text:
Does the law of independent assortment apply to homologous chromosomes or alleles, or both?
My textbook is giving me two definitions

1st def: "random orientation of homologous chromosomes at the metaphase plate in meiosis 1."
2nd def: "alleles for one gene separate into gametes independently of alleles of any other gene (only if genes are on non-homologs or very far apart on same chromosome)."

It's kind of hard to explain but here are my thoughts on this:
It seems to me that the 1st definition is exclusively taking a look at each pair of homologous chromosomes:  It looks like it is talking about alleles on certain homologs themselves and how there's 50% chance that a gamete will get a paternal and maternal allele of a gene after anaphase I.
And I'm guessing that the 2nd definition is an extension of the first by comparing gene assortment in all the homologous chromosomes:
It looks like it is primarily talking about the genes that are on each pair of homologous chromosome and how they (the genes) separate independently of each other (because they are on different homologs) in addition to the "random orientation of homologous chromosomes".
Can someone please clarify?

Check out these answers to other questions: one two

Possible duplicate of What is 'independent assortment'?


text:
What is meant by "heads" and "tails" in the context of gene orientation?
I have a hard time understanding what this paper is talking about when it says:

We observed maximal cleavage at sites oriented tail-to-tail and separated by -10 bp to +30 bp (Fig. 2d). Finally, adjacent sites on the same DNA strand (head-to-tail orientation) did not show damage by NHEJ

Then it shows a figure/chart that I don't understand. I don't know the head and tail or the gene is, in terms of what it is relative or with respect to.
Any help would be appreciated.
Thanks.

The heads and tails, in this paper, refer to the orientation of sgRNA binding sites. If there are two tandem sites in the same orientation then they are referred to as head-to-tail (end of the first site followed by the beginning of the second site). It is also apparent from the excerpt that you have included in your question.
Head-to-head and tail-to-tail refer to the site pairs that are placed in the opposite strands; the former (H2H) refers to a configuration in which the beginnings of the two sites are closer whereas the latter (T2T) refers to the case where the ends of the two sites are closer.

Regarding your question about the placement of sites within -10 to +30 bp of each other:
I think the point of the paper is that the two cuts by the nickases should be close enough and in the T2T orientation for a maximally disruptive double strand break. If the distance between the single stranded cuts (nicks) is increased then they effectively are just two single strand breaks which are repaired efficiently. The authors also conclude that using two nickases in this fashion produces has lower chances of mistargeting compared to that of a normal Cas9 (that makes double strand cuts).

source: Stack Exchange

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

sort: votes


text:
How do some deep sea creatures lower their metabolism to stay alive for a long time?
I was watching some bio related videos and saw in one that some deep sea creatures  and other organisms purposefully limit their movement to decrease metabolism rates. Do they live longer?
If we apply this same theory to humans, doesn't it mean that exercising less and regulation of diet may help decrease metabolic rates? I know exercise is extremely good for the body but this just got me thinking...

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


text:
Do antimuscarinic drugs increase cAMP or cGMP
Activation of muscarinic receptors M2 and M4 inhibits adenylate cyclase which reduces cAMP levels. It would be expected that antimuscarinics such as ipratropium would increase cAMP levels. However, the pharmacological action of ipratropium is said to be mediated through increased cGMP levels [1]. Why is this the case?
[1] https://www.ncbi.nlm.nih.gov/pubmed/138578

M2 and M4 receptors are Gi-coupled receptors. M3 which is relevant for the effects of ipratropium is Gq coupled. Similar receptors have different effectors and therefore different effects on cAMP/cGMP.


text:
Mechanism of redirected blood
I've read several fitness articles mentioning redirected blood flow to muscles that are in use. However, they never mention how it works. Is it local and specific to the muscles in use? Or, for example, I guess more blood has to flow through the entire arm if I am training my forearms..? So, won't the entire arm benefit to a certain extent?
I did some research and discovered the vascular shunt mechanism through the opening and closing of capillary sphincters. However, I cannot find any resources discussing how local this effect is. So, as an example, how much does blood flow to the arm improve if someone is training their forearm for six months?

I'm voting to close this question as off-topic because this is a biology site not a sports training site.

@David Well  I originally posted this at the physical fitness SE. They apparently felt it belonged here, and it got migrated. So, apparently it's too technical for them and too sports related for you. I clearly need to edit this question to make it belong in one of the SEs.

I think could be on topic, though it should be changed to keep it on-topic here: 1) Your question contains aspects of both acute (immediate) changes during exercise and also chronic (long-term) changes. It would be better if your question focused on one or the other to focus on a specific biological question. We like questions that have some prior research here, too. 2) The background on conditioning/training is a bit problematic, because some people might interpret the question as asking for personal advice.

@BryanKrause Alright, thanks for the feedback! I have now tried editing it to make it on-topic for the biology SE.

A major determiner of blood flow redirection among muscles is increased oxygen demand in the working muscles.
When a muscle works, it uses oxygen, so the partial pressure of oxygen (PO2) in the muscle falls, which signals small arteries (arterioles) to dilate, which results in increased blood flow and hence oxygen and nutrients delivery to the muscle (Skeletal Muscle Circulation, NCBI Bookshelf).

When you exercise your forearm muscles without exercising upper arm muscles, the arterioles in the forearm muscles will dilate but in the upper arm muscles will not. The blood will just flow through the large arteries of the upper arm toward the forearm, but it won't be delivered to the upper arm muscles.
A long-term effect of exercise is the formation of new capillaries in the exercised, but not in other muscles (PubMed, 2008). So, six months of exercising forearm muscles without exercising upper arm muscles will result in better circulation only in the forearm muscles.


text:
What is a "pan-specific" antibody?
I am new to biology. I searched a lot to find an article that explains what "pan-specific" antibody is but I could not find anything substantial that would help me understand what it is.
An example from an article

In this report, we address this long-standing analytical deficiency by
  developing a pan-specific antibody against the pHis modification. We
  show that this antibody can be used to detect protein histidine
  phosphorylation in vitro and in vivo.

Another definition
I appreciate if someone helps me with finding a scientific explanation (article/ book) on what "pan-specific" antibodies are.
Kind Regards,

What does pan-specific antibody mean?

The combining prefix pan- means "all" or "every".
Antibodies are specific because they bind specifically to an epitope ('target') on a molecule. A pan-specific antibody is one that binds specifically to all desired targets, within a defined range.
Here are three correct examples of how the word could be used, to help you understand. Only the first two are relevant for your particular case:

In your case, there is an antibody for the phosphoprotein, the unphosphorylated protein, and both. The antibody that targets both is pan-specific because it binds both ("all", or "every") forms of the protein.
Another possible use for pan-specific is that some antibodies bind to some members of a protein family, but not all, so they are not comprehensive enough. Other time, antibodies bind to all members of a protein family, but bind additional targets, so they are not specific enough. Pan-specific is a great way to describe an antibody (monoclonal) or set of antibodies (polyclonal) that are both specific and comprehensive enough to adsorb an antigen of choice.
An antibody that binds specifically to a protein called pan.

Thanks a lot. Can you please share a link to a website or an article that I can find this sort of explanation there? It's a bit weird that I can't find an explanation about these concepts on a website! I think I'm using the wrong keywords!

It's a Greek prefix and it's commonly used. You won't get a technical definition of it, it's just jargon that you pick up over the years studying science. This goes for other Latin and Greek prefixes, like -epi or -con or -inter or -intra. Now that you know that science takes loanwords from Latin and Greek, I'm sure you'll be better prepared for novel words. For instance, you may be able to tell the difference between epidemic and a pandemic, and that pandemics are much worse.

In the paper quoted in the question the term clearly related to phosphoamino acids, but did not have the meaning suggested in answer 1 of @S_Pr. The paper was from Nat Chem Biol. and entitled:

“A Pan-specific Antibody for Direct Detection of Protein Histidine
  Phosphorylation”

The idea is that the antibody is:
‘pan’ in that it will react with all phospho-histidine residues on proteins, but
‘specific’ in that it will not react with unphosphorylated histidine residues or other phospho-aminoacids e.g. phospho-serine.

Thank you, David. I liked to vote up your answer as it was helpful as well. But, as I'm a new member I can't vote up with reputation less than 15. However, thanks.

@Tooba — No problem. It’s not a big deal and I have plenty of points.


text:
How does the emerson effect produce a higher rate of photosynthesis?
Can anyone explain how the emerson effect works to increase the rate of photosynthesis, and as the original studies were done over 50 years ago, how much research is still done into this area? Or is it well understood now as to not need further work?
I am obviously not a biologist but from what I have been reading, photosystem 2 absorbs light at 680nm due to the primary electron donor p680 and photosystem 1 at 700nm due to p700. The rate of photosynthesis when exposed to light at these 2 wavelengths simultaneously is greater than the sum of the rate of photosynthesis if exposed to these wavelengths separately. Sorry for any mistakes, I am just starting to try to learn about it. I'm interested to find out how this higher rate of photosynthesis occurs when using light in the red and far red end of the spectrum at the same time.

You are expected to show some attempt to answer this on your own, even a brief description of what you know about the emerson effect would be beneficial. You may also want to look up photosystem 1 and photosystem 2.

I have added some more info into the question to show what I think I know so far.


text:
The correlation between a leaf's age and its length in the initial stage of growth
I am building a machine learning algorithm which predicts the age of a leaf before its maturity period based on its measured length or area. I would like to know whether there is a mathematical relation to describe this or a repository of data on this topic.

Your question is very broad. Please narrow it down to a specific issue that can be answered in a few paragraphs. Moreover, we expect you to show some research from your part.


text:
Is it possible for human beings to feed through the nose?
There is a prediction on a futurology site that food can be eaten by inhalation
https://2050.earth/predictions/smell-can-feed-you
Although aerosol foods do exist they are still eaten by the mouth.
Is there any biological evidence that human beings can feed through their noses?

I'm voting to close this question as off-topic because it belongs to SE Worldbuilding.

@David I've come to Worldbuilding to say that this is not a worldbuilding question, as it deals with real human biology, and not fiction.

@AndyD273 — You could have fooled me!

