is calculated by determining the ratio of positive to negative compartments and comparing to a Poisson distribution for discrete probability distrubutions. It can have much finer resolution than qPCR, supposedly capable of reliably detecting a 1.2-fold difference in concentrations, with the trade-off that it has less dynamic range with reduced confidence in quantification estimates near the top and bottom of that range. Plus the entire system is usually much more expensive at just about every level (equipment, reagents, and consumables). But with most gene expression assays, you really need to ask yourself if a 1.2-fold change in transcript level is even going to be meaningful in your biological system.


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Glycogenolysis & Gluconeogenesis
Is glycogenolysis and Gluconeogenesis is the same in the terms of product formed?
This doubt arrived when I was attempting true & false and the question was
Glucocorticoids stimulate glycogenolysis, lipolysis and proteolysis
The answer given was false because "Glucocorticoids stimulate gluconeogenesis, lipolysis and proteolysis"

Obviously not from the feedback you received. Have you done an Internet search or consulted Wikipedia. Please do that before posting here.

Hello and welcome A learner,
Glycogenolysis is the breakdown of the molecule glycogen into glucose.
Gluconeogenesis is the metabolic process by which organisms produce glucose and other sugars from non-carbohydrate precursors.
These processes arrive at the same product (Glucose).
Glucocorticoids stimulate the process of Gluconeogenesis but not the process of Glycogenolysis.
To elaborate...
Glucocorticoids are steroid hormones that stimulate production of glucose in the liver via Gluconeogenesis. But Glucocorticoids are not involved in the pathway of Glycogenolysis.
Therefore: Glucocorticoids do not stimulate glycogenolysis, lipolysis and proteolysis.
And the answer is false.


text:
Why both forward and reverse primer are added in asymmetric PCR?
If the purpose of Asymmetric PCR is to amplify single targeted strand of dsDNA then instead of adding just one primer for targeted strand why do we add both forward and reverse primer? Upon addition of only one type of primer won't we will get linear amplification of that strand?

The other primer is at least 30 times less. I suppose this is done for amplifying the template to a certain extent. If you have a pure template (i.e. the exact length as the final product) of good enough concentration then the other primer is not required at all.

I'm not 100% sure about it as I haven't done it personally and I couldn't find any material on this topic. So it is just a guess.


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If bacterial plasmid DNA is methylated then how do we digest it using restriction enzyme in cloning experiments?
So, I was reading about how bacteria protects its own DNA by methylation against restriction enzyme. But if the plasmid DNA is also methylated then we can't cut plasmid using restriction enzyme for doing cloning. And if we are isolating this plasmid from Methylase deficient strain so that the plasmid is not methylated, won't it would be digested by the bacterial restriction enzyme. Do we isolate these plasmid from a strain that is also unable to produce restriction enzyme ?


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Sex determination in Drosphila
Ive been taught that its based on genic balancing.
But I recently saw this question that has caused me some doubt.
I thought it would be the 1st option but unfortunately they said it to be the 3rd.
But in the answer key, they mention the same line of that of the 1st option.
Ive only been taught genic balance in a general sense .I solved by finding the ratio of no. of X chrom. to no. of autosomes. It would help if someone could give me some clarity.

could you rotate the image or type the question? Hurts my neck to turn it D:

Do not post questions as images. Have the decency to type them out properly so people can read them, especially those who are partially sighted. This is a disgrace.

I think the first possible answer is wrong because maybe by "set" they mean the total number of autosomes. Where as in the figure below it states that the autosome is only responsible for a repressor(Dpn), and that in normal conditions (in pairs i assume) they product equal amounts for females and males.
If the chromosome 2 was not in a proper pair, then I assume the dosage of the Dpn repressor would be off.
The gene dosage is with the activators produced also, sis-a, and sis-b. So I guess in females they produce twice as much activator for the Sxl protein, which later on allows for the repression of male genes and activation of female genes.

There are certain questions that should not be answered. See Not all questions can or should be answered here. The presentation of this makes it fall into that category. Please help to maintain the standards of this site.


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Why was Achromobacter xerosis removed from the NCBI taxonomy?
The Global Catalogue of Microorganisms lists a bacterium called Achromobacter xerosis which is mentioned in several papers and patents. It once existed in the NCBI taxonomy database, with ID 216898. However, it is no longer there - going to https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=216898 just yields a "No result found" page.
Why was this species removed from the NCBI's taxonomy? I haven't managed to find any documentation on why the NCBI would purge a species from their database, nor can I see any obvious reason to do so.

For whatever it's worth, I queried NCBI support about this and got a reply:

To: info@ncbi.nlm.nih.gov
  Subject: Reason for removal of a species from the taxonomy?
Hi,
I notice that the species Achromobacter xerosis used to be listed in the NCBI taxonomy at https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=216898 but no longer is. I haven't been able to track down any documentation hinting at why a species would ever be removed from the taxonomy. Is there any such documentation that I've missed, and are you able to explain why this species in particular was removed?
Thanks in advance for your time,
  Mark

Reply:

Dear Mark Amery:
  The NCBI Taxonomy database records exist to support data that are in other NCBI databases. A review of the Taxonomy database must have identified that we have no records for which Achromobacter xerosis
  is designated as the organism name.
regards,
  Bonnie L. Maidak, Ph.D.
  NCBI Help Desk
  DHHS/NIH/NLM/NCBI


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Why do autumn leaves on the eastern sides of trees change and fall before the western leaves?
I've noticed that for the autumn leaves in my area (Great Lakes region of United States), if a tree's leaves are changing or falling asymmetrically, they almost always change first on the East-facing side of the tree.
I can't find any explanation for this phenomenon online; but in the spirit of "showing my work", I'll give some hypotheses from this non-biologist. :)

If there is a temperature at which direct sunlight destroys chlorophyll or reduces its effectiveness, there might be pronounced coloring effect on eastern leaves. The air temperature at dawn is usually 5-10 degrees Celsius less than at sunset.
If direct sunlight instead prolongs color change or leaf detachment, it could be that this asymmetry is caused by an increase in cloud cover in the mornings relative to the afternoons.

Any thoughts? I've noticed this in past years, but this year seems really extreme: many trees in the region have lost all of their eastern leaves but have a western side covered in bright orange leaves; they also had orange eastern leaves while the western sides were green, so wind gusts aren't the culprit.

Nice question. Do you have a photo to illustrate this?


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Why are the sympathetic and parasympathetic axons different, in terms of presynaptic and postsynaptic length?
Does the parasympathetic system have a long presynaptic efferent axon because it takes a great distance to reach target organs from the brain stem or sacral region of the spine? Does the sympathetic have a long postsynaptic efferent axon (that reaches the target organ) since the presynaptic neurons are centrally located in the thoracic and lumbar regions of the spine? What purposes do these different axon lengths between the presynaptic and postsynaptic parasympathetic and sympathetic neurons serve? I'm looking for an answer that explains their benefits.

Seems similar to this question (also not answered): https://biology.stackexchange.com/questions/42168 :)

Does anyone know the answer to this question?


