text:
Why doesn't the human skin grow back exactly how it was before being damaged?
Very simple: Why (and how) is regenerated skin different from original ?
As we know we lose skin cells that becomes the dust in out homes and it always grows back to full thickness right ? So when I have a cut, I imagined it to heal provisionally with whatever possible and then after some time to replace itself with the normal skin that is coded in my chromosomes. So why doesn't it do that ? Scars remain and the color is always different from the neighbor parts.
Update:

Why we get scars?
What about skin transplants ?
Why doesn't skin actually grow/replace itself?

Update 2:

(I've been thinking) Skin has lots of different layers, right ? So when an area is damaged does it regenerate all layers or just one for being simple and efficient (in "hope" the subject will take precautions not to damage this part of body again, so that regenerating everything back to 100% would be overkill) ?
I'm not a scientist, I have only the basics from school, so I'll probably not understand most of the technical terms
also I'm more interested about an explanation that goes towards the "survival of the fittest" rule, and not so much about the biochemical reactions in our bodies (because it was just some random mutation that turned out to be the better choice for us → why?)

This is a very large topic regarding wound healing (http://en.wikipedia.org/wiki/Wound_healing) and the scaring is primarily caused by inflammatory factors, which are important in initiating wound healing response, leading to a trade of!

I totally agree with Bez with this. And you if you are asking about scars specifically,this might help http://en.wikipedia.org/wiki/Scar

There are other reasons for scars.. If the underlying collagen fibers are damaged then the new ones dont get incorporated in the exact same orientation.. You dont get scars that easily.. You can also refer any book on clinical anatomy..

Is that a lie scientist are telling us ?... What sort of a statement is this? Scientists don't lie, governments and profiteers do.

@WYSIWYG It is not a statement but a question. In general now I wonder why this site is trying to exist. If all I need is to open Wikipedia or buy a book ... (which both I wouldn't understand I guess)

@Leck.. 1. you are not supposed to attach your social assumptions when asking a scientific question. 2. This site is not your school classroom where the TA is supposed to teach you. If something is already there in wikipedia then why are you asking it- why dont you simply read it from there. If you can't understand what is written there then ask your professor or a friend. Though it is allowed here to ask something that you don't understand but all that is expected is that you make an effort. Nobody is obliged to teach you.

And I didn't vote to close the question, I just asked you to refine your language.

@WYSIWYG You've been rude here. I was reading this before I commented (AND I answered the "I wonder why" by myself if you read what's in the brackets). And I also can't see the close votes because I'm too low on rep (don't really care). If I find no answer here then I'll keep it as one of those life's mysteries that make my life worthwhile. Bye!

Is it better Now?

@Leck there are different kinds of scars (scaring) caused by different kinds of insults and treatments.  In a healthy individual, your skin is constantly growing and replacing itself.  It dies and sloughs off as new skin is formed under it.  I'm still not sure what your question is asking for beyond the wiki link.  After you've read some more (or perhaps now) please take another stab at wording your question, and we'll see if we can't get on the same page.

scar tissue evolved long before humans, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5057359/#:~:text=Animals%20respond%20to%20traumatic%20organ,reproduction%20of%20the%20missing%20tissue.

Human skin is made up of three layers [1]:

Epidermis; it contains no blood vessels; it has 5 cellular layers (starting from surface):

stratum corneum
stratum lucidum
stratum granulosum
stratum spinosum
stratum germinativum

Dermis; it is separated from the above by the basal membrane; made up of connective tissue (with blood vessels and nerve endings)
Hypodermis - it is not even considered part of the skin

"Gray940". Licensed under Public domain via Wikimedia Commons.

Why (and how) is regenerated skin different from original ?

Why? Skin is a very important organ. It protects from pathogens, it maintains body temperature, it keeps body water [1], etc. How? That depends on what causes the regeneration. I've emphasized two terms in the above list.