Do you actually mean inhalation, ie that you'd absorb nutrients through your lungs? Because otherwise, the nose is connected to the stomach via the esophagus and you can be fed through that: https://en.wikipedia.org/wiki/Nasogastric_intubation

Certain vitamins, for example, vitamin B12, can be absorbed through the nasal mucosa by simple diffusion.
Many nutrients can be absorbed through the intestinal mucosa only by the help of specific carriers. These carriers are not likely present in nasal mucosa, so the nutrients in question may not be absorbed there.
The other problem, especially with macronutrients (carbs, proteins, fats), is if the surface area of nasal mucosa is big enough to absorb large amounts of macronutrients (carbs, proteins, fats) needed to meet nutritional demands. In one experiment, only 0.1 mg of glucose from a given dose was absorbed through the oral mucosa.
In another experiment, some amino acids were absorbed from oral mucosa.


text:
Spatially Encoded GPCRs?
I'm reading this paper, and I'm already lost in terms of what they mean by GPCR signaling is spatially encoded.

The trafficking of G protein coupled‐receptors (GPCRs) is one of the
  most exciting areas in cell biology because of recent advances
  demonstrating that GPCR signaling is spatially encoded.
   …
  …
  Some GPCRs appear to regulate their own endocytic rate through
  modulation of clathrin‐coated pit (CCP) maturation.12-14 This
  regulation, which can differ between ligands acting at the same GPCR,
  is an additional method by which GPCR signaling can be spatially
  encoded.

How can signaling be spatially encoded?

Looks like they're just using a fancy way of saying that the signaling pathways and outcomes depend on where the GPCR is located in the cell: "GPCRs, acting in a diverse array of physiological systems, can have differential signaling consequences depending on their subcellular localization."

How can (GPCR) signaling be spatially encoded?

Terse explanation: During endocytosis the G protein-coupled receptor can be spatially constrained.
Your paper refers to: "Fulfilling the promise of “biased” G protein-coupled receptor agonism", by Luttrell LM, Maudsley S, and Bohn LM, in Mol Pharmacol. 2015;88(3): 579-588. https://doi.org/10.1124/mol.115.099630.

Abstract: The fact that over 30% of current pharmaceuticals target heptahelical G protein–coupled receptors (GPCRs) attests to their tractability as drug targets. Although GPCR drug development has traditionally focused on conventional agonists and antagonists, the growing appreciation that GPCRs mediate physiologically relevant effects via both G protein and non–G protein effectors has prompted the search for ligands that can "bias" downstream signaling in favor of one or the other process. Biased ligands are novel entities with distinct signaling profiles dictated by ligand structure, and the potential prospect of biased ligands as better drugs has been pleonastically proclaimed. Indeed, preclinical proof-of-concept studies have demonstrated that both G protein and arrestin pathway-selective ligands can promote beneficial effects in vivo while simultaneously antagonizing deleterious ones. But along with opportunity comes added complexity and new challenges for drug discovery. If ligands can be biased, then ligand classification becomes assay dependent, and more nuanced screening approaches are needed to capture ligand efficacy across several dimensions of signaling. Moreover, because the signaling repertoire of biased ligands differs from that of the native agonist, unpredicted responses may arise in vivo as these unbalanced signals propagate.".

A relatively simple explanation is offered in another paper: "Temporal Bias: Time-Encoded Dynamic GPCR Signaling", by Manuel Grundmann and Evi Kostenis DOI: https://doi.org/10.1016/j.tips.2017.09.004:

"The notion that information is not only encoded by the chemistry of the signaling components but also by their spatial and temporal occurrence, brought about the term of ‘spatiotemporal signaling’ $^{[3]}$. Signal transduction can thus be categorized into at least three dimensions, (i) quality (which substances take part), (ii) space (where the event takes place) and (iii) time (when the event takes place). The interplay between these dimensions will hereinafter be designated as ‘dynamic signaling’ or ‘signaling dynamics’. Dynamic signaling is deeply entrenched in GPCR signal transduction as an increasing number of reports provide us with a glimpse into spatiotemporal aspects of receptor function $^{[4, 5, 6, 7, 8, 9, 10]}$.".
[3] Kholodenko B.N. et al. Signalling ballet in space and time. Nat. Rev. Mol. Cell Biol. 2010; 11: 414-426
[4] Irannejad R. Functional selectivity of GPCR-directed drug action through location bias. FASEB J. 2017; 31 (664.2)
[5] Mullershausen F. et al. Persistent signaling induced by FTY720-phosphate is mediated by internalized S1P1 receptors. Nat. Chem. Biol. 2009; 5: 428-434
[6] Irannejad R. et al. Conformational biosensors reveal GPCR signalling from endosomes. Nature. 2013; 495: 534-538
[7] Eichel K. et al. β-Arrestin drives MAP kinase signalling from clathrin-coated structures after GPCR dissociation. Nat. Cell Biol. 2016; 18: 303-310.
[8] Thomsen A.R. et al. GPCR-G protein-β-arrestin super-complex mediates sustained G protein signaling. Cell. 2016; 166: 907-919
[9]  Jean-Alphonse F.G. et al. β2-Adrenergic receptor control of endosomal PTH receptor signaling via Gβγ. Nat. Chem. Biol. 2016; 13: 259-261
[10] Plasma membrane localization of the μ-opioid receptor controls spatiotemporal signaling. Sci. Signal. 2016; 9: ra16

See: "Spatial encoding of GPCR signaling in the nervous system", by Zara Y Weinberg, Stephanie E Crilly and Manojkumar A Puthenveedu, DOI: https://doi.org/10.1016/j.ceb.2018.12.006:

"Several GPCRs, including receptors previously thought to signal primarily from the cell surface, have been recently shown to signal from many intracellular compartments. This raises the idea that signaling by any given receptor is spatially encoded in the cell, with distinct sites of signal origin dictating distinct downstream consequences.".

During endocytosis the G protein-coupled receptor can be spatially constrained.
See: "Spatial resolution of cAMP signaling by soluble adenylyl cyclase", by Giusi Caldieri and Sara Sigismund
DOI: https://doi.org/10.1083/jcb.201606123 which offers a easy to understand image:

Figure 1. Spatial and temporal control of GPCR signaling by ACs. In hippocampal neurons, CRHR1, upon binding to agonist CRH, activates the trimeric G protein complex, composed of α, β, and γ subunits. Stimulatory Gα subunit is released and activates tmAC and cAMP production (Irannejad and von Zastrow, 2014). In parallel, activated GPCR can also induce local Ca$^{2+}$ release that activates sAC, followed by an increase in cAMP levels (Inda et al., 2016). (1) These two sources of cAMP at the PM contribute to the early phase of ERK activation via the effectors protein kinase A (PKA) and EPACs (Inda et al., 2016). Activated GPCRs once released from the G proteins are phosphorylated and recruit β-arrestin (β-ARR) to be internalized via clathrin-coated pits (CCPs; Irannejad and von Zastrow, 2014). (2) At the endosomal station, GPCRs activate sAC to trigger a second wave of cAMP production and to sustain Erk signaling in an EPAC-dependent fashion. sAC activation at the PM and at endosomes requires Ca$^{2+}$ and bicarbonate (not depicted for simplicity; Inda et al., 2016). The signaling cascade leading to Ca$^{2+}$ and bicarbonate release (particularly at the endosomal station) and the exact mechanism of action of sAC are not completely characterized. The different forms of ACs, and the corresponding cAMP gradients generated by them, are depicted in different colors to highlight their different roles. Whether this specificity reflects different isoforms and/or regulation remains to be clarified.

"The work reported by Inda et al. in this issue integrates and expands our emerging knowledge of localized GPCR signaling at the endosomal level. In a previous work, these authors showed that Erk activation by corticotropin-releasing hormone receptor 1 (CRHR1) signaling is biphasic, with an early response originating from the PM and a late response that is endocytosis dependent (Bonfiglio et al., 2013). In their new work, Inda et al. (2016) reinforce these findings, showing that distinct cAMP sources are differentially involved in the two phases of Erk signaling. Whereas tmAC and sAC both contribute to the acute Erk signaling response, sAC is specifically involved in the sustained “endocytic” phase of Erk signaling in hippocampal neuronal cells (Fig. 1).".

Note phase 1 and 2, targeting one phase or another, rather than continuous action, is spatially encoded.

In the paper (same as link 1 in the my original question), the authors state:
"there a multitudes of known GPCR interacting proteins, but only a subset of these have been shown to participate directly in basal GPCR organization"
what does basal GPCR organization even mean?


text:
Evolution versus Creationism
If nature, or any aspects of it, are intelligently designed, how could we tell? How would we be able to test that hypothesis?

Consider this: if a potter makes a pot, does it make sense to search the pot for direct evidence of his/her existence, or would doing so only possibly imply that someone made it? Does lack of finding the potter in this instance mean (s)he doesn't exist? In the same vein, if the Christian God created all the universe and reality that we know, would lack of finding direct evidence for such a God inside that universe mean that God does not exist?? (by the way, we have a lot more universe to explore anyway).

The scientific process could provide evidence supporting the potter's existence, but one could never prove the existence of the potter unless one expanded his/her viewpoint beyond the pot. Similarly, the scientific process could potentially provide evidence supporting God's existence or his resulting created design, but it can never prove that a god does not exist because of the endless possibility for searching. In other words, "science" cannot prove existence (or lack thereof) of a God.

To answer your question: verly likely not. The world and universe is an amazingly complex and beautiful existence, but we have no objective way of demonstrating definitively where it all came from. In science, hypotheses have to be testable and falsifiable, but in your case, we do not know what intelligent design should look like, so we have no truly objective test to perform...

By the way, I think your post will be closed as being primarily opinion based (i.e., potential answers will likely only be based on opinion). You could try to rewrite to avoid having your post closed. Unfortunately, no matter how much you edit, this community typically reacts quite negatively toward religious-slanted posts, so get ready for copious downvoting

lots of natural things are intelligently designed, they are called artifacts or tools and they tend to stick out. If you mean nature a s a whole that's not biology that would be physics.

While we can't disprove design, we can certainly test the hypothesis of INTELLIGENT design, by finding any number of things - the human lower back comes immediately to mind - that no intelligent designer would have designed that way.