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How Does The Presence of Livestock on Land Increase Net Methane Production?
It's a hot topic, and I've just read this article that debunks the claim I'm about to make - But even though I read it, I still don't really understand it. I'm happy to change my opinion if I understand the facts.
Suppose we have a closed system, imagine a pasture in an aquarium. Light goes in, grass grows, dies, decays, is recycled, all that good stuff. I imagine the air going into the aquarium is pretty atmospheric, and the air exiting has been changed depending on the amount of CO2 that is absorbed through photosynthesis, the amount of O2 is absorbed through plant respiration, and the amount of greenhouse gasses produced from decaying plant material in the thatch/soil.
(I think I have that right - my biology education doesn't go past high school level)
Now suppose we add a cow into the mix. If anything, to me, the cow reduces net emissions while it grows because less grass decays, and is instead turned into cow. Once the cow is mature, in this closed system, it's only eating and "processing" the grass that was already part of this natural cycle of growth/decay.
Here's where I think I am possibly going wrong:

Does the cow increase the amount of "decay"? Does eating the grass make it re-grow faster, thus speeding up that natural cycle?
Or, does the cow output different (more harmful) greenhouse gasses than the grass would normally produce through decay?

In short, how does the cow increase emissions? It can only have eaten what has already been grown -  And what has grown is doomed to someday decay and be re-released into the atmosphere anyway. I don't particularly like having contrary opinions, so help me out!

Are you familiar with the phrase "gut microbiome"?

@Cell I am -- Is the bacteria in our gut so different from the bacteria in the soil that would break down the plant material? Do they release different gasses? If so, that's probably the answer I'm looking for

Consider that the methane problem isn't really about cows grazing on land, it's cows in factory feedlots.  After all, a couple of centuries ago North America had a similar biomass (estimated 30-75 million, and they're bigger than domestic cattle) of buffalo grazing, without apparent problems.  Buffalo are similar enough to cows that they can interbreed, producing "beefalo".

@jamesqf I had just looked up bison populations then vs. cattle now, funny that you mention it. I understand the process has been industrialized, but they're still consuming organic compounds, right? We're just moving them elsewhere.

@Aww_Geez: I don't know why buffalo grazing, or FTM open range cattle grazing, should result in different amounts of methane being emitted, or even if it does.  Maybe it's a different diet, feedlot animals eating hay or silage instead of fresh grass.  Or maybe it's just statistical manipulation by anti-meat people.  I just think it's something that seems to have been overlooked, and needs explanation.

Ruminant digestion produces a lot of methane.
Cows are ruminants, and ruminants produce a LOT of methane. Sheep and goats are also ruminants but their are far fewer of them. Ruminants use methanogenic bacteria to breakdown their food, these bacteria, as there name implies release methane as a byproduct.  Ruminants produce a lot more methane than other herbivores becasue of this.
Decaying grass normally produces CO2 as do many native herbivores. Cows like most herbivores only convert a very small amount of the grass they eat into cow. Herbivore digestion is not terribly efficient, not surprising the grass does not what to be easy to digest.
Farming also puts a lot more herbivore mass on a piece of land than it would normally have, further increasing the effect, that is the purpose of farming to get more out of the land than simple hunter/gathering could. This is an issue becasue methane is a FAR more effective greenhouse gas than CO2.
Feeding cattle often involves replacing existing ecosystems which high yield feed crops and this can release a lot of CO2 and/or Methane depending on the original ecosystem just from the change, but it also means that feed is now producing methane instead of CO2 it would be if eat by non-ruminants.
Source
Source 2

I see, I think my error in thought was that "all decomposition will release carbon into the atmosphere, what does it matter if it comes from a cow or a pile of compost?". . . Turns out different methods of decomposition create different gasses, of varying harm.


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Did humans evolve the ability to swim? Or is it just luck that we are able to swim?
Many animals like ducks have evolved features to be able to swim. Even not so aquatic animals like a tiger evolved so that its feet can act as paddles. In humans I don't see any direct feature that has specifically evolved for the purpose of swimming. So is it just luck that we are able to swim and some of our cousins like gorillas are not able to swim? Or did we evolve in some way to be able to swim

I think you have the question backwards.  It'd seem to be more reasonable to ask whether there are animals that CAN'T swim.  I can't think of any offhand: certainly most of those I'm familiar with can.  Some, like dogs, actually enjoy it.

Well, of course, with questions of this sort nobody knows. However before posting you might ask whether there is any reason that the ability to swim has been so advantageous to our ancestors that it has been subject to evolutionary selection. You might also think about the habitat of such ancestors. It is interesting that in fishing communities (e.g. in Scotland) most fishermen had never learned to swim. Why not? Because if your boat flounders in a gale you drown, whether or not you can swim.

@jamesqf oh... I thought there are many animals that can't swim. I know hippos drown in water, but they can maneuver easily and water is their forte, there maybe animals that don't float and may not be able to learn to swim

@David interesting to know. I thought there are some definite traits in humans which show how we evolved to be able to swim, which I don't know, but many people who study these things may know.

@user41965: I don't think there are many.  For just mammals, it seems that the only ones that actually can't swim are giraffes: http://www.bbc.com/earth/story/20170320-the-cruel-experiments-that-revealed-most-mammals-can-swim  (I suppose you could argue about whether what hippos do in the water actually counts as swimming.)  The difference seems to be that with most mammals, swimming is pretty much instinctive, while with humans & other great apes, it has to be learned - even if, as in my case, the learning was a matter of the bigger kids pushing you into the deep part of the creek :-)

The Jane Goodall website says: "You’ll rarely see a chimp paddling about in the water as they don’t like to swim. Their low body fat ratio causes them to sink and their top heavy body composition makes it difficult for them to keep their heads above water.  However, some chimpanzees do enjoy a good splash around in shallow water."
Some monkeys have been taught to swim, see this video: https://www.youtube.com/watch?v=q2vekGuV8xA
So, the answer is, it's just luck that humans are quite good swimmers compared to other monkeys, because strong bipedal running and legs also gives humans good stability in water. After us the best swimmer is the proboscis monkey. Many other monkeys do play in water and swim: https://www.youtube.com/watch?v=sn-M1kCvzLg
There are many studies that theorize that modern humans have evolved beside seas and rivers.
Here's a massive infographin on the subject: https://visual.ly/community/Infographics/science/possible-aquatic-adaptations-human
Humans crossed the open ocean at least 50,000 years ago, i.e. to colonize Australia, the oldest evidence of fishing is currently from East Timor, 42,000 year old fishing hooks: https://www.livescience.com/17186-oldest-fish-hooks-early-humans.html#:~:text=Their%20discovery%20uncovered%20fishing%20hooks,%2C%22%20O'Connor%20said.

I was also thinking the same, the fat and size of our lungs can be attributed to our energy needs.  Which are probably not meant for swimming, but I'm guessing they play a role. I've heard theories about the reason we lost body hair may be due to living in seas. Of course water is the source of life and it makes sense that humanity thrives near water bodies. But I don't see any features in humans (that I know of) that have evolved to make swimming easier. But such an important skill like "swimming" just being our luck and not evolution.. I mean, what're the odds, Idk...