Stratum corneum represents the "skin cells that becomes the dust in our homes and it always grows back to full thickness". It is lost during a physiological process called desquamation [2]. The cells that are lost are non living corneocytes. Their only purpose is to from a protection barrier [3].
Basement membrane holds the germinativum layer of the epidermis. Injuries that do not affect it are repaired by complete regeneration of all destroyed layers. However, if the injury destroys membrane continuity, the germinative cells on the edges will fail to "reconnect" with each other, thus the layers derived from them will follow the same rule. A process of fibrosis is triggered. The result of  extensive fibrosis is a scar, containing collagen secreted by the granulation tissue with dermal origins. Yet, the germinative layer tends to join back together [6], but probably the excess collagen production, without the limiting basement membrane, bulges into the epidermis and limits germinative layer extension. That's why keeping the edges of the tissue close to each other reduces excessive fibrosis and allows germinative layer regeneration, thus resulting in none to small, barely visible scars.

How deep should an injury be in order not to affect basement membrane? No more than 0.06 to 0.08 mm [5].

What about skin transplants ?

Skin grafts contain at least a part of dermis [4], which will allow granulation tissue formation thus permitting revascularisation and making the graft stick. Otherwise it would fall off and/or be lost by necrosis.

References:

Wikipedia contributors, "Skin," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Skin&oldid=619454074 (accessed August 4, 2014).
Wikipedia contributors, "Desquamation," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Desquamation&oldid=614028888 (accessed August 4, 2014).
Wikipedia contributors, "Stratum corneum," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Stratum_corneum&oldid=615247326 (accessed August 4, 2014).
Wikipedia contributors, "Skin grafting," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Skin_grafting&oldid=603324006 (accessed August 4, 2014).
Sandby-Møller J, Poulsen T, Wulf HC. Epidermal thickness at different body sites: relationship to age, gender, pigmentation, blood content, skin type and smoking habits. Acta Derm. Venereol. 2003;83(6):410-3. doi: 10.1080/00015550310015419. PubMed PMID: 14690333.
Dawn A. Tamarkin, Ph.D. Repair of skin. 2011 STCC Foundation Press. Available from http://faculty.stcc.edu/AandP/AP/AP1pages/Units1to4/skin/repairof.htm (accessed 04.08.2014)

You're confusing an emergent system with a determined system. Your cells have programming which emerges as the form you see. You are using determinism to decide what your form should be. Determinism gives one reaction for every action. Biology is emergent, not deterministic. The biological mechanisms which are responsible for healing exist in a different information space, with different evolutionary pressures from those which generated your form. The close approximation of scar tissue to undamaged flesh is an emergent property of these two instructions sharing the same physical location. There is no communication between the information which patterned your form and the information which heals your body.

I don't understand q_q. Or explain the information space you're referencing. Are chromosomes the deterministic information space ? What is the "different information space" ?

Genes are the buildings blocks of biological information. Different genes are selected for and against and the fact that you can differentially regulate them is what separates them into their own information space. What you look like comes in large part from hox genes which have very different evolutionary pressures from genes regulating collagen production during healing.


text:
Found lots of these insects on my study desk today. What are these?
I came home today, switched on the lights and saw many of these running around my study desk. Any help in identifying these little insects? The picture is zoomed in so it doesn't really do justice to how tiny it is.
Approximate Size: 1mm
Location: Mumbai, India
What are these insects ? How do I get rid of them ?

Additional Images:
Additional Image 1
Additional Image 2
Additional Image 3
Additional Image 4
Video 1
Video 2
Any help in identifying these is really appreciated. We are freaking out crossing our fingers that it is not bedbugs. What are the chances these are baby bed bugs?

Welcome to Biology.SE! If possible clear, closeup photos of the creature from multiple angles would be helpful — the picture you posted is so blurry I'm not sure how many legs it has! ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

I've zoomed it 2x on my iPhone and this is the clearest view I could get of this insect. I'll see if I can get a few more.
Also, Is there a way it can be confirmed that it is not a bedbug?

The "Camera+ 2" app (and probably many others) has macro functionality, so you can take clear close-ups easily. It's free, as far as I recall.

Added some more photos and a 4k video. Does that help?

None of those photos seem any clearer to me ... ——— If you are concerned about bed bugs please search on this site — there is an excellent answer that shows pictures of all stages of bed bug development. ———— In general, please do a search before asking questions as that is more efficient for you and prevents the accumulation of duplicate questions, which just makes more work for the moderators of this site. Thanks!

From the main photo this looks like a booklouse to me; which one (and there are a lot of them sharing human living spaces) does need a very good photo.  Searching this site for "book louse" or "booklouse" will (if memory serves) lead to at least one thread that either discusses or links to control measures (which may be justified given the numbers mentioned).