Visit Physics.SE. During the 1st 10$^{-43}$ seconds everything was smaller than anything thereafter. All of the universe was compressed smaller than a molecule of DNA. For a considerable period of time after that there were not atoms (from which we are made). It took billions of years for chance to happen, and the earliest form of self-replicating chemicals (RNA) came into existence. Modern science does not praise the ingeniousness of the design, but notes it's flaws; those early chemicals we came from were not life, that came ltr.

I am voting to close because the question ask for testable hypothesis for a fundamentally non-scientific concept.

You would work through the millions of examples of evolution processes and proofs, DNA, morphology, geographical, etc, which show that volcanoes, meteorites, weather, and evolution are all equally based on chaos... are the pebbles rolling around on a beach intelligently arranged individually for a plan or chaos, you decide.

Only someone who believes in intelligent design can answer that question for you and that answer will most likely be unscientific (therefore not fit for this site). The reason is because intelligent design is a claim that is not based on observable reality rather divine revelation so it is impossible test any hypothesis regarding it.
Evolution on the other hand is based on two observable, testable facts: (1) all living things on Earth inherit their traits from their parents and (2) those traits are not always copied and passed on with perfect fidelity. With these two facts we can theorize on what other observable facts lead to the variation in life that we see today i.e. evolution by natural selection.

I have never read any testable hypothesis from the Intelligent Design (ID) community. As such ID is not wrong or right, it is just not testable.
To be fair, ID contains a lot of logical fallacies. Not only does it not offer any testable hypotheses but it often just does not make much sense anyway!

To be fair, Old Earth Creationists are more literate than their "young" group and do offer hypotheses that are "testable" to some degree. As an alternative to whale evolution for example, Dr. Hugh Ross from Reasons to Believe proposes that God iteratively created new species of whales over millions of years. He argues that God did this to lower CO2 levels in the atmosphere so that Earth remained habitable with the increasing brightness of the Sun.

Regarding that hypothesis, it could be tested whether CO2 levels have decreased significantly as whales became larger in size. I can imagine what would happen if the hypothesis was proven or disproven. If a negative correlation was shown, OECs would show it as evidence for good design and thus, God. If it was positive or null, they would shrug off their shoulders and say that they were mistaken in what constitutes good design; not that it's proof against God (which would the logical extension).

Your whale hypothesis is non-sense too. 1) Whales are big but they aren't that numerous. If you combine all krills together you'd get a mas much higher than all whales together. The same would be true for termites, ants, humans and many other things. 2) Also, the mass of whales is so, soooo negligible compared to the quantity of carbon in the world. 3) The hypothesis is not testable as it would it so full of much stronger confounding variables (evolution and demographic changes of other life forms)

As you said, showing a correlation or another would not in anyway prove any intention anyway. If whales were to stuck a lot of carbon, nothing would suggest that someone "created" whales for that purpose.

Actually it turns out that whales are vital for oceanic carbon absorption (scientificamerican.com/article/whales-keep-carbon-out-of-the-atmosphere), mainly because they enrich they "fertilize" the surface with nutrients when they dive and defecate.

But still, that's for our Earth. We can't tell if a world without them would be worse or better, since predicting how ecosystems would develop for millions of years is a virtually impossible task. IDers are way too confident to assert how unlikely our world is as evidence that it is the best possible one.

Yep. Going up to suggest that bananas easiness to eat are evidence of god forgetting what wild bananas looked like before being selected by us (here).

The "banana argument" is truly embarrasing, perhaps only comparable to the "crocoduck". What's interesting to note is that the wild precursor of bananas are full of seeds and not nice to eat. Those sold at the market are triploid mutants of the original plant (le.ac.uk/bl/phh4/openpubs/bananacytogenetics.htm).

What's even more bizarre is that Comfort praised how bananas were designed to "perfectly fit our hand". It would make far more sense to state that it is the human hand which is intelligently designed to grab a wide range of objects of different shapes and sizes. Following his reasoning, we could state that a pebble in the shores of a river is rationally designed because it is smooth, we are able to hold it and we can use it to open up nuts. All while considering erosion a "fairy-tale" and disregarding the entire field of geology.

Saying that almost all animals have eyes could imply there is a common cause. But creationists affirm, I think, humans are the last step, there will be nothing after (implying we will destroy everything ?) ? Or is it humanism ?


text:
Sulforaphane vs. Hyperthermic conditioning (sauna use) which would induce a greater heat shock response in the human body?
I’m curious to know which would induce a greater upregulation of heat shock proteins, consuming sulforaphane or putting the body through heat stress such as using the sauna.
Sulforaphane reference- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2975177/#!po=79.7872
Hyperthermic conditioning reference-
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3418130/
There are many more articles/studies done on these two subjects, these are just 2 references of the many.

Could you please edit your post add the references you are referring to regarding the upregulation of heat shock proteins by sulforaphane? This might not be common knowledge. I addition, the answer to your question might depend on the concentration of sulforaphane and the temperature/humidity/duration of the sauna use.

Do the references added suffice for you?  @Arsak


text:
Can someone help me identify this Brazilian spider?
Does anyone know anything about the identification of this spider? Sorry, but it's the only image I have. It was shot at 2004, January 25th (summer), at 11:27 AM, in Cerrado biome at Minas Gerais state, Brazil. It was walking over a Paepalanthus inflorescence (Eriocaulaceae), probably waiting to prey on its pollinators. A small section of web can be seen raised to the left (where it apparently comes from another inflorescence), touches one of the small flowers, and then it's apparently still connected to the spider, in a pattern that reminds me of Salticidae, though I'm not sure. I think its size is around 1 cm. I doubt a specific identification will be possible, but family, superfamily, subfamily, anything will be fine.

Interesting!  See those long spines on the legs?  Only two groups of spiders (that come to mind, anyway) have that sort of arrangement:
Lynx Spiders (Family Oxyopidae) and Pirate Spiders (Family Mimetidae).
Lynx Spiders are wandering hunters, and the ones I'm familiar with tend to have a body shape more like the familiar Grass Spiders (longish, tear-drop shaped abdomen and hunters cephalothorax - roughly rectangular, and often very blocky at the face.
For instance:
https://bugguide.net/node/view/1965

https://bugguide.net/node/view/1489229/bgimage
So, your spider looks to be a South American Lynx Spider, which unfortunately I'm not at all knowledgeable about.
I'm going to discount Pirate Spiders as a possibility, even with the association there with a bit of web (Pirate Spiders invade other species' webs and kill the occupants), because they're much more 'orb-weaver'-like in their general body shape.  This one is so Lynx Spider-like that I am pretty confident that it is one of those.


text:
What does "crude" mean in this context?
Taken from Ian Freshney's Culture of Animal Cells:

The enzymes used most frequently for tissue disaggregation are
  crude preparations of trypsin, collagenase, elastase, pronase, Dispase, DNase, and hyaluronidase...

What does crude mean in this context?

In this context crude means naturally occurring or unrefined.
Purified trypsin alone, for example, is usually ineffective for tissue dissociation since it shows little selectivity for extracellular proteins.
Source: Worthington Tissue Dissociation Guide


text:
What's the benefit of the average human body temperature?
Why would the body choose a resting temperature of 36.1c to 37.2c? It seems a very inefficient mechanism of survival considering the typical ambient temperatures on Earth. If there is a benefit to needing to continuously do extra work, what is it?

what have you searched so far to answer this?

What's the benefit of the average human body temperature?

It's a balance between preventing infection and not requiring excessive food intake. It is has also been claimed that this is the temperature at which the most essential enzymes are most reactive, without becoming damaged by excess temperature.
References:

"Mammalian Endothermy Optimally Restricts Fungi and Metabolic Costs", by Aviv Bergman and Arturo Casadevall, DOI: https://doi.org/10.1128/mBio.00212-10
"Fungal virulence, vertebrate endothermy, and dinosaur extinction: is there a connection?" (.PDF), by Arturo Casadevall, DOI: https://doi.org/10.1016/j.fgb.2004.11.008

"The number of fungal species that can thrive and therefore infect an animal declines by 6 percent for every 1° C rise in temperature. This means that tens of thousands of fungal species infect reptiles, amphibians and other cold-blooded animals, but only a few hundred harm mammals.".

It is useful to refer to ectotherms (an organism in which internal physiological sources of heat are of negligible importance in controlling body temperature, which permits them to operate at very economical metabolic rates) as poikilotherms when applicable.

"Poikilothermic animals include types of vertebrate animals, specifically some fish, amphibians, and reptiles, as well as a large number of invertebrate animals. The naked mole-rat is the only mammal that is currently thought to be poikilothermic.".
"Poikilotherm animals must be able to function over a wider range of temperatures than homeotherms. The speed of most chemical reactions vary with temperature, and in order to function poikilotherms may have four to ten enzyme systems that operate at different temperatures for an important chemical reaction. As a result, poikilotherms often have larger, more complex genomes than homeotherms in the same ecological niche. Frogs are a notable example of this effect, though their complex development is also an important factor in their large genome.
Because their metabolism is variable and generally below that of homeothermic animals, sustained high-energy activities like powered flight in large animals or maintaining a large brain is generally beyond poikilotherm animals. The metabolism of poikilotherms favors strategies such as sit-and-wait hunting over chasing prey for larger animals with high movement cost. As they do not use their metabolisms to heat or cool themselves, total energy requirement over time is low. For the same body weight, poikilotherms need only 5 to 10% of the energy of homeotherms.".

This update speaks to the theories on enzymes (solitary from metabolism), offered in other answers.
Articles and theories that are not discredited:

Enzyme assays by Hans Bisswanger:
That article is mostly concerned with the temperature used to conduct assays of enzymes.