I put some other evidence of monkeys swimming, It's interesting the difference between baboons who swim and run very well like dogs, and big forest apes like chimps which swim completely differently.

@com.prehensible however the way each kind of ape/monkey is swimming, I think the main reason we're able to swim (as long as we don't have paddles) is because we're able to float reasonably well and we can put our nose out of the water while maintaining the position. Now that I think of it, and I've searched and found this link news.com/biology/science-chimpanzees-orangutans-swim- maybe many animals can swim, but maybe they just don't learn to do it


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Nutrient agar as the medium for antibiotic susceptibility testing
I couldn't get Mueller Hinton agar to conduct antibiotic susceptibility testing. I'm thinking of just choosing nutrient agar as the growth medium for the bacteria Staphylococcus epidermidis. Will there be any major issue in choosing nutrient agar as the growth medium?
Thanks in advance

The standard breakpoints used in clinical susceptibility testing (Kirby-Bauer/disc diffusion assay) are considered reliable when every part of the testing method is standardized. If you change any part of that standardized method without properly validating those changes, it may or may not affect the outcomes and there would be no way of knowing without some sort of comparison study for validation.
Difficulty obtaining the proper media would seem common enough that this exact problem has been studied. This study did a head-to-head comparison of nutrient agar (NA) and Mueller-Hinton agar (MHA) for susceptibility testing on 149 clinical isolates along with a few QC reference strains. They found that NA agar did not produce acceptable results for the QC strains according to the relevant Clinical & Laboratory Standards Institute (CLSI) guidelines. Use of NA also resulted in many errant determinations among their clinical isolates (including many isolates of Staphylococcus aureus).
Given the error rates in this study, I would say that you should not rely on susceptibility testing results using nutrient agar in any sort of clinical context.
Reference:
Nassar, M.S.M., Hazzah, W.A. & Bakr, W.M.K. Evaluation of antibiotic susceptibility test results: how guilty a laboratory could be?. J. Egypt. Public. Health. Assoc. 94, 4 (2019). https://doi.org/10.1186/s42506-018-0006-1


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Are there any animals whose genome haven't been sequenced yet?
I referred to a few websites and it seems like almost every animal's genome has been sequenced. However, are there any animals that haven't yet been sequenced? If so, can you provide the list here or provide the link to the website which provides that information??

There are 60,000 species of beetles, you really think people have sequenced them all?

@swbarnes2 We're on our way to doing so...

Wikipedia maintains an (incomplete) list of sequenced animal genomes here.
There are a few million living species of animals, we're not that close to sequencing them all, and listing them all doesn't make much sense.
I'd recommend starting from the animals that have been sequenced, and in particular, animals from particular families or smaller taxa, if you'd like more detailed information.

I see there are a lot of animals that we haven't yet sequenced but I mean are there like any animals that are beneficial to humans in some way, hence it's worth sequencing, but it hasn't yet been done? I thought about choosing chimpanzee but it has already been sequenced.

@ZetaFox "Beneficial to humans in some way" is a pretty broad criterion that could likely include every animal there is with some justification.

@ZetaFox A lot of focus is actually on those that are harmful to humans, which is why you'll find thousands upon thousands of sequenced strains for many pathogens.

@jakebeal I kind of read OPs comment as "beneficial to sequence" but that's a good point to emphasize in case I was reading too much into it.


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How much percent of image does our eyes focus at any instant?
I learned in highschool that even thought we have a wide view, we only observe a tiny fraction of that view through our eyes. So at any instant we are not really looking at all the objects infront of us, this is why we need to individually focus at each object at a time.
Question: What is the % of view that is in focus at any instant of time compared to the full view we observe thorough our eyes?

What you learned in high school isn't exactly true (or is misremembered). Human eyes get visual input across about 120 degrees of visual angle, and some herbivore mammals see near 360 degrees total between their two eyes.
However, the resolution is not constant. The fovea is an area of high-density receptors in the retina. When you look at something specific, you are directing light from that area of the visual field to the fovea. The fovea is limited to about 2 degrees of visual angle.
Additionally, your attention is often limited to a small section of the visual field. When viewing a scene, your eyes will naturally make saccades to bring various points into high acuity vision to get a good sense of the entire scene, but you are still seeing all the surrounding area, even if you aren't paying much attention to it. Importantly, you are still sensitive to surprising stimuli (especially those that are high-contrast or moving) in those areas that might cause you to redirect your attention, otherwise you would be very easy to sneak up on.

yes its the 2 degrees of visual angle that i remember now. So still a small fraction around 1/60th area of the whole view is in focus at any one time. You mentioned that the "attention" is limited to small section of visual field, can we say that its limited to 1/60th of the visual field? So to say some entity is in attention is in the fovea as we are focusing on it?

@gfdsal It's roughly spherical so more like 2^2/120^2. For attention it's a bit complicated and there are no sharp boundaries, but you could say it's on a similar spatial scale.

note the rest of the eye is still used but it is more to detect change (usually movement) , once something changes your attention and focus move to that point. you focus is constantly moving around to what you think is important, so although you only get a god image of about 2% your brain can reconstruct a much larger image.

To be precise, I think the answer (and the question) are mixing focus and resolution. For example, a myopic eye wouldn't focus the image, regardless of the fovea resolution. Focus would depend on the quality of the lens, not the sensor.

@jinawee Did you notice I didn't use the word focus at all? OP used that word, but it is clear from context that they are referring to the target of gaze (which is also what a properly working eye focuses on), rather than the specific processes that go on in focusing.


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Movement of few ion during changes in membrane potential
My question is very simple: why is it sufficient for a very few ions (such as 1 in 100000 K+) to move across the membrane to generate a remarkable variation in the membrane potential (like a change of 100mV) ??
I took the examples from my university textbook, which, though, doesn't explain the reason behind this statement. Is it because during this event the permeability changes so dramatically that the number of ions doesn't have to be so big?
Can someone help me? Thank you!

See this answer: essentially, it's because when you are talking about the charge from moving ions across a membrane, 100mV is actually not that remarkable, from an electrical standpoint. You only need 1 microcoulomb of charge per sq cm of membrane to change the membrane potential by 1 VOLT and a cell has a lot less membrane than that.


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Biological Neural Network Training for Babies
I am concerned by the fact that babies cant walk because the muscles in their limbs arent developed and tuned to give directional control, it takes years before babies gain mobility and dexterity. So technically the neural nets in the motor cortex requires years of training before that capability is achieved.
However, when the babies are born they dont need training for ocular muscles for directional control of their eyeballs (which is quite computationally challenging problem due to high degree of freedom compared to hinge movement) . Do biological neural network for occular muscles come pre-trained while the neural network for limb muscles come untrained by birth?

well nice observation, are you saying that rotational or ball-joint mechanisms are hard to tune then hinge mechanisms in the limb? Do you have reference for this?