Thank you all ! It was book louse / book lice.

source: Stack Exchange

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sort: votes


text:
Plants with nutritional requirements similar to Cannabis
What are some short plants that preferably could be grown indoor which have similar nutritional requirements (in terms of N-P-K ratio, doses etc.) as Cannabis?
The purpose of this is testing a mineral fertilizer for Cannabis, without actually growing Cannabis as it is illegal in my country.
I was looking into Cannabaceae family and found out that Hops are closely related. However, due to its size/height it won't be convenient to grow it at home. Also, I'm not sure if being in the same family implies similar nutritional needs.
Plus bonus for valuable/exotic plants.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular, I’m voting to close this question because it seems like [Gardening.SE] would be a better fit, but please don't crosspost (instead request migration). ———— In addition, we expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

@tyersome Although I'm not new to SE generally (been here for almost 10 years already), I've taken the tour and looked into How to Ask. I didn't find anything new or specific to this SE. There's a clear question in my post (well, I'll add a question mark). It is a general question "about biological concepts". It is not anything personal, philosophical, ethical or having many possible answers. It is well tagged. Regarding cross-posting: as I'm happy to accept both some plant names and/or directions to research myself - I'm expecting the former from Gardening.SE and the latter from here.

As for the research done - you can see I've started looking into the plant family. Of course before asking this question I've googled it only to get names of plants that have similar leaves or otherwise are visually similar. That's not what I'm looking for. With all due respect, I'm not expecting scientific papers from Gardening.SE (which I expect to get those here) and vice versa - probably there could be people with practical experience and name a plant right away which is improbable here.

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text:
How does gas equilibration occur in the alveolus, numerically?
I am attempting to model gas exchange across the alveolar membrane.  My main question is there a direct exchange of O2 molecules for CO2 molecules?  If so, then my model predicts (assuming alveolar PO2 107mmHg and CO2 40mmHg; and venous PO2 40, PCO2 46) an arterial PO2 107mmHg, but PCO2 of only 37mmHg (taking into account pH change and equilibration with bicarb and haemoglobin carbamates).  If I remove the plasma bicarb equilibration process (as this takes ~15 seconds, but alveolar transit time is ~0.75 seconds), then the arterial PCO2 is even lower, ~33mmHg.  The expected results should be somewhere in the range of an arterial PO2 of 107 and PCO2 of 40.
The only alternative I can think of is that there isn't a molecule for molecule exchange, with the O2 absorption and CO2 removal being separate processes.  If this is the case then overall there will either be a reduction in alveolar air pressure and/or volume during gas exchange.  However, I can find no references to inhaled tidal volume being different to exhaled tidal volume.  Nor does there seem to be any evidence for N2 or H2O molecules to participate in this process (at standard atmospheric pressure).
Any ideas??
Ultimately I want to then extrapolate model to deal with pathology (eg high alveolar CO2, high venous CO2 etc).
EDIT to include references...
Mechanistic physicochemical model of CO2 transport in the blood
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5341128/
Modeling of the oxygen transfer in the respiratory process
https://hal.archives-ouvertes.fr/hal-00714239/document
Modeling pulmonary gas exchange and single-exhalation profiles of CO
https://www.frontiersin.org/articles/10.3389/fphys.2018.00927/full
Respiratory Physiology
https://derangedphysiology.com/main/cicm-primary-exam/required-reading/respiratory-system
Other materials I have read include:

Pilbeams Mechanical Ventilation
Nunn's Applied Respiratory Physiology
Guyton and Hall Medical Physiology

Can you explain your model in a bit more detail? How does it predict a PCO2 of 37 mm Hg? Why should it cause a reduction in alveolar pressure/volume?

Hi Adhish, thanks for replying.

In my model I know both the venous PCO2, the pH and from there can also calculate the total CO2 content (ie plasma HCO2, CO2 and erythrocyte content (CO3, HCO3 and HbCO2)).  At the alveolus I first calculate the new oxygen content (based on the alveolar/venous oxygen gradient, diffusion coefficient, haemoglobin content etc).  Knowing the alveolar volume I can calculate how many mols of O2 has been extracted.