"The essential requirements for enzyme assays are described and frequently occurring errors and pitfalls as well as their avoidance are discussed. The main factors, which must be considered for assaying enzymes, are temperature, pH, ionic strength and the proper concentrations of the essential components like substrates and enzymes. Standardization of these parameters would be desirable, but the diversity of the features of different enzymes prevents unification of assay conditions. Nevertheless, many enzymes, especially those from mammalian sources, possess a pH optimum near the physiological pH of 7.5, and the body temperature of about 37 °C can serve as assay temperature, although because of experimental reasons frequently 25 °C is preferred. But in many cases the particular features of the individual enzyme dictate special assay conditions, which can deviate considerably from recommended conditions.".
...
"Enzymes display their highest activity at their respective optimum conditions, deviations from the optimum cause a reduction of the activity, depending on the degree of the deviation. Moderate deviations produce only small activity decreases which can be tolerated (Figure 1), and so the physiological conditions prevailing in the cell may be taken as standards for at least of the mammalian enzymes. However, assay procedures are usually adapted directly to the features of the individual enzyme and not to obey general standards. Enzymes are sensitive substances present in small amounts and their activity in the cell can often be detected only at their optimum conditions.".

Royal Society of Chemistry - "Enzymes - Function and structure":

"As the temperature rises, reacting molecules have more and more kinetic energy. This increases the chances of a successful collision and so the rate increases. There is a certain temperature at which an enzyme's catalytic activity is at its greatest (see graph). This optimal temperature is usually around human body temperature (37.5 °C) for the enzymes in human cells.
Above this temperature the enzyme structure begins to break down (denature) since at higher temperatures intra- and intermolecular bonds are broken as the enzyme molecules gain even more kinetic energy.".

Note: Wikipedia: "Wilson's temperature syndrome":

"The American Thyroid Association (ATA) describes Wilson's syndrome as at odds with established knowledge of thyroid function. The ATA described the diagnostic criteria for Wilson's syndrome as imprecise and non-specific, and raised concern that the proposed treatments were potentially harmful. Florida State Medical Board members described Wilson's syndrome as a "phony syndrome" and a scam during disciplinary action against Wilson."
...
"The ATA stated in 2005 that a "thorough review of the biomedical literature has found no scientific evidence supporting the existence of 'Wilson's Temperature Syndrome'." The statement added that the mean temperature of normal persons in the AM on waking is 97.5 °F, not 98.5 °F, and that many of the symptoms described by Wilson are nonspecific and typical of depression, anxiety, and psychological and social stress. It also notes that a similar set of symptoms occurs in the alternative diagnoses of neurasthenia, chronic fatigue syndrome, fibromyalgia, multiple chemical sensitivity, chronic Epstein-Barr virus syndrome, and chronic candidiasis. Finally, the Association notes that chronic supplementation with triiodothyronine (T3) is particularly difficult and problematic, since various tissues set their own cellular levels of this hormone by making it individually from thyroxine, and supplementation of T3 may overwhelm this normal regulatory mechanism in some of these tissue.".

Reference: Wilson's Temperature Syndrome

"Metabolism Dependent on Enzymes"
"Enzyme Function Dependent On Temperature":

"... when an enzyme-dependent chemical reaction is monitored for how well it takes place at various temperatures, the lower the temperature, the slower the chemical reaction. As the temperature is increased, the reaction rate will go faster with each increase until it reaches its optimum reaction rate. If the temperature is increased too much, the rate of reaction will diminish due to denaturing or change in shape of the enzyme.".

The treatment suggested by Wilson is what was discredited, the fact that enzyme reactions proceed differently at different temperatures is still supported. Reference to his article was included due to the partial overlap with established knowledge.

I think you are the only one that answered the rather indirect question of why body temperatures are above ambient.

Those are some interesting citations, but I think this answer misses the other advantages of an elevated body temperature.

@BryanKrause I am expanding my answer.

Interesting. I was hypothesizing that perhaps our DNA developed in a warmer environment and we developed adaptations for cooler environments. Is there any possibility of that scenario?

@NonSecwitter I've made another update, I believe it explains that. Poikilotherms adapted to be conservative while homeotherms adapted to high energy activities and maintaining a larger brain. I think your 'DNA question' deserves its own space, but the short answer is that each developed its own taxa in either environment.

First, let's learn about the vocabulary to describe how living beings deal with their internal temperature with this answer. Now that you have read this answer, you understand that humans are homeo-endo-therms.
There are pros and cons of homeothermy. Those pros and cons depend upon the species and esp. upon the type of environment experienced by the organism. Here is one pro and one con. In the specialized literature, you;d find a much more exhaustive list of pros and cons
Pro
The activity of most chemical reactions are affected by temperature. See this post, this post and this post for examples (this post might also be of interest). Enzyme activities are typically highly dependent upon the temperature.
Homeotherms have the advantage that their internal working is not too affected by the outside temperature allowing them to maintain a high metabolism and a high level of activity in a variety of environmental conditions.
Con
Depending upon the environment and the species, it may take a lot of energy (and other ressources) to maintain a constant temperature. For example, in mammals we see behaviours such as shivering, hair positioning (piloerection), vasoconstriction, sweating, change in body posture and other systems such as non-shivering heat production by brown adipose tissues.

Consider if cavemen would be efficient at defending and fighting each other and predators if they took 15 minutes to warm up from a cold nap before they can start to move.
Animals with wider temperature ranges have to maintain many enzyme genes for enzymes that work at different temperatures, and that's inefficient.
If an animal is warm, it processes food and grows a lot faster, so it makes sense for all growing animals to be warm day and night if they can. Older animals can build up fat and reserves and milk and offspring faster if they are resting warmly also. So a female human would benefit from being warm from age 0-37 to breed.
Bears can be dormant at 33'C and alaskan marmots can adjust to 3'C.
Humans that don't hybernate have to be active every day, and have to survive the nights, and grow fast, and build up fat reserves, and keep the immune system enzymes and antibodies at their most performant.

You perhaps need to consider that it's not just humans.  All mammals have body temperatures in a fairly narrow range - 97-103 °F/36-39.5 °C.  Birds likewise have a narrow temperature range, though a bit higher, around 105 °F/40.5 °C.
The advantages seem fairly obvious, at least if you've seen reptiles in cold weather torpor.  As another answer points out, the speed of chemical reactions varies with temperature.  Maintaining a constant temperature allows those reactions (which ultimately determine the speeed of everything the body does) to happen at a constant rate, so animals can be equally active in everything from polar ice to tropical jungle.


text:
Are phylogenetic tree construction algorithms any different than general clustering algorithms?
I suspect the answer is no. But I don't know enough to be sure that that is the case. Of course phylogenetic tree construction uses biological knowledge, e.g special distance metrics, but does it brings anything new at the level of clustering agorithm (e.g hierarchical, neighbor-joining etc).

Not all methods are based on distance matrices. There are methods based on  parsimony, others on maximum likelihood, and others taking MCMC approaches. Even with methods based on distance matrices, there are complications that are specific to phylogenetic (e.g. the cluster need to be rooted somehow, sometimes a network is a better descriptor of the relationship among lineages than a tree). Now, cluster algorithms is a very broad field of knowledge and I am not sure whether all cluster algorithms are based on distance matrices.

One difference is that phylogenetic tree construction algorithms will typically try to jointly estimate the tree and the transition parameters.  A general clustering algorithm might assume that a difference in one feature would make the same contribution to 'distance' between clusters as a difference in another feature. In phylogenetic tree construction, it is explicit that not all differences between taxa represent the same evolutionary distance between taxa, and the parameters governing the distribution of distance/difference may be jointly estimated with the tree.


text:
In oscillometric blood pressure measurement, why do we assume that highest oscillations correspond with mean arterial pressure?
As far as I've seen, the point on the oscillometric curve where there are greatest oscillations represents the mean arterial pressure (MAP).
My question is - why? What is the logic behind this assumption? Or is it just an empirically observed coincidence?


text:
Why clotting does not occur during Menstruation
As we know when we get injured our body's clotting systems stop the bleeding. So why does it take days for menstruation to stop ?

http://medcell.med.yale.edu/histology/female_genital_tract_uterine_cycle.php

The endometrium changes throughout the menstrual cycle in response to hormones. During the first part of the cycle, the hormone estrogen is made by the ovaries. Estrogen causes the lining to grow and thicken to prepare the uterus for pregnancy. In the middle of the cycle, an egg is released from one of the ovaries (ovulation). Following ovulation, levels of another hormone called progesterone begin to increase. Progesterone prepares the endometrium to receive and nourish a fertilized egg. If pregnancy does not occur, estrogen and progesterone levels decrease. The decrease in progesterone triggers menstruation (the shedding of the uterine lining). Once the lining is completely shed, a new menstrual cycle begins. (ACOG)

The uterine lining secretes an anti-clotting factor during periods to assist the blood flow. If the substance is not sufficient to overcome the natural clotting factor menstrual blood clots can form, a process known as hemostasis. Flow may slow down toward the end of a period, and blood can clump. When women are reclining for a time, such as while sleeping, the discharge will pool, and blood clots will be dislodged when upon standing. The blood darkens as it sits and sometimes looks brown or black.
During menstruation, the endometrial cells that line the uterus strip away and leave the body. As this happens, the body releases proteins that cause the blood in the uterus to coagulate. This coagulation prevents the blood vessels in the uterine lining from continuing to bleed. The blood that the body has already shed also contains these coagulation proteins. When the flow is most substantial, the coagulation proteins within the blood may start to clump together, resulting in menstrual clots. This generally occurs when menstrual blood pools in the uterus or vagina before leaving the body.
Menstrual blood clots can be caused by an imbalance in the clotting and anti-coagulating factors in blood or by hormonal changes. Fibroids and endometriosis contribute to excess buildup of the uterine lining, which breaks free as clots.