@JhonnyS yes, a hinge mechanism gives rise to 2 degrees of freedom (you move in planner axis mainly), while eyeballs move with 3 degrees of freedom (non-planner) so the optimization space is bigger.

That is not my understanding of how eyes develop. Would you care to cite that?

I think you need to get over this computer science idea of "pretrained neural networks" and "computational intensity", because what is going on is far, far more complex, and the brain is not a CPU. There are no "degrees of freedom" issues when comparing the movement of an eyeball with that of an elbow, it's a matter of controlling the muscles that are attached.

@MattDMo I think he is right, and there is no contradiction to your view. The computer science side is far, far more complex, if it is needed, and with a neural network, the CPU is possibly not used except for simple unrelated tasks like handling data. The aspect of degrees of freedom is expressed in the muscles needed.

@gfdsal Movement up/down and left/right of an eye is 2 degrees of freedom, the movement is on a sphere, which has a 2D surface. It is embedded in the 3D space differently, but that is not relevant for the movement.

@MattDMo I do agree with you to some degree but I was not comparing brain with computer CPU, they both solve different computational models, CPU does mainly add/shift/compare while the processing in brain as you said far more complex. My question was agnostic of specifics of any hardware implementation. For any task to be done, in any platform, a computation of that task must be executed and information to execute that task must be present, whether its CPU, human brain or alien tech. So what I was asking that a pre-trained computation model in the from of NN is in place by birth for babies..

@VolkerSiegel Yes i guess its is indeed 2 DOF but that was just to give a hint of complexity of the control problem.

Biological neurons function in a very different way, as compared to the simplistic artificial neural networks of machine learning. For example, see how real neurons work and how they connect with each other. The types of neurons themselves are very varied:  "...neurons to take specialized forms such as unipolar,bipolar,  multipolar,  anaxonic,  pseudounipolar,  basket  cells, purkinje cells, Lugaro cells, spindle cells and more.".
As for the eyes, light passes through a large network of neurons before hitting the rod and cone cells. It's the opposite for the octopus retina. Animal babies are able to learn to walk much quicker than human babies. Also, have a look at videos of how blind children learn to walk.
So essentially, there's a lot lot lot more going on in the creation and working of the human body than just "neural network training". A really nice paper titled "facts and anomalies" gives perspective into this complexity.
Nobody fully understands how the system of cells and the equilibrium works. It's extremely complex and multi-dimensional. When you look at the complexity inside a single cell and the electron transport chain, you'll notice that there's a heck of a lot of things that are already pre-programmed and designed to make use of the molecular properties of nature to create structures and motors using the equilibrium of chemical properties. When such an equilibrium is created, evolution and adaptation can happen, but only in a very controlled manner. So I do not believe a baby's neural network is getting trained to walk or see. It's pre-trained from millions of years of evolution. The reason it may be taking some time to mature, is probably because the corresponding neurons in the brain are taking some time to get created, grow and find their way in the brain to form the right synapses.

So I guess what you are concluding that in human babies, its the combination of molecular properties and pre-trained neural nets and these pre-trained neural nets that happens due to pre-existing information in DNA which got encoded over time, millions of years of evolution?

@gfdsal: Personally, I do not believe only DNA contains the information. There's a lot more in the cytosol we haven't even discovered. Just have a glance through the "facts and anomalies" paper that I linked to, and you'll see why it's too early for us to make conclusions.

your answer coupled with @MattDMo 's answer made lots of sense. I am accepting this due to references.

I am just curious why did you mention that light passes through a large network of neurons before hitting the rod and cone cells. isnt this other way round, because rods and cones are the main receptors of light which then passes to visual cortex instead of visual cortex passing the information to rods and cones?

@gfdsal: Do a bit of Google searching to see and understand the function of the layers of the retina. I didn't mention anything about the visual cortex, but I have reason to believe that data is transferred from the brain to the retina too. Could you please do plenty of Google searches about the questions you have: https://neuroecology.wordpress.com/2017/03/29/the-retina-receives-signals-from-all-over-the-brain-and-that-is-kind-of-weird/

Alright I will google that. For me its actually quite werid to know that eyes receive the stimulus from brain, but i think it should make sense cause when we dream, we actually see "as now i presume" with eyes, "and not just visual cortex."

Some babies start walking by 12-15 months, so it's not exactly years before they can do it. They can also grasp things with their hands from birth. When first born they still don't have full ocular control, and especially can't focus except on strongly contrasting objects. If you watch a newborn, their eyes are often moving from place to place, even when a parent's face is in view.
As for why they don't have much muscular control, just think about their circumstances – they've spent the previous 9 months in a very cramped uterus, with barely any room to move around and no chance to fully extend their legs when they're in the third trimester and increasing in size quite rapidly. It's not that their muscular control neural networks aren't trained at all, they're just not trained to their full extent yet. The eyes are a bit more trained, because light can penetrate inside the womb, especially at the latest stages of pregnancy when the mother's abdominal skin is stretched tight, and they have plenty of chances to move their eyes around, even if they have nothing to focus on.

But doesnt child need data to train the cornea muscles? Also are you saying the light can penetrate moms belly onto the womb, but do you think its significant? are there any references for this as I am also curious to know.

@JhonnyS yes, light can penetrate skin rather easily. As a simple experiment, stand in front of a mirror in a very dark room, then open your mouth and shine a flashlight into it. You'll see your cheeks light up quite nicely. As far as specific references, I'm not sure - it's in just about every baby book I've read. Sound also penetrates easily, so assuming both parents are living together, the baby already responds to the sound of their father's voice when they're born.

So is the answer that biological neural network in babies come with partially pre-trained networks? So this partial pre-training happens in the womb as you suggested or its due to genetics (half from mother and half from father)?

@gfdsal Both. There is plenty of information and organization in our brains that is influenced by DNA, and plenty that comes from experience. It's not either/or. Biology is extremely complex, as the answer by Julia points out. We don't understand all the interactions that take place, or how exactly the brain develops.

Walking is about more than having strong legs moving in a hinge motion.  It's about coordinating all your leg muscles and your torso muscles.  Babies have instincts which tell them how to coordinate all the muscle movements for suckling, but they still have to practice all the muscle movements for eating (and again, while learning to coordinate all the torso muscles for sitting).  Eye movements are far simpler.


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What is the best way to find which domains in a list of InterPro IDs are catalytic?
What is the best way to find which domains in a list of InterPro IDs are catalytic?
(In this case, we are looking at human enzymes and their domains' InterPro IDs.)
Thanks in advance!
Setz

Welcome to SE Biology. Please finish reading the [tour] to find out how this and other SE sites work. Your question may have a better response on our sister site, SE Bioinformatics, but in any case you should give an indication of the steps you have taken yourself to answer any question you posed here. Personally I would have submitted a ticket from the Interpro Help page. Some of these large web facilities have very good support (others less so).

In InterPro you can do a search "by text" and type in "catalytic". It gives you a list of IDs with description and you can download the list.

Thanks for your reply!