If I then assume the exact same number of CO2 molecules have entered the alveolus in exchange, then I can calculate the both the new alveolar CO2 and (after redistribution through the CO2 compartments) in the now arterial PCO2.  Doing this gives me an arterial PCO2 of 37mmHg (and an alveolar PCO2 increase from 40mmHg to 41mmHg).

My assumption of 1:1 molecule exchange was based on presumed preservation of pressure/volume within the alveolus (as temperature is constant), as per Henry's Law, PV=nRT.

I understand your question now. I will try to write an answer when I have time.

Hmmm... So I'm thinking may be truly independent of each other, and that the alveolar volume must decrease with each breath, inferring from this summary that discusses the rate of atelectalsis formation at different FiO2's
https://www.openanesthesia.org/atelectasis_during_anesthesia_etiol/

There is no known mechanism for exchange of $\ce{O2}$ and $\ce{CO2}$ in a one-for-one fashion. Their transport across the alveolar membrane takes place by diffusion alone: both of them attain their equilibria with blood independently.
Note that it is not necessary for inhaled and exhaled tidal volumes to be the same. In fact, under physiologic conditions, the exhaled tidal volume is slightly less than inhaled tidal volume. This is because humans normally produce slightly less $\ce{CO2}$ than they consume $\ce{O2}$. In other words, the respiratory quotient is less than $1$.
Thus, we see that the assumption of preservation of alveolar volume and pressure is not valid. Apart from inspiration and expiration, the diffusion of gases to and from blood also affects alveolar volume.

Reference and further reading:
Boron WF, Boulpaep EL, editors. Medical physiology. 3rd ed (international edition). Philadelphia: Elsevier; c2017. 1297 p. (I found this textbook an excellent resource for learning physiology in general and respiratory physiology in particular.)

Brilliant thanks! I'll look at adding that text to my collection, cheers :)

Adhish, don't know if you check these after you've answered, but just wanted to let you know my copy of Medical Physiolgy arrived today, and it's everything you promised it would be.  Thanks again.

@ArkoFlake15 Glad to be of help. :)

No direct exchange, but there is interaction.
I used these wikipedia articles:
https://en.wikipedia.org/wiki/Hemoglobin
https://en.wikipedia.org/wiki/Bohr_effect
For Oxygen transport nearly all is transported bound to hemoglobin. Only one part in 71 is transported as soluble unbound oxygen.
For carbon dioxide, only about 20-25% is transported by hemoglobin. But it sticks to the amine groups and so doesn't directly compete with oxygen which binds elsewhere.
The Bohr effect causes the oxygen to bind more strongly where there is little CO2 and vice-versa. The wikipedia article has a mathematics treatment of this.
The rest of the CO2 is transported as hydrogen carbonate through the action of a carbonic anhydrase. CO2 is not very soluble at body temperature.
The volume of CO2 in the breath is still small.

I'm sorry, this is not at all detailed enough for my purposes.


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What is the genetic basis of blood type (ABO) system?
What is the genetic basis of the A/B/B+/O/etc. blood type system? Are there definitive loci that correspond to each or can multiple different genotypes produce the same antigen profile? Also, is the blood type of a child necessarily one of the blood types of the parents, or can an A/B female cross to A/B male produce a child with blood type O?

There is only one locus involved in ABO blood type, the ABO gene on chromosome 9. It has three alleles: A, B, and O.
We have two copies of every gene, one from each parent. Because the O allele is recessive to A and B, there are blood types with multiple genotypes. AO and AA will both produce blood type A, and BO and BB will both produce blood type B. Only OO will produce blood type O, and AB will get you blood type AB. The specific cross you mentioned (AB x AB) will never produce a child with blood type O, because neither of the parents had any O alleles for the child to inherit. However, any other blood type is possible with this particular cross.
The + or - you sometimes see is a separate system called the rhesus blood type system. The genetics involved in that are actually a bit complicated, but they don't involve the ABO gene at all.

I can answer only half your question.
It is not necessary that the child has to have the blood group of parents.
The inheritance is like this :
1.There are 3 alleles Ia , Ib and Io.
2.Ia and Ib are codominant i.e. they will both be expressed if present together.
3.Ia and Ib are dominant over Io. So, blood group O can only be expressed if the genotype is IoIo. IaIa or IaIo is blood group A and IbIb or IbIo is blood group B.
5.IaIb is blood group AB
So in the case of both the parents being AB blood group,the child can not have O group.S/he can have any other blood group.
The inheritance of negative and positive blood group follows simple mendelian inheritance.
Please feel free to correct me!