Under normal physiological circumstances menstruation is a highly regulated, complex process that is under strict hormonal control. During normal menstruation, progesterone withdrawal initiates menstruation. The cessation of menstrual bleeding is achieved by endometrial haemostasis via platelet aggregation, fibrin deposition and thrombus formation. Local endocrine, immunological and haemostatic factors interact at a molecular level to control endometrial haemostasis. Tissue factor and thrombin play a key role locally in the cessation of menstrual bleeding through instigation of the coagulation factors. On the other hand, fibrinolysis prevents clot organisation within the uterine cavity while plasminogen activator inhibitors (PAI) and thrombin-activatable fibrinolysis inhibitors control plasminogen activators and plasmin activity. Abnormalities of uterine bleeding can result from imbalance of the haemostatic factors.
Endometrial haemostasis is a vital process for the control and cessation of menstruation. It is influenced by systemic clotting systems that react to the hormone induced shedding of the endometrium, forming the haemostatic platelet plug and fibrin deposition. Local factors within the endometrium are paramount to ensure the process is highly regulated, with adequate blood vessel occlusion, breakdown of thrombus, and tissue regeneration.
Davies, J., & Kadir, R. A. (2012). Endometrial haemostasis and menstruation. Reviews in Endocrine and Metabolic Disorders, 13(4), 289-299. doi:10.1007/s11154-012-9226-4

Coagulation & Fibrinolytic Pathway in 5 minutes - Simple and Easy

Fibrinolysis Wikipedia


text:
What are the predators of Glaucus atlanticus?
I'm researching the Glaucus atlanticus, also known as the blue glaucus, among various other names, but after reading quite a few articles and searching on the Internet as many different ways as I can think of, I can't find any of its predators, or any indication it has no natural predators. Everything I've read is just silent on the issue. Does anyone know what, if any, predators this has? Thanks!

While I don't really know anything about that animal, it doesn't really need a specific predator (to keep its population in check) if it has to compete with other organisms for the same food source(s).

Try out using Google Scholar to take a more scientific literature-based approach to your search.
Frick et al. (2009)1 found that about 42% of logerhead sea turtle (Caretta caretta) stomachs contained remnants of G. atlanticus.

We were able to identify G. atlanticus in the diet of loggerheads because whole or nearly intact specimens were present.

 Loggerhead turtle mouth and throat with sharp papillae. Source NCSU CMAST (Photo by Craig Harms)
Bieri (1966)2 observed G. atlanticus frequently attacking one another and biting off pieces of each other. In one case, one individual ate all but the head and trunk of a smaller specimen.

Citations:
 1, Frick, M.G., Williams, K.L., Bolten, A.B., Bjorndal, K.A. and Martins, H.R., 2009. Foraging ecology of oceanic-stage loggerhead turtles Caretta caretta. Endangered Species Research, 9(2), pp.91-97.
2. Bieri, R., 1966. Feeding preferences and rates of the snail, Ianthina prolongata, the barnacle, Lepas anserifera, the nudibranchs, Glaucus atlanticus and Fiona pinnata, and the food web in the marine neuston.

Good answer (+1), however I fail to see the function of the somewhat gross picture of the loggerhead. Note2self: stay well away from the beak of loggerheads...

RHA just for the FYI nature is cool factor.


text:
Do the left half and right halves of the diaphragm undergo the same displacement during breathing?
Do the left half and right halves of the diaphragm of a normal person move exactly the same distance between inhaling and exhaling?

Did you check diaphragm muscle images? They are fairly symmetrical.

A short answer is that the displacement of the right and left part of the diaphragm during breathing may not be the same.
ASYMMETRY
Thoracic diaphragm (Wikipedia):

In humans, the diaphragm is slightly asymmetric—its right half is
  higher up (superior) to the left half, since the large liver rests
  beneath the right half of the diaphragm. There is also a theory that
  the diaphragm is lower on the other side due to the presence of the
  heart.

Genetic specification of left–right asymmetry in the diaphragm muscles and their motor innervation (PubMed):

The diaphragm muscle is essential for breathing in mammals. Its
  asymmetric elevation during contraction correlates with morphological
  features suggestive of inherent left–right (L/R) asymmetry.

EXCURSION
Excursion (displacement during breathing) of the right and left part of  the diaphragm may or may not be the same, which may differ from case to case.
Manual evaluation of the diaphragm muscle (PubMed):

In most cases, the diaphragm shows a symmetrical respiratory excursion
  of ~2–10 cm...

Imaging of the Diaphragm: Anatomy and Function (RadioGraphics):

The excursion may be somewhat asymmetric and there may be a slight
  delay or lag on one side, typically the right.


text:
Mother's physiological response to baby crying
I have read several articles [1,2] that talks about the physiological response in mothers when their babies cry. Is there any studies performed and published that show that this is not true ?

https://www.sciencenews.org/blog/growth-curve/how-baby-cries-bore-mom%E2%80%99s-brain
https://www.livescience.com/36964-baby-cries-women-men-brains.html

Hello Noor. It is better to cite a peer reviewed publication when citing references. Anyway, to prove that something exists you just need a single evidence; to disprove the existence of something you have to exhaust all possibilities. First, step to verify the authenticity of a research is to check if it is designed and conducted properly. Then you repeat the experiment and see if it is reproducible. Having said that, I would insist that you should also try looking for articles that dispute this claim. Here, we appreciate if users show some effort from their side before asking.

Some women do not respond emotionally and physiolocically to their own crying infants. It is highly abnormal, and deleterious to the emotional development of the child. Women are hard wired to resopnd to their infant crying. If it weren't true, we would not have survived as a species.

@WYSIWYG, i take note of your advise, thanks


text:
Identify This Plant (Flower)
I just bought this plant from flower shop, after it flowered it was very beautiful red flower, can anyone tell me what is this flower?

This is a Gerbera, which belongs to the daisy family (Asteraceae). Compare:

There are various species.

The domesticated cultivars are mostly a result of a cross between Gerbera jamesonii and another South African species Gerbera viridifolia.[5] The cross is known as Gerbera hybrida. Thousands of cultivars exist.

(from Wikipedia)


text:
What is the difference between Warburg effect and Crabtree effect in metabolism?
In addition to answering my question, please suggest a good review article that provides comparison of the above effects. Which pathways affect central carbon metabolism to produce these effects? Also, how many unique metabolic effects are known for metabolism in general? Is there a good article which covers such unique aspects of metabolism?

Your question is quite broad (multiple questions and overall broad nature). Can you please narrow it down a bit so that it is answerable in a few paragraphs at most?

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!


text:
Is cannibalism part of mainstream food-chain?
There are some species who sometimes eat their own kinds. Is this cannibalism considered their regular food? Do the link in food-chain for those animals make a loop on themselves?
Can this statement: "Food chains are found within the population of a species." be held true?
Disclosure: The above statement was part of a question that asked to identify the correct among statements. I tried to find relevant content in books and internet but couldn't find any. I'm not trying to get my assignment solved, but I want opinion on cannibalism and it's impact on food chains.

A food chain is a linear network of links in a food web (wiki). If you consider species as the nodes of the network, cannibalism could be represented as an edge that connects the species whit itself. This makes the network non-linear, So I suggest to used food web instead of food chain I think your statement can be true if you consider individuals of a given cannibalistic species as the nodes of your network.

Cannibalism can be found across most animal groups. For some groups of organisms (e.g., spiders, fishes) cannibalism can be common within a single generation. Sometimes it will be between siblings, but more often with other members of their species.
As @heracho pointed out, from a network/food web/flow-diagram perspective, yes, cannibalism is repressed as a negative feedback loop on itself.
Evaluating the statement: "Food chains are found within the population of a species," I interpret is as, within species, there are subgroups that consume subgroups, that consume subgroups. You'd need at least 3 levels for it to be considered a chain (i.e., you don't have a chain with two species/a single link). Cannibalism would be a single link/two species, and not considered a chain. As to whether or not chains exist within a species, I suspect it is not common if it exists at all. If it did, I would guess it'd be found in a group like fishes where prey are often size dependent.


text:
How hot water burn works?
At age of 6 I accidentally dipped my hand into a boiling indian curry(Sambar) which was in a large pot.
I got a Boiling Water Burn(Just like in the picture but with a little more radius) in my hand right away and my grandma applied some toothpaste on the area. It has been 11 years now and I still have that mark in my hand.

The question is why is the mark in the center(In circle form)  of my hand and not spread down the whole hand which was  completely submerged a little above the mark. The curry's temperature was pretty uniform around the whole mixture.

The heat takes some seconds to travel through the skin into the deeper layers of the skin, and the deeper it gets, the bigger the scar zone is, it also depends on the skin thickness. Perhaps when you shook and treated your hand, you managed to cool down all the zones further away than the scarred zone fast enough so that it was superficial, or the scar zone had thinner skin, or it was both. AFAIK you should dip a burn into cool water to prevent it getting deep ASAP?


text:
Why aren't all strongly self-recognizing T cells made into regulatory T cells?
Negative selection in T cell development is often simply described as preventing effector T cells from recognizing self-antigens. This is complicated by regulatory T cells developing from T cells with moderate affinity for self-antigens. If recognition of self is useful for immune tolerance, why don't T-cells with strong affinity for self-antigens also become regulatory T cells?

The selection is based upon the strength of the binding. A strong bond causes a signal in the T-cell to self destruct (apoptosis).
Wikipedia has a post on T cells. Perhaps the moderate bonding become regulatory cells, because these cells have to recognize those T cells that survive negative selection, which are most likely to cause autoimmune responses over a long period of time.
Strong affinity to self means the immune response will become a danger to the host.

I understand that effector cells should have a weak affinity for self so that they do not attack the host, but why shouldn't regulatory cells? If moderate affinity for self is used by regulatory cells for tolerance, why wouldn't strong affinity for self do the job better?

@BatWannaBe To my knowledge the strength of the self-reactivity of Tregs can differ by subset, and those cells have different roles. The problem, and some evidence here, is that high self-reactivity is associated with autoimmunity.

@CKM The article you linked seems to claim that higher self-reactivity makes Tregs better at SUPPRESSING autoimmunity. See the discussion paragraph starting with "Our study showed that the level of TCR self-reactivity alone can be used to identify superiorly functional Tregs in preventing tissue-specific autoimmunity."

@BatWannaBe Sorry, I was unclear and that comment was less helpful than when I was typing it up. They do state that clearly in the discussion. There are also some tidbits that continuous TCR signaling can potentially make the Tregs dysfunctional and ablate their ability to control the autoimmunity.


text:
Why do spinner dolphins spin?
Spinner dolphins have a behavior where they jump out of the water and spin a bunch of times in the air. Wikipedia's article on this just states

These spins may serve several functions

and doesn't anything. Are there any known reasons for their extreme spinning behavior?