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Shrinking size of Y chromosomes
I read on the web that the size of Y chromosomes decreased in earlier period of time and the picture below tells that it is still occurring.
So basically I want to know what caused  this shrinking and if it has stopped now then what caused this break ??

you can find at least the beginnings of the answer on Wikipedia: https://en.wikipedia.org/wiki/Y_chromosome#Degeneration

@Ben Bolker what about the second part ?

Welcome to SE Biology. As a new user, you should finish reading the [tour]. Please do not post text as graphics, which discriminate against people with visual deficiencies and which cannot be indexed. Rewrite it as text.


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Why do babies urinate when they hear "SHHH.." sound?
I have noticed it many times in the region where I live. I don't know if its common World wide. But I think someone else would have noticed it. So why does this happen ?

I have no sense of the tags to be used here . So please someone add it if possible .

This sounds like hearsay; we appreciate questions that are founded on scientific grounds. I would suggest this to be carried over to Reddit or a similar nonscientific forum

I think it's necessary to show evidence (not merely anecdote) for a phenomenon before asking "why" it occurs.

In general, babies do not naturally urinate when hearing that sound.
However, there is a technique of instilling a Pavlovian response in your baby to urinate when hearing that sound.  You start by holding the baby diaper-free, and making the sound when they urinate, so that they make that association between the sound and the sensation of urination.  After lots of reinforcement, you can get the baby to urinate when it hears the sound, so babies are potty-trained earlier than they otherwise would be.
It's part of a process called "elimination communication"
https://en.wikipedia.org/wiki/Elimination_communication
It's less common in Western countries, probably because most people prefer to, and have the means to either buy lots of disposable diapers, or have the means to easily wash their cloth ones over and over again.

I always thought that it is the onomatopoeia for the sound of peeing, invoking the same response as the sound of running water.


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Are the IRV and ERV equal in amount?
I am reading about Inspiratory Reserve Volume and Expiratory Reserve Volume in my textbook. So my general question is aren't the two terms show the same amount of air ?
I would like to tell you why I think so. Like IRV tells us about the maximum amount of air we can intake other than normal intake. So this extra amount is what going inside our lungs and I think this is the part which comes out in the form of ERV .
So shouldn't the total capacity of lungs be equal to (Tidal volume + IRV + Reserved Volume) only ? Why do we need to include the term ERV in the above equation ?

You're misunderstanding a bit. Here are some definitions from Wikipedia, where I added some bold for emphasis:

Expiratory reserve volume: the maximal volume of air that can be
exhaled from the end-expiratory position

Inspiratory reserve volume: the maximal volume that can be inhaled
from the end-inspiratory level

In plain terms, ERV is how much you can still breathe out after you've breathed out all you normally would. You can try it out yourself: when you're finished breathing out and ready to start breathing in, try to blow out a bit, you'll find there is still air there. You don't need to breathe in extra to be able to breathe out this extra.
Similarly, IRV is how much you can still breathe in after you've breathed in all you normally would.
If you were to do a "fullest possible breath" that would include inspiring as much extra as possible, plus the normal breath volume, plus exhaling the last little bit you can:
IRV + Tidal Volume + ERV
There's still a little bit of residual air left over (RV), though, so:
IRV + Tidal Volume + ERV + RV
gives you the total capacity.


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Is this a deathstalker?
I caught a scorpion in my house and wondering if it is a deathstalker? This was caught in Central Asia Northern Tajikistan.

No, it is not a "Deathstalker". The members of the Genus Leiurus are what are commonly referred to as the "Deathstalkers". I do not like using vernacular or common names as they can be too broad in iverlap for multiple species and so to avoid confusion and for clarity utilize Genus and where can be determined species and subspecies. The scorpion you found appears to be a member of the Genus Mesobuthus. While superficially similiar to Leiurus sp., the pedipalps in Mesobuthus are shorter and more bulbous...among several other features.
In 2018 there was a good paper on Mesobuthids in that region. A quick google scholar search should provide you sites for the paper to be viewed at.

Revision of the Mesobuthus caucasicus Complex from Central Asia, with Descriptions of Six New Species (Scorpiones: Buthidae)

I am not that familiar with types or some terminologies you specified in your answer. Is it a deathstalker?

@Dilshod No.  Deathstalkers are members of the Leiurus genus (as RCampbell says), which is a different genus from Mesobuthus

Dilshod, sorry for any confusion. I shy away from use of common names as many times they are apied to multiple species or multiple Genera. I posted with the Genus of the scorpion you found so you could further investigate avenues of identification for Mesobuthids of your region.

@RCampbell, your answer would be improved by editing the question to include the useful information in these comments.  @Punintended seems to provide a good direct answer, so maybe add something like thisNo. Deathstalkers are members of the Leiurus genus. I shy away from using common names as many times they are applied to multiple species or multiple Genera.


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Why doesn't repeated Mantaux testing for Mycobacterium tuberculosis cause an immune response?
I have never had TB but have had multiple TB tests for work. All negative. If you are introducing TB antigen with each test, why isn't a memory of that formed by the adaptive immune system?

It's an interesting question; I've had PPDs yearly for decades. May I ask what you found when you tried to answer this question with a search? Please edit your findings into you question and refine your question accordingly. Thanks!

Some antigens are poorly immunugenic i.e. they do not cause appreciable T cell activation and memory cell formation.
Such antigens require something called as an 'adjuvant' to trigger an appropriate immune response. This is the principle for many vaccines like DPT in which the pertussis  component acts as an adjuvant for diphtheria and tetanus toxoids and results in appropriate T cell stimulation and consequent development of immunity to these pathogens.
With this in mind let's come to your question. I would like to cite a research that explored a similar question-
Tuberculin skin test and interferon gamma release assay false positive
EST-6 and CFP-10 are two of the antigens administered in Montoux test(there are others also which are a part of the 'mixture' injected ID and may actually induce T cell response but we will focus on these two for the discussion)
Turns out these are weakly immunogenic and cannot trigger an immune response in a previously unexposed person. When infection by M.tuberculosis happens the other components of bacteria like lipopolysaccharide layer act as adjuvant and trigger T cell response to these antigens. Hence, interferon gamma release essay is positve in only those who have been exposed to the 'whole' bacillus and not merely these 2 antigens in a montoux test.
Montoux test is unlikely to become positive by repeat administration as adaptive immunity is not stimulated so no memory for the next encounter is present. However you are not completely off the mark as there is a small chance that these antigens might trigger an immune response and sensitise the person as they do have  some immunogenicity after all.
Due to to its propensity for false negatives and false positives for various reasons it is not preferred anymore and interferon gamma release assay is the gold standard to detect latent TB nowadays.


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Why do Pelicans seem to disappear when circling high in the sky on a sunny day
When I watch Pelicans circling high in the sky on a sunny day, at a certain point in that circle, they disappear from view, then reappear again further along in that circle.
Is it something to do with the angle of the sun reflecting off the feathers?


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Neutral genetic mutations in eukaryotic cells
Why are most mutations in eukaryotic cells neutral? i.e. have no effect on the phenotype.