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Lyonization and X-linked disorders?
Lyonization or X-chromosome inactivation is the conversion of all but one, X-chromosomes in Females into non-coding heterochromatin (i.e. deactivated) leading to the formation of one or more Barr bodies. The selection of the X-chromosome to be inactivated is different in different animals. In female Marsupials, the inactivation is always of the Paternal X-chromosome while in placental mammals, the selection is random. (Although the extent of lyonization is not completely random and varies directionally with age).
My question is

If the X-chromosome to be inactivated is randomly selected in
  placental mammals (including humans), then why don't the females
  heterozygous for a X-linked recessive disorder do not show the
  phenotype of the disease though the functional gene is equally likely
  (as compared to the defective) to be the one to be lyonized?

There are some evidences of genes escaping inactivation and managing to exhibit themselves but I don't think they can account for all the recessive x-linked disorders.

The simple answer is that which X chromosome is inactivated varies in different cell lineages, so typically a female will have cells exhibiting either wild-type or mutant phenotypes. It was Mary Lyon's observation of mosaicism in heterozygous mouse coat colour that gave the phenomenon its name. So in the case of a recessive disease there will be a phenotype, but in many cases the 50% of cells expressing the normal gene will provide sufficient functional cells to get by. From the Wikipedia article about Mary Lyon:

Her research has allowed us to understand the genetic control mechanisms of chromosome X, which explains the absence of symptoms in numerous healthy women that are carriers of diseases associated with this chromosome.

Edit - response to comments:
Plug, I et al. (2006) Bleeding in carriers of hemophilia. Blood 108: 52-56
Abstract:

A wide range of factor VIII and IX levels is observed in heterozygous carriers of hemophilia as well as in noncarriers. In female carriers, extreme lyonization may lead to low clotting factor levels. We studied the effect of heterozygous hemophilia carriership on the occurrence of bleeding symptoms. A postal survey was performed among most of the women who were tested for carriership of hemophilia in the Netherlands before 2001. The questionnaire included items on personal characteristics, characteristics of hemophilia in the affected family members, and carrier testing and history of bleeding problems such as bleeding after tooth extraction, bleeding after tonsillectomy, and other operations. Information on clotting factor levels was obtained from the hospital charts. Logistic regression was used to assess the relation of carrier status and clotting factor levels with the occurrence of hemorrhagic events. In 2004, 766 questionnaires were sent, and 546 women responded (80%). Of these, 274 were carriers of hemophilia A or B. The median clotting factor level of carriers was 0.60 IU/mL (range, 0.05-2.19 IU/mL) compared with 1.02 IU/mL (range, 0.45-3.28 IU/mL) in noncarriers. Clotting factor levels from 0.60 to 0.05 IU/mL were increasingly associated with prolonged bleeding from small wounds and prolonged bleeding after tooth extraction, tonsillectomy, and operations. Carriers of hemophilia bleed more than other women, especially after medical interventions. Our findings suggest that not only clotting factor levels at the extreme of the distribution, resembling mild hemophilia, but also mildly reduced clotting factor levels between 0.41 and 0.60 IU/mL are associated with bleeding.

Bimler, D & Kirkland, J (2009) Colour-space distortion in women who are heterozygous for colour deficiency. Vision Research 49: 536-543
from the Introduction:

About 15% of women are heterozygous for some form of colour vision deficiency (CVD). That is, they possess a genetic abnormality on one of their two X chromosomes, affecting the photopigments (opsins) which subserve colour vision. The retina of a heterozygous woman is a mosaic in which some cone cells express the aberrant gene while others express the normal copy, depending on which X chromosome is active (inactivation of one X chromosome occurs randomly in retinal stem-cells at some stage of fetal development). The normal cells are sufficient to provide full trichromatic vision.

Thank you for the answer. In case of a female heterozygous for haemophilia, can we observe the defective $\beta$-Hb chain in atleast a part of the total RBCs? That, if possible, would greatly simplify identification of Heterozygous carriers.