No single factor is considered to be the reason for the aerial spinning behavior (Hester et al., 1963; Norris and Dohl, 1980; Norris et al., 1994). The various factors include leadership or dominance, alertness, acoustic communication, courtship display, defining positions of members in the school, and dislodging ectoparasites. The most notable ectoparasites are remoras and whalesuckers (order Perciformes, family Echeneidae). ... Hester et al. (1963) suggested that the aerial maneuvers executed by spinner dolphins are involved in the removal of remoras. ... While aerial spinning maneuvers may not have developed specifically to remove ectoparasites like remoras, dynamically it is plausible that this proves to be an added benefit.

--Dynamics of the aerial maneuvers of spinner dolphins

From Lammers - Spinner dolphins of islands and atolls, Ethology and Behavioural Ecology of Odontocetes, 2019 (https://link.springer.com/content/pdf/10.1007/978-3-030-16663-2.pdf) :

Invariably, the question arises: Why do they do it? Probably the most
common answer is to rid themselves of parasites, including remoras
(Hester et al. 1963; Norris and Dohl 1980; Norris et al. 1994b).
However, this answer alone is rather unsatisfying, as most odontocetes
face the problem of parasites yet do not display the acrobatic
aptitude of spinner dolphins. Thus, additional explanations are
necessary that account for the spinner dolphin’s distinct behavioral
ecology. Norris et al. (1994b) proposed that the bubble plume produced
underwater by reentering spinning dolphins would offer a strong target
for echolocating pod-mates and therefore serve as a beacon of sorts to
help define the envelope of the pod or perhaps act as a target to more
distant subgroups.
Similarly, the reentry sound produced by a leaping dolphin could serve
as an Fig. 17.3 A collated sequence of a spinner dolphin, Stenella
longirostris, performing a spinning leap. This sequence was taken from
Twitter, with permission by the Wyland Foundation. In this compilation
of a video sequence, the leap begins on the right side, and the
dolphin turns on its axis two times, until it lands to the left. Leaps
can be in this vertical stance, but also horizontally to the water,
and can incorporate over three turns of the body axis while in-air 380
M. O. Lammers omnidirectional cue to nearby animals. Still, these
explanations probably cannot reconcile the large variety of aerial
behaviors in the spinner dolphin repertoire. Perhaps an additional
clue lies in the fact that behavioral state can be inferred from the
pod’s aerial displays. Thus, it may be that spinners use aerial
displays to regulate the pod’s state in their perpetual effort to
achieve and maintain group cohesion. These acrobatic leaps are perhaps
designed as a signal of group social cohesion for entering or leaving
a bay, or for signaling an after-feeding “party mood” as has been
suggested for dusky dolphins (Würsig and Würsig 1980).


text:
x-linked recessive inheritance and correlation for males
I was inspired by a discussion in this thread. Wikipedia lists a number of disorders linked to recessive genes on the x-chromosome. One typical example is red-green color blindness. Now wikipedia says that up to ten percent of men and up to one percent of women suffer from red-green color blindness. This is due to the fact that the recessive gene for red-green color-blindness sits on the x-chromosome and men have only one copy of this chromosome while women have two.
Now if you take a random male that suffers from red-green color blindness there is a ten percent chance that his father also has red-green color blindness. There is also a ten percent chance that his mother has red-green colorblindness. She must have one copy for red-green color blindness, and if so there is a ten percent chance that she is homozygote and thus suffers from color blindness herself.
So if you did not know the gene causing red-green color blindness and investigated, say 1000 red-green color blind males you will find no correlation between their color blindness and the sex of a parent that also have color blindness.
If you do it the other way around you will of course find that 100 percent of the sons of color blind women be color blind, there is total correlation. So you get very different results depending on the way you set up your investigation.
Now there are also polygenetic traits such as length or intelligence that might be affected by recessive genes on the x-chromosome. The y-chromosome is much shorter than the x-chromosome and contains fewer genes than the x-chromosomes so you would naively expect that somewhat more of the variance in polygenetic traits in male are due to genes inherited from their mother than from their father.
Now if you set up a large scale investigation trying to find out how much of the variation in a polygenic trait in a male that is due to genes from his father and from his mother will the contribution from x-linked recessive genes be accurately determined?
If a man has an x-linked recessive gene making him, say, one centimeter taller than if he had another gene variant, there is equal likelyhood that his father and his mother is affected by this gene perhaps making the correlation "invisible"?
If a man does not have a recessive x-linked gene there is zero likelihood that his mother is affected by this gene but his father could still be affected by that gene.
Question:
1. How does the fact that some of the x-linked genes contributing to a polygenic trait are recessive influence large scale investigations based on correlations trying to determine how much of the variation in a polygenic trait in a male that is due to genes inherited from his mother?

Now if you take a random male that suffers from red-green color blindness there is a ten percent chance that his father also has red-green color blindness. [..] She must have one copy for red-green color blindness, and if so there is a ten percent chance that she is homozygote and thus suffers from color blindness herself Can you please somehow justify this claim?

you will of course find that 100 percent of the sons of color blind women be color blind Can you please justify this claim?

If a certain percent of all x-chromosomes in a population contains a certain recessive gene a women must be homozygotic in that gene in order for the gene to be expressed in her. If the women is homozygotic, her son must inherit one copy of that gene and as he receives no copy from his father that gene must be expressed.

@Remi.b It is just conditional probabilities: if the frequency of the recessive X allele is p=0.1, and the son is colorblind, it means his mother definitely has one recessive X allele. The probability that her other X allele is also recessive is then p=0.1. Similarity, the father has only one X allele, which is recessive with provability p=0.1. If a woman is colorblind, her both X alleles are recessive, and her sons will inherit a recessive allele with 100% probability. The described experiment design of simply sampling from population is however flawed.

@Agerhell your argument holds only if fir every child you consider only one parent. Once both parents (or more complicated genealogies) are included, the things become less ambiguous.

@Remi.b If there is a ten percent chance that a random x-chromosome codes for colorblindedness and you know that the mother must carry one of those for her son to be colorblind. Then there is a ten percent chance that her other X-chromosome codes for color blindedness which would make her colorblind. If both her x-chromosomes codes for color blindedness her son must inherit one of them.

I see several separate questions here, please narrow it down to a single discreet question. Honestly most of your questions don't require any of the lead up.

The correlations you are looking are all based on some unusual and arbitrary subset of the data. The one type of correlation that people generally look at is the one that we call heritability.
For a detailed definition of the term heritability, please have a look at this post. In short, heritability (in the narrow sense; again see above link) is the fraction of the overall phenotypic variance (for a specific trait) that is caused by additive genetic variance.


text:
Identify This Glowing Insect
When I was walking in my garden at night I saw this small glowing insect, can you identify what is this insect?
Location: Middle-East Palestine
Size: Length about 1 CM
This image in the dark (see the light of the insect)

These images taken by flash.

Please [edit] your post to provide your location and the approximate size of the insect. See here for guidelines for writing well-received [tag:species-identification] questions. Thanks

I voted down because we have clear species ID guidelines, and without them your question can, at best, attract guesses. ID questions lacking details lead to answers without details and we end up with a bunch of internet noise. We're trying to be more accurate than sites like Yahoo Answers or Quora where Q and A quality is minimal. Downvoting is my way of enticing users to put in the little bit of extra effort (which will lead you to getting a more accurate ID). Thanks! :)

@theforestecologist np I edited my question bro

Appears to be a larviform female firefly (order Coleoptera; family Lampiridae).
I cannot find a good source for listing/IDing Palestinian fireflies, so I unfortunately cannot give you a definitive answer. I do want to provide some of an answer and an example specimen to get you going on the path of accurately IDing your specimen.
To get you started, your specimen appears similar to Photinus bromleyi (seen here) and below:

Photinus are a group of North American fireflies, so not likely your species.
According to firefly.org, the subfamily Luciolinae is found throughout Eurasia, while the genus Lampyris is a "wastebin taxon" used as a "catch all" for misfit fireflies that is found throughout the world. So I'd start looking in those groups.
I'll dig around for a more Palestinian-oriented bug guide. Again, this is not meant to be an exact answer but just a starting point for you or another user who might have access to Palestinian resources. I'll update if I find something definitive.


text:
How to prevent mold from building on food and how to kill it along with neurotoxins?
I have some food/fruits chopped in very small parts, whatever it is that needs to be conserved during long time, when it is given to me it can be somewhat wet or humid, after some time of keeping it in a plastic Sterilite it builds mold.
After reading a bit I've learned that an autoclave can kill mold at 100°C at 10psi (68.9kPa) for an hour, but it won't kill toxins. My All American pressure cooker with gauge says it can reach 120°C at 15psi (103.4kPa), however this is not much of a difference.
Vinegar, bleach and borax can all be used, but food becomes unusable.
So here are the two questions:

How can I safely keep that food without building mold?
If mold does appear, how do I exterminate it along with toxins safely for human health?

No way to distinguish toxins from nutrients. If it's molded, better throw it away.

I think this is possibly better asked at Cooking.SE - you are basically asking for something like canning , though there are other approaches too - it mostly depends on the type of food you wish to preserve and how it handles each approach. Vinegar, for example, works well for some foods: though it's not as simple as just soaking your food in vinegar, we typically call it "pickling."

@BryanKrause Then take the approach at industrial level, suppose the food is blended rice, could something be done? Disposal is not an option.


text:
Exocytosis of synaptic vesicles
I'm reading the following paper:
http://jcs.biologists.org/content/123/6/819
The part I am really confused about is when they say:

Exocytosis appears to use two alternative pathways: clathrin-mediated endocytosis (CME), which is well established by numerous lines of evidence, and the more controversial ‘kiss-and-run’ pathway, which involves direct retrieval of a vesicle at the site of fusion

My question is .. How can exocytosis (contents inside of cell are transported to outside of cell) use clathrin mediated endocytosis?
I thought endocytosis is the opposite of exocytosis, so why do synaptic vesicles use clathrin mediated endocytosis as a method of exocytosis?