Your premise that most mutations in eukaryotic cells are neutral is dependent on where in the genome the mutations occur. Most of the genome of eukaryotes is non-coding, so mutations are frequently neutral unless they occur in some signaling region. In protein coding genes, all mutations in 2nd codon positions, and about half of the mutations in 3rd and 1st codon positions change the amino acid, and this is most often deleterious. It is informative to distinguish between mutations and substitutions. Many mutations are never observed because they are lethal. Substitutions are mutations that have survived the filter of selection long enough to be observed. Lethal mutations are never observed because they kill the embryo before it is born. And seriously deleterious mutations are removed from the population quickly as well. So selection acts to favor the observation of neutral substitutions, but most mutations are deleterious.


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Why do certain ferns have roughened spore surface?
Ferns such as Anemia phyllitidis, Blotiella lindeniana, Ctenitis hirta, Cystopterix fragilis, Hemionitis palmata and many others have roughened splity spore surface.
I ask, why is it evolutionary so? Does it have something to do with Equisetales spores, which has long derivates to join up together to spread more effectively? Or more like a convergention with polen of Asteraceae, which is morphologically adapted to zoogamy?


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How to learn and memorize animals classification to get an intuition about them?
I would like to have a good intuition on how close is what animal to which one and how large each group is by number of species and population. I was wondering if there is a good website with good demographics and graphs that could help me memorize it because it's really so hard to make up the tree myself from wikipedia pages!

There is a very good website and application for that. It's called Onezoom tree of life explorer which I believe is for London imperial collage.

OneZoom won't be of much help for sometimes to get a broad vision of the most considered branches of the tree of life. It is too detail for such purpose.

I'm not choosing this answer so as to gain more attention in hope of getting some better alternatives. If I don't get anything better in a few days I will accept it.

Another alternative is the Tree of Life web project, which includes species richness information in the lower levels of the tree and allows reasonably easy navigation of subtrees. You can find the animal portal here.
EDIT -- another alternative, which is in active development, is this integration of Wikipedia and the Open Tree of Life Hyperbolic Tree.

It is very good! but the problem is that it is very slow! with onezoom it's like a map but with this you have to load the page again each time you navigate which becomes frustrating.

@ladybug you may find that open Tree of Life has a smoother browsing interface. Not sure about number of taxa, though.


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How do I interpret SNP nomenclature?
I am combing through my 23 & me raw data and I am a little confused on SNP terminology. I am using NCBI's genome browser and SNP database. As an example we can all follow here is a link to a CYP1A1 SNP https://www.ncbi.nlm.nih.gov/snp/rs28399430. When you open this link you will see alleles listed as G>C. Which one of these is the reference genome and which is the pathogenic allele? Is the relationship always constant (like in x>y, x is always the reference and y is the substitution). If you scroll down to the genome browser view, there also doesn't appear to be any way to tell + vs - sense strand (ie making it difficult to tell G for C mutations or vice versa). I would just assume its the top strand? The ultimate goal here is for me to look through 23&me and compare my SNP genotype to the reference genome and see if my genotype exhibits pathogenic SNPs in certain genes.

"Which one of these is the reference genome and which is the pathogenic
allele?" How have you concluded that the less common, non-reference allele is pathogenic? I don't see any clinical data for that

For specific examples I’m looking at it’s the case. Not globally- should have made my self clear sorry

Quick answer is yeah, the G is the "reference allele" as you put it.  The greater than symbol is acting as an arrow, ie, G goes to C, that is, G is replaced with C.
Actually you get a pretty clear indication of that if you look down a line it two where it mentions the frequency:

C=0.000419 (104/247982, GnomAD_exome)
  C=0.000494 (62/125568, TOPMED)
  C=0.000538 (62/115296, ExAC)

The C frequency is way too low to be the "normal" allele.  It's rather the substitution which results in a missense variant. You can see more specific stats by clicking on the frequency button.  In this case they basically just say that in all studied populations the G variant is by far the most common.


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Do plasma B cells express the BCR or only produce soluble antibodies?
Is the B cell receptor still expressed on a B cell once it has begun to produce soluble antibodies? Is there a gene change that prevents the membrane-bound form from being produced anymore?

B cells can secrete antibody before they are terminally differentiated into plasma cells, so there is a phase during which both membrane-bound and secretory antibodies can be produced by the same cell:

When a naïve or memory B cell is activated by antigen (with the aid of a helper T cell), it proliferates and differentiates into an antibody-secreting effector cell. Such cells make and secrete large amounts of soluble (rather than membrane-bound) antibody, which has the same unique antigen-binding site as the cell-surface antibody that served earlier as the antigen receptor (Figure 24-17). Effector B cells can begin secreting antibody while they are still small lymphocytes, but the end stage of their maturation pathway is a large plasma cell

--Molecular Biology of the Cell. 4th edition.
Plasma cells, generally speaking, have little or no surface immunoglobulin, but it's been claimed that some subsets of plasma cells do have surface Ig:

Surprisingly, although IgG PCs downregulated surface IgG expression, IgA and IgM PCs expressed their respective isotype both intracellularly and on the plasma membrane (Figure 1A, lower panel). Importantly, concordant Ig’s were also detected on the plasma membrane of IgA and IgM, but not IgG, PCs isolated from BM or colon LP indicating that this property is a characteristic of PCs present in their physiological niches

--A functional BCR in human IgA and IgM plasma cells

Once B cell starts secreting soluble antibodies, it is no longer a B cell, it is called a plasma cell hence normal B cells do not secrete soluble antibodies before becoming plasma cells. It is the BCR that is secreted. B cells can either differentiate into memory or plasma cells.  Plasma cells produce soluble antibody molecules closely modeled after the receptors of the precursor B cell. The plasma cell continuously produces soluble antibodies.
I hope this helps since I did not directly answer your questions because they were based on inaccurate information/bases. Please let me know if any other questions based on the information I provided

Welcome to Biology.SE! Your answer sounds reasonable, but it is much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support non-specialists in immunology will have difficulty in verifying your claims. ——— That you for taking the [tour], however you may also benefit from consulting the help pages for additional advice on [Answer] effectively on this site and then edit your answer accordingly. Thanks!


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How accurate are Illumina microarray chips for genotyping?
What is the error rate for these machines in genotyping (like for 23&me)? What is the chance of a false positive or false negative?

23andme uses DNA microarrays ("chips") to perform genotyping. These methods only assay a set of previously known single nucleotide variants, so the probability of missing some specific variant (false negative) is high if that variant is not specifically assayed. It is not quite 100% as frequently known variants missing from the chip are closely associated with a variant that is on the chip, so you can sometimes impute missing data.
Sequencing-based methods will in theory pick up unanticipated variants, but they have their own foibles.
Generally both methods are quite good at single nucleotide variants (SNVs) but are bad to only ok at other kinds of variants. See for example (this paper (chosen somewhat at random, there are many similar papers) to see what the state of the art is for sequencing-based non-SNV calls.
Getting back to chips, these themselves depend somewhat on what version of the genotyping chip is used. For specific information on different versions of 23andme chips, I recommend this blog. For tech specs on the most recent Illumina chip used by 23andme, you can see their product sheet, and specifically Table 5. Their data claims that call rate among targeted variants is >99%, and among those the reproducibility is >99.9%. However things can be reproducibly wrong, so that's not exactly false positive that you requested.
Though it's somewhat old, this paper will give you a sense of both technologies in terms of variant ascertainment, claiming 89% sensitivity and 99.6% specificity (for European genotypes only) for either low coverage sequencing or a then-current chip.
To learn more about how these stats work for chips, specifically for false positives, this video may help.
Hope that helps.

Thank you for the thoughtful response. Am I correct in saying that since what they refer to as the "call rate" is >99.5%, that out of 650,000 SNPs 32,500 are erroneous?! That seems ridiculously high especially if those SNPs are for disease variant alleles

Hi Joe, I am understanding "call rate" to mean the rate at which the chip provides enough information for the chip-reading software to be confident enough to give a genotype in the first place. To state it differently, <0.5% of the SNP data will be missing. So not a false positive, but maybe a false negative. Also, SNPs are usually present in triplicate/quadruplicate on a chip, so there is backup for failures. For serious disease though, a chip is not a great detection tool for this reason, I believe chips are generally not used medically (?). Mostly for research cause they're quite cheap.


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What is the purpose of getting a rabies vaccine after exposure?
After exposure to the virus, it is already inside you and your immune system will start to recognize it. Is the vaccine then just a way to kickstart this process so the body can fight off the infection sooner? Is it just a way to introduce much more antigen to the system than would be present only a few hours post exposure from actual virus replication? Or is the boost coming from adjuvants?

Rabies virus enters the body, typically from a bite, and then enters nerves which it follows up to the brain. An immune response to a first exposure of a pathogen generally takes many days, perhaps weeks, to develop to the point where it's protective. This is often even slower when the pathogen is in nerves, which are relatively sheltered from the immune system, and when there's only a small amount of virus present.
After rabies exposure, people are given two treatments: They're given  rabies immune globulin, which contains pre-formed antibodies against rabies, and they're also given the vaccine.
The rabies immune globulin is the most important of these. It provides immediate protection, beginning within minutes of injection. If the virus has not yet entered the nerve cell (which often takes quite a while) then this globulin will bind to and inactivate all, or almost all, of the virus.
Giving the vaccine as well is an added precaution. It will give a faster, probably much faster, response than would the natural virus. There may be only a few rabies viruses present -- it only takes one! -- and of course the natural virus is doing everything in its power to avoid making a strong immune response, whereas the vaccine is the opposite. It has large amounts of antigen, and it's optimized for making a strong immune response. (Rabies vaccine post-exposure is boosted on days 3, 7, and 14 after the first dose. That's an extremely aggressive vaccination procedure that you don't see with any routine treatments.) The vaccine might drive a protective immune response within a few days, while the natural virus might take a month, or never.
If the rabies immune globulin doesn't catch all the virus, or if it temporarily blocks it but then some escapes -- then the vaccine-induced immune response might protect them.

CDC page on post-exposure vaccination
CDC page on post-exposure globulin


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How to remove protein contamination in plasmid isolation.
I have already tried phenol chloroform extraction, isopropanol precipitation, did not work. It is giving high 280 reading.

Can you please give some more details on your protocols and probably also show some spectrum?

I used Resuspension(mixed with RNase) buffer,then vortexed and added lysis buffer,shaking and then neutralization buffer and centrifuged. Took the supernatant,added 100%ethanol and incubated for 1hour,centrifuged,took the pellet(huge pellet came,must be because of protein), 70% ethanol wash ,dried and resuspended in TE buffer.

i also did phenol chloroform step next time after collecting the Supernatant after neutralization, protein layer did not come much.


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Do ants know the direct (approximately shortest) path to their nest from the food morsel?
I've been studying a bit on the foraging habits of ants, and one of the things I'm not clear on is whether ants know the shortest path from the food that they find to their nest. I understand that ants can leave different types of pheromones$^{[1,2]}$, they can change their behavior based on those trails, and those trails are often volatile. What I'd like to know is how do ants find their nest once they find a food morsel. In one of the papers,$^{[3]}$ it was shown that ants change their foraging strategy based on the number of encounters they have: they follow a straighter path when the ant density in an area is low, while they follow a more tortuous path if the ant density is high.
Considering a lower ant density, an ant will travel pretty far from the nest in search for food in a path that is not always straightforward. Assuming that the pheromone trails it leaves behind do not evaporate by the time it finds the food, will the ant travel back on the same path laid down by its pheromone trail, or will it actively find a more direct path towards its nest? I might also be missing something in the sense that ants always know where their nest lies when they are foraging, and thus can find the shortest path whenever they find any food. If so, any work reflecting such research would be of great help.
References:

Dussutour, A., Nicolis, S. C., Shephard, G., Beekman, M., & Sumpter, D. J. (2009). The role of multiple pheromones in food recruitment by ants. Journal of Experimental Biology, 212(15), 2337-2348.

von Thienen, W., Metzler, D., & Witte, V. (2016). How memory and motivation modulate the responses to trail pheromones in three ant species. Behavioral ecology and sociobiology, 70(3), 393-407.

Adler, F. R., & Gordon, D. M. (1992). Information collection and spread by networks of patrolling ants. The American Naturalist, 140(3), 373-400.

Terms that may help you research are dead reckoning or path integration. From Wikipedia:

In navigation, dead reckoning is the process of calculating one's current position by using a previously determined position, or fix, by using estimations of speed and course over elapsed time. The corresponding term in biology, used to describe the processes by which animals update their estimates of position or heading, is path integration.

There are many animals and certainly some species of ants that use dead reckoning/path integration for navigation. Here are some papers about the Cataglyphis genus by one scientist and some colleagues:
Wehner, R., & Räber, F. (1979). Visual spatial memory in desert ants, Cataglyphis bicolor (Hymenoptera: Formicidae). Experientia, 35(12), 1569-1571.
Wehner, R., & Wehner, S. (1986). Path integration in desert ants. Approaching a long-standing puzzle in insect navigation. Monitore Zoologico Italiano-Italian Journal of Zoology, 20(3), 309-331.
Müller, M., & Wehner, R. (1994). The hidden spiral: systematic search and path integration in desert ants, Cataglyphis fortis. Journal of Comparative Physiology A, 175(5), 525-530.
Collett, M., Collett, T. S., Chameron, S., & Wehner, R. (2003). Do familiar landmarks reset the global path integration system of desert ants?. Journal of experimental biology, 206(5), 877-882.
The last one on the list is particularly relevant because it seems to show that the ants are not using landmarks as markers of position, because moving landmarks doesn't alter their paths.
My intuition is that the extent of path integration will depend on the environment. Species living in a fairly "flat" terrain can gain a lot from knowing the direction towards their home. In a tree canopy, however, the direction "home" doesn't matter a whole lot if your path is constrained by paths down foliage, etc.
Therefore it's unlikely to be able to make any general statement about ants as a whole group, and better to investigate individual genera/species.
However, the Cataglyphis genus from the papers above live in a desert, and their dead reckoning abilities seem to be the ones most studied (there are many many more papers than the ones I pasted here, try searching Google Scholar for "path integration" ant or "path integration" Cataglyphis).