That sentence is located in a paragraph titled "Stages 5-7: Endocytosis and recycling": it's talking about recycling exocytosed membrane which is necessary for making vesicles for further exocytosis.
The sentences before the part you quoted are:

Synapses possess highly efficient mechanisms for retrieving SVs from the plasma membrane of the presynaptic terminal after exocytosis. Fast regeneration of functional SVs is a prerequisite for synapses to function during prolonged activity.

I think the passage is just somewhat confusingly worded, in that "exocytosis" is used as the subject of the sentence which is strange in this context. You could rewrite that sentence:

There appear to be two alternative pathways to recycle membrane for exocytosis: clathrin-mediated...

The author likely intended the word "exocytosis" in the original sentence to mean "the entire process of releasing synaptic vesicles, including formation of those vesicles" rather than the specific event of vesicle fusion with the membrane. Kind of like if I referred to "planting trees" as part of "logging" - you typically think of "logging" as cutting down trees, but in the right context it can make sense to refer to the process: you need to have a tree there to be able to cut it down. I could say "Trees are necessary for logging. Logging uses two alternative pathways: planting trees directly as saplings, or leaving land to grow new forest naturally over a number of years."


text:
How are electrons entering the electron transport chain in cellular respiration energised (excited)?
In photosynthesis, electrons are excited by light energy from the sun (photoactivated).
How do they become excited in human cellular respiration?
I believe it has something to do with NADH and FADH2.

It may be useful to start with a quotation from the Introduction to Ch. 9 of Berg et al. Biochemistry (6e) that addresses the question, more or less as asked. I can’t find a link to the pages in the 5e online so I will transcribe it from my text:

“A principal difference between oxidative phosphorylation and
  photophosphorylation is the source of the high energy electrons. In
  oxidative phosphorylation these electrons come from the oxidation of
  carbon fuels to carbon dioxide. In photosynthesis these electrons are
  excited to a higher energy level by the energy from photons.”

It is important to think about one of the ways in which the excited electrons are used in photosynthesis. To quote from earlier in the Introduction:

“In essence, light is used to create reducing potential.”

What this means chemically is that in photosynthesis the electrons have sufficient energy to reduce NAD+ to NADPH. In the biosynthetic (dark) reactions of photosynthesis the NADPH can be used to reduce carbon dioxide to sugars from which glucose can be produced.
So glucose is a reduced compound and can be thought of as ‘embodying’ the excited electrons, as its oxidation to carbon dioxide generates NADH (from NAD+). Hence:
There is no need for any additional excitation of electrons — that was done originally in photosynthesis.


text:
What are the (evolutionary) advantages of secondary transport?
Secondary active transport uses electrochemical gradients as a source of energy for the uphill transport of substrates (coupled to downhill transport of the ion).
However except for in a few cases (e.g. Electron transport chains) the electrochemical gradient is formed by ATPase pumps which use energy from ATP to pump the ions.
So why not just use ATP in the first place (and not have to set up the gradient). (I do understand that the gradients are useful for signalling, action potentials etc. but that is a seperate issue.) i.e. What is the advantage of secondary transport.
My (complete) speculation:
Is secondary transport perhaps used because it allows a sort of inherent regulation. Stop the gradient forming pump and you immediately stop all the secondary transport using that particular gradient? If that is the case are secondary transport proteins in groups with similar functions/pathways utilising the same gradient?

I'm not sure if I understand the question properly. Essentially, it seems like you are asking why the protein network is one way compared to another simpler design. The answer to that is likely to be speculative; something to do with evolutionary ancestry of the proteins and possible functional redundancy built into the network. These types of questions at the organism level are often closed as duplicates of "Why do some bad traits evolve, and good ones don't?"

@James, I was actually presuming that there is an evolutionary reason for secondary transport, i.e. it has some sort of advantage and thus is so pervasive. My question is whether there are any hypothesises (preferably with evidence) as to what that advantage may be? I've tried to make the question more explicit.

I have not read the post but the title question (Why have secondary transport?) is grammatically wrong and does not mean anything. You should edit that.

I think an easy analogy for why this approach evolves is to think of how humans use electricity (or energy more broadly).
Although it is feasible to have localized electricity generators (for example, a solar panel on a simple calculator), it's typically more efficient to have centralized electricity production. With that organization, changes to the electricity generating machinery can proceed without any changes needed at the end user. If the power plant improves efficiency by 10%, that improves the efficiency of the entire system without a change needed in every lightbulb, refrigerator, and phone charger.
Once an ion gradient is established, different independent systems can use it to perform otherwise energetically unfavorable tasks. Of course this is not the only way evolution could proceed: as linked in a comment there are several general explanations for why evolution doesn't produce every possible combination. There are in fact a lot of proteins that use ATP directly.
The sodium-potassium ATPase that powers one of the major secondary transport systems is particularly interesting because it moves 5 ions at a time, making it very efficient. It would waste ATP if it only exchanged 2 ions at a time. By producing that gradient, other proteins can then evolve to use this gradient at an appropriate energy level rather than needing to work on a "1 ATP = 1 cycle" basis.

also keep in mind a common active ion being transported out that drives it is sodium and it is easy to see why the transport of sodium out of the cell would evolve by itself in some environments. once it exists it can be exploited for other purposes. the other common ion is H+ which can be used on it own to regulate PH.


text:
Does the yolk sac for Danio rerio form at the vegetal pole?
Does the yolk sac in general form always at the vegetal pole?
If so, is this the case for Danio rerio (the zebrafish)?

Generally, yes, yolk is at the vegetal pole. There may be exceptions but I am not aware of them.
You can read about zebrafish (Danio rerio) embryology in great detail in this paper. Figure 3 from this paper (see image) shows the immediate post-fertilization zygote, in which the animal-vegetal axis is first set up by the migration of non-yolk to the animal pole.

UPDATE: very explicitly labeled yolk figures.

Thank you! I read a paper but it was not clear to me where the yolk sac was eaxctly.

See new figures from paper in update.


text:
In biological nitrogen fixation, the electrons required to reduce dinitrogen to ammonia are provided by which compound?
The reaction is as follows:
N2 + 16ATP + 8e- + 8H+ → 2NH3 + H2 + 16ADP + 16Pi
From where are the 8 electrons coming from?
We know that in photosynthesis, the electrons are supplied by the oxidation of water to evolve oxygen gas. What about here?

Welcome to SE BIology. Please take the Tour and read the Help on asking questions. You will find that you are expected to do some research yourself before posting. I would start with a source that explains the biochemistry of the process — Berg et al online will give you the answer. Then, if there are still specific points you don't understand you should repost explaining precisely what these are. At present I am voting to close your question.


text:
Does every protein starts with Methionine amino acid
During process of protein synthesis we need AUG Codon to start translation .As we know this codon codes for Methionine amino acid so can we say that every protein starts with Methionine amino acid ?

No, not every protein starts with a methionine. When the methionine is removed, it is called N-terminal methionine excision. Abstract excerpt below:

N-terminal methionine excision (NME) is the major proteolytic pathway
  responsible for the diversity of N-terminal  amino  acids  in
  proteins.  Dedicated  NME components have been identified in all
  organisms, in all compartments  in  which  protein  synthesis  occurs:
  cytoplasm, plastids and mitochondria. Recent studies have revealed
  that NME is regulated at various levels and plays an important role in
  controlling protein turnover. NME is essential  in  Eubacteria  and
  lower  eukaryotes  and  is  the target of many natural and synthetic
  inhibitors. Such inhibitors  have  considerable  potential  for  use
  in the  treatment of various human diseases, from cancer to bacterial
  and parasitic infections.

And from a recent review focusing on the methionine aminopeptidase enzyme that cleaves the first methionine:

Protein synthesis is initiated by methionine in eukaryotes and by
  formylmethionine in prokaryotes. N‐terminal methionine can be
  co‐translationally cleaved by the enzyme methionine aminopeptidase
  (MAP). When recombinant proteins are expressed in bacterial and
  mammalian expression systems, there is a simple universal rule that
  predicts whether the initiating methionine will be processed by MAP
  based on the size of the residue adjacent (penultimate) to the
  N‐methionine.

Mitochondria and other organelles also have different start codons. Their alternate start codons are well-characterized (AUA and AUU in humans and mainly - but not exclusively - GUG and UUG in prokaryotes).


text:
Do birds require cilia for left/right symmetry during their embryological stages?
I know that in humans ciliary dyskenisia can lead to a Situs inversus, is this also the case for birds and reptilians?

Here is a paper that talks about left-right patterning across bilateral organisms, discussing both Xenopus (frog) and chicken.
It looks like it may be hard to generalize, but the answer appears to be "yes" for Xenopus and "no" for chicken (see e.g. Figure 2, and text immediately following).
However, it looks like the question of what exactly is going on in chicken is not well understood, according to this other paper. Chickens do have lethal ciliopathy mutants homologous to mutants causing left-right defects in other organisms, but these mutants appear to have normal left-right asymmetry development in chicken.
It is also not clear that the requirement of motile cilia for left-right asymmetry is generalizable within clades though, as pigs have apparently also lost the dependence on cilia for L-R, whereas mice and humans do require cilia for L-R. It appears that pig and chicken have dispensed with cilia by the same histological mechanism (see image below, Figure 7 of first paper).
I do not know whether the mechanism has been investigated in other birds.
Hope that helps.


text:
Are the processes on afferent neurons that go from the sensory receptor to the cell body considered axons or dendrites?
References on pain fibers say impulses move along axons to the CNS, but I thought that by definition axons carry impulses away from the cell body.

They are considered axons. Pseudounipolar cells have a bit of an odd morphology.
The reason you consider the entire length an axon is because it all grows from a single process from the soma which then branches. Terminology is just terminology, so "rules" are often made to be broken in biology: yes, an axon typically carries information away from the soma, but that's not the case here for neurons where the information sort of bypasses the soma.
Besides the developmental origin from a single process, the initiation site for an action potential is out in the distal end of the axon, rather than at an axon hillock connected to the soma, and if you had a section of axon on either side of the soma it wouldn't be apparent which end you were looking at.