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Exploring speed of ants
I'm working on developing a model of ant foraging. To do this, I have simulated food morsels distributed randomly within an area, with the minimum distance between morsels being variable. I'm trying to get a good idea of the scale at which I should define the distances. This has to depend on ant walking speed and their usual foraging distance.
I'm not very species-specific in my approach. One study (1) shows a survey of foraging distance for different species. They found that most of the species had a maximal foraging distance of less than 1m. Some species did go upwards of 10m. I presume this distance would increase with the presence of trails, but to only focus on finding food by exploring, I can keep the distance between food morsels to be 2m-3m.
Now, I also want to figure out the time that it would take an ant to start from the nest and reach the food given its distance. This is where I'm stuck. I wasn't able to find any survey or study on walking speeds of different ant species. I need an approximate 'exploring speed' of ants, which is just time taken to reach a morsel after leaving the nest. Are there any references I could use to estimate this value for my model?
References:

Eguchi, K., Bui, T. V., & Yamane, S. (2004). A preliminary study on foraging distance and nesting sites of ants in Indo-Chinese lowland vegetation. Sociobiology, 43(3), 445-457.

I don't think it's reasonable to try to do this in a species-independent manner, since there is so much difference between ant species. Leaf-cutter ants, for example, will build trails to forage 200 meters away from their nests. Likewise, ants vary by two orders of magnitude in size and the walking speed of an ant will vary accordingly as well. Finally, I don't think that you can reasonably exclude trail-building from your simulation, since that's a key ingredient of foraging.
Bottom line: pick a species to model and look for information on its specific mobility.


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Effect of cold showers after intense training
What is the effect of cold showers after very intense training (body fully covered in sweat, high pulse, increased body temperature)?
I'm especially interested in how it affects perspiration.

I haven't done a full case-control study on this but I'm pretty confident one will stop sweating a few seconds after entering a cold shower ; ) What do you mean  exactly?

I assume, because the pores close, but after the shower the body would continue sweating, at least if the temperature is still too high, I guess? Also are there any health issues involved in this delayed perspiration?

A shower is very good at transferring/absorbing heat, if anything your body temperature will cool down significantly faster in a cold shower then by sweating alone. The recommendation of cold showers/cooling post exercise has to do with reducing inflammation in the muscles.

Taking cold showers(10-15 ℃) after training or workout have many benefits:

It helps in lowering the damaged tissues temperature by constricting blood vessels.
Cold helps numb nerve endings which provides instant localised pain relief.
Brings down heart rate and increases circulation.
It minimises inflammation and help you recover faster.
It is more effective in relieving delayed-onset muscle soreness,
which generally occurs one to four days after any physical activity.
It reduces uric acid levels, so it is beneficial for people suffering from gout.
It boosts glutathione levels in the body which is a very beneficial antioxidant.

Those who should avoid cold showers:
1] Those who suffer from heart diseases as constriction of blood vessels can lead to a heart attack.
2] People having high blood pressure, because blood vessels will constrict and can reduce the supply of blood to different organs, especially the brain.
Ice bath:

In sports therapy, an ice bath, or sometimes cold-water immersion or cold therapy, is a training regimen usually following a period of intense exercise in which a substantial part of a human body is immersed in a bath of ice or ice-water for a limited duration. While it is becoming increasingly popular and accepted among athletes in a variety of sports, the method is controversial, with a risk of hypothermia, with the possibility of shock leading to sudden death. Many athletes have used cold water immersion after an intense exercise workout on the belief that it speeds up bodily recovery; however, the internal physical processes are not well understood and remain elusive. Generally research into the health effects of cold water immersion as part of an athletic training regimen is inconclusive, with some studies suggesting a mild benefit such as reducing muscle damage and discomfort and alleviating delayed onset muscle soreness, with other studies suggesting that cold water immersion may slow muscle growth and interfere with an overall training regimen.

[Source 1]
[Source 2]
You also maybe interested in:
[Question 1]
[Question 2]

References:
 - A cold shower maybe more beneficial to your fitness[Dr. Mercola].
 - Cold shower after exercise.
 - Effects of hydrotherapy on various systems of the body(NCBI)
 - The effects of cold water immersion and recovery of inflammation
 - Ice bath (Wikipedia)
 - 8 do's and don't's of Ice bath

Thx for the answer! Could you add some information on the effects of showers below 10-15 ℃? And are there any side effects, because of (possibly temporarily) suppressed perspiration due to closed pores?

Almost all of the claimed benefits you list here are unlikely to be true, even your own reference (http://onlinelibrary.wiley.com/doi/10.1113/JP272881/full) doesn't support your claim about inflamation! A Cochrane review of Ice Baths found only Delayed Onset Muscle Soreness showed any effect, and even here the evidence was weak: http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD008262.pub2/abstract

The claims you make may or may not be in your references, it's hard to tell since you don't link your claims to particular references, but your references are a pretty mixed bag - including a link to a site that credulously discusses Spleen Qi, for example - and the more credible of them are more skeptical.

Dr. Mercola is, at best, highly controversial and, at worst, a dangerous AIDS-denialist and anti-vaccine crank, q.v. https://en.wikipedia.org/wiki/Joseph_Mercola. I do not consider his site "credible".


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Why are the most heat tollerant organisms prokaryotic?
Prokaryotic organisms are able to grow at far higher temperatures than are
eukaryotes.
Archaea are known to group, among some mesophiles, the most extremophiles organisms (es. Pyrococcus furiosus), but also some bacteria can reach quite high-temperature habitats, such as Thermus aquaticus.
Eukaryotes instead are far less tolerant in terms of maximum growth temperature.
Also most of the hyperthermophiles are chemoorganotrophs or chemolithotrophs, being autotrophs (Cyanobacteria) far less heat tolerant.
My question is about the physical or chemical limitations that block eukaryotes from adapt at extreme habitats like prokaryotes do.

Isn't it true that champions of resistance to extreme environments (whether extreme hot, extreme cold, extreme salinity, extreme drought, ...) are often prokaryotes? I feel like it might not be specific to heat alone.

I think so, for what I know Archaea are the champions of resistance to extreme environments sensu lato, but I was concentrating on heat alone to pose a question that can be answered in a concise and specific manner.

The premise, that only Prokaryotes tolerate high temperatures, might not be true. For example, the Pompeii worm can tolerate high temperatures. Since Prokaryotes developed earlier, the diversity might be greater and examples of extremophiles more extended.


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What is the tissue structure of bamboo?
If the xylem and phloem of the bamboo is not in the hollow center than where is it located/situated? cannot get clear cut answers from the above discussions

Was this not answered in : https://biology.stackexchange.com/questions/26123/what-does-the-empty-space-in-the-bamboo-stem-do

What above discussions? If this question has been asked before you cannot duplicate it.