Tandrup, T. (1995). Are the neurons in the dorsal root ganglion pseudounipolar? A comparison of the number of neurons and number of myelinated and unmyelinated fibres in the dorsal root. Journal of Comparative Neurology, 357(3), 341-347.


text:
How is Pseudomonas aeruginosa diagnosed?
I know that P. aeruginosa is cultured on an agar plate, but which media or assays make it distinct from other Gram-negative bacteria?

Welcome to SE BIology. Please take the time to take the Tour and find out about this site. After that, the Help on asking questions should be your next call.  You need to show that you have done some research for yourself first before posting here. Tell us where you have searched an dwhat you have or have not found.

Well, the answer is actually a Wikipedia search away. But from the 7th edition of the book Microbiología Médica and Todar's Online book of Bacteriology:

Nutriotional needs. Simple. Part of why Pseudomonas spp. grows everywhere is that it can metabolize a wide array of carbon and nitrogen-containing compounds. Blood agar and McConkey are enough for its growth.
Colonies. They generally show a mucoid appearence and are flat.
Respiration. Practically an obligate aerobe. Usually oxidizes glucose, but it is capable of anaerobic respiration as well, using nitrates or arginine as electron donors. The cytochrome oxidase assay is positive, unlike Enterobacteriaceae and Stenotrophomonas.
Pigmentation. P. aeruginosa synthesizes pyoverdin (fluorescent and green) and pyocyanin (blue and water-soluble). Pyocyanin is produced when the presence of iron in the media is low, however, and not all strains synthesize it.
Temperature. Its optimal temperature is 37ºC, but its survival range is quite wide, from as low as 4ºC to as high as 42ºC.
Antibiotic resistance. And to many antibiotics. The presence of beta-lactamases makes P. aeruginosa withstand penicillin, carbapenems and cephalosporins.
Odor. Cultures emit a pleasant aroma that most associate with grapes or soap.

Wikipedia does show a nice battery of tests that identify P. aeruginosa, but if I were you I would compare them to other sources.

Positive: oxidase, citrate, motility, gelatin hydrolysis, acid production (from glucose and mannitol), nitrate reduction, lipase, pigmentation (green or blue), catalase and beta-hemolysis.
Negative: Gram staining, indole production, methyl red staining, Voges-Proskaeur (?), hydrogen sulfide production, urea hydrolysis, phenylalanine deaminase, lysine decarboxylase, acid production (from lactose, maltose and sucrose) and DNAse.


text:
Can motor neurons in the brain stem start movements?
Supposedly (consciouss) movement is started in the cerebral cortex. But some time ago I've read a research which stated it might be possible some movements (not specified which ones, probably mean automated ones) start in the brain stem. That research was in one of those research file websites, it wasnt an article and it didnt have any mainstream visibility. Then I didnt hear anything more in this line, but you hear many times about these babies "born without a brain" who lacks most of its brain, 80% of its brain or who lacks cerebral cortex yet they move. Where are those movements started? Can motor neurons in the brain stem start movements?

Yes, movements (including fairly complex ones) can start in or be driven by the brainstem (and spinal cord).
Central pattern generators are key to producing coordinated rhythmic movements, including those for locomotion, chewing, and breathing: these are also located in the brainstem and spinal cord.
There have been many experiments done to study brainstem control of locomotion (see Shik and Orlovsky, 1976), particularly in decerebrate cats. You can induce a walking motion independent of cerebral control in these animals just by moving the floor (e.g., using a treadmill).
More generally, voluntary motor commands from cortex are mostly just a "suggested plan" - the specific patterns of muscle activation are determined in the brainstem and spinal cord, with input from proprioception and modulation by the cerebellum and brainstem nuclei such as the red nucleus.
In humans, spontaneous movements are also common in ~50% of brain-dead patients (Saposnik et al. 2005), although definitions of brain death typically include the brainstem, so these should be thought of as spinal rather than brainstem movements.

Saposnik, G., Maurino, J., Saizar, R., & Bueri, J. A. (2005). Spontaneous and reflex movements in 107 patients with brain death. The American journal of medicine, 118(3), 311-314.
Shik, M. L., & Orlovsky, G. N. (1976). Neurophysiology of locomotor automatism. Physiological reviews, 56(3), 465-501.


text:
Is it possible for a human being to live on a different day cycle?
I am considering writing a story where a character lives on a 30-hour day cycle.
That is, this person sleeps for 9.5 hours and is awake for 20.5 hours.  Then this person repeats the schedule.
I'd like to know from those of you whom are more knowledgeable about biology and physiology whether this is possible.

Yes, it is certainly possible. Whether or not it's healthy is a different question!

Any chance this is motivated by https://xkcd.com/320/ ?

Ha.  Nice find.  I hadn't seen that one.


text:
Why do bulls-eye rashes look like they do?
People infected with Lyme Disease often present with an erythema migrans ("migrating redness") rash. Most often, these rashes are in the shape of a bulls-eye.
Rash image.
Presumably, this is a reaction that many of our bodies have to the Borrelia burgdorferi pathogen.
Lyme disease also sometimes presents with different-looking rashes, and other pathogens also sometimes produce a bulls-eye-looking rash. CDC Link on Lyme Disease Rashes and Look-alikes.
What causes the bulls-eye shape of these rashes?
Thought process: A gradient of redness from the site of the tick bite makes sense--an immune response might be strongest at the bite site--but I'm still stumped on why there would be a spot of redness surrounded by a no-rash-ring surrounded by a rash-ring.

Note: If I remember correctly, external links to images are usually frowned upon. Although the images linked in this post aren't super graphic, I decided to make them external links for the sake of anyone who is sensitive to medical images.

The spreading of the rash is caused by dissemination (migration) of the Lyme spirochetes (Borrelia) through the skin out from the initial site of infection.
The spirochetes trigger a immune reaction that involves macrophages entering the skin and releasing pro-inflammatory factors.
The clear areas (when present) apparently represent areas where macrophages have been cleared from the skin and thus are no longer triggering a inflammatory response.
The different patterns associated with the rashes can be explained by differences in how fast macrophages are cleared from the skin.
Reference:
Vig, D. K., & Wolgemuth, C. W. (2014). Spatiotemporal evolution of erythema migrans, the hallmark rash of Lyme disease. Biophysical journal, 106(3), 763-768.


text:
How does the zygote divide much faster than other cells?
Normally a cell has a mechanism that controls its division. As far as I know, it checks surface area and stuff like that to decide to go for mitosis or not.
However, this is not the case for a zygote. A zygote, after around ~14 days starts to divide rapidly and forms the blastula. What mechanism controlls this "rapid division"?
Why can zygote divide rapidly when it has not reached a high surface area or doesn't have enough mitogens to induce the cell division? Does the zygotes mini-cells have a cell cycle like other cells but they are really fast? Or do they just copy the DNA and divide rightaway?
And when I first saw the video of this stage, I was surprised. The DNA is a one long molecule; how fast do those replicators work?

A zygote generally has a lot of nutrients, essential biomolecules like RNA and proteins and cytoplasmic organelles for rapid division. So the cell does not grow and divide but rather undergoes "cleavage" (there is no G1 phase of cell cycle). However, it still undergoes DNA replication. And yes, DNA replication is fast because it is initiated at once from several parts (origins of replication) of the long DNA (it still takes a few hours† ).

 † See:

Confusion about the duration of different phases of the cell cycle such as G1, G2 & S
Time spent in phases of cell cycle


text:
Living potato clock?
Could a potato stay alive and power a clock while growing in the ground?
I know how a potato clock works as a electrochemical cell  and involves chemistry, but I am only interested in a growing plants ability to grow and recover lost compounds, water or otherwise during this process while in the ground.

Side question:
How much power could come from one potato?

Source is in the picture.

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

I’m on the phone so I can’t cut and paste, but read the line in the Tour that states the purpose of SE Biology.

Cross-posted on Physics in 2016 by the same user: A live potato light?

@David is this better?

Better. But I still regard it as off-topic. However others do not. Whether they will give you an answer is another question.

Copper is toxic. The potato may develop a toxic wound at the copper site until it made a barrier there. You should try for yourself, it's such an easy experiment.

@com.prehensible can you make an answer out of that so I can award you the bounty?

Muze, please stop reposting this question. You’ve asked it here before (https://biology.stackexchange.com/questions/69376/potato-power-self-sustaining-medium-using-a-living-potato-plant-possible/69543) and on Physics as well (https://physics.stackexchange.com/questions/277693/a-live-potato-light). If the answers are unsatisfactory to you in those places, please comment or edit your previous q’s rather than reposting duplicates.


text:
Does a bird nest out of its breeding range?
I have a book by the Audubon Society on building bird houses and for each bird they show a breeding, wintering and all year range.
Do the birds only breed in their breeding range, or in both breeding and all-year range?
For example, the northern flicker is shown as breeding in Canada, but its all-year range is in the United States. So, am I wasting my time building a bird house for a northern flicker in the United States which is south of the breeding range, but inside the all-year range?

An all-year range for a bird species is obviously a range where a population exists year round, and since birds generally breed each year, there will be individuals of the species breeding within this range.  Precisely speaking, this is part of the breeding range of the species, but maps of bird ranges commonly call this range the all-year range, and will reserve the term "breeding range" for that part of the range map where birds breed but are not present during part of the year.  This is helpful since it communicates which times of the year the birds can be expected to be present.
Because in temperate zones summer is the time when breeding most always occurs, maps commonly show the summer-only breeding range in a warm color such as red. For migratory species, a range where they spend the winter but do not remain during the breeding season is usually shown in a cool color such as blue.  Typically such maps will show the year-round range in a combination of these two colors, e.g. purple.  (Some maps also show a migratory range, where birds transit but do not stay for long periods, in some other color.)


text:
Why are there fewer ospreys in upper New England?
I have a book by the Audubon Society on building bird houses. In this book the chapter on ospreys shows their breeding range to include Canada and then a pocket around the Connecticut and New York coasts, but no upper New England (Massachusetts, New Hampshire and Maine).
This corresponds to my own experience. I have seen a lot of Osprey nests in Connecticut, but they seem much rarer in Massachusetts and New Hampshire. Why is this?
If the answer was that they prefer a warmer climate, then it makes no sense because they have a widespread breeding range in parts of Canada that are colder than New England.