I don't know the answer, but I think that you are getting your diseases mixed up - it's sickle cell anaemia that's a haemoglobin disorder. I seem to recall however that the most common genetic disease in humans, glucose 6-phosphate dehydrogenase deficiency (X-linked) is an example of a blood disorder in which heterozygous females have two populations of red cells.

I am sorry. I was in quite a haste and blundered because of it! Thank you anyway.

@SatwikPasani I got quite interested in what you said in the first comment if we apply it to some other disorder as sickle cell anaemia isn't X linked ( As alan boyd already pointed out). Why shouldn't the concentration of say, a clotting factor differ in haemophilia carriers from that of homozygous female ?

@biogirl Analysing the cone constitution in females heterozygous for color-blindness is equally intriguing since there is a possibility of there being a random distribution of color-blind and normal cones, in the retina. Anyway, I am looking up the Haemophilia case at the adjacent pathology centre and will keep updating here. P.s.( I know I did a mistake in my first comment but editing comments after 5 min is disallowed :))

@SatwikPasani Cool ! Would love to follow up !

@AlanBoyd Does extreme lyonization (in the first paper) mean inactivation of X chromosome carrying the normal allele in most of the cells ?

@AlanBoyd As a co-incidence, it was this very paper(first one) the pathology department asked me to look at (they didn't have the latest research papers directly on lyonization for they rarely came across haemophilia cases, let alone carriers). Though the link they gave was behind a paywall, I got a free link here.http://bloodjournal.hematologylibrary.org/content/108/1/52.full.pdf The second link was unknown. Thank you for it.

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text:
Scrotal temperature and vascularization
The testes (at least in human males) are vascular organs, the vascularization extending even o the interstitial spaces of the seminiferous tubules. The function of the scrotal sac, is to isolate the testes from the abdominal cavity, and provide a lower temperature ($1-2^\circ \text C$ lower than normal body temperature of $37^\circ \text C$).

But since the blood is the main temperature-buffer maintaining the
  normal body temperature and the scrotal (testicular) tissues are
  considerably vascularized, why doesn't the blood flow raise the
  scrotal temperature to normal body temperature?

If the reason is the location of scrotum external to the abdomen, then all limbs and limb-extremities are located in the similar way (and in those cases, heat dissipation would be faster than in case of scrotum due to less surrounding insulation by thighs and clothes), and hence the temperature of all parts except the interior of the head and abdomen must be at considerably lower temperature? Is this the case?

well... fingers and toes do become cold and pale in winters.. :P

The fingers and toes (for example) ARE at lower temperatures than the interior of the torso.  It's why it's so easy to get frostbite on the extremities. As for temperature regulation of the testes, you have to also consider that humans evolved without clothes...i.e. The testes just "hang out" and get lots of airflow, as opposed to modern times, when they are typically under (usually) more than one layer of clothing.
Also, for reference, I took some quick IR temp readings on myself:
Room temp: 19.9C
Fingertip: 27.0C
Palm: 31.8C
Axilla: 34.6C

You didn't include your scrotal temperature, the area of interest here.

I thought it would be odd to use the kitchen thermometer to measure the temperature of my "junk". Next best thing I could come up with was the axilla.

A quick question, why do you think the presence of excessive clothing does not cause increased temperature due to reduced dissipation in all cases?

It probably does reduce heat dissipation in all cases, the reduction dependent on the nature of the clothing.  Scrotal temperature is actually regulated by a couple of methods however: blood flow can be adjusted by changing the flow resistance of the vascular beds, and scrotum itself contains muscles that adjust how closely the testes sit relative to the body.  Take a cold shower, and you will notice the scrotum will pull up snugly against the body. A hot shower and it will hang loosely. Of course, if temperature is not perfectly regulated, it's not the end of the world either.

The lower temperature optimizes sperm production conditions, but a degree here or there will not render one sterile. It may slightly reduce sperm count, but you'd probably be hard pressed to measure a difference. The outside of the body will probably always be about 1C lower than the core body temp, so you aren't looking at a huge alteration in the testicular temperature even if all thermoregulation were stopped by the clothing.

http://www.ncbi.nlm.nih.gov/pubmed/7496419
Apparently special undergarments can reduce male fertility significantly. I'm not sure about how rigorous that particular study is, but I suppose it's something to consider.
I'm not going to attempt to replicate their work, at any rate :D


text:
cell proliferation assays for research proposal
I'm an undergrad Biology student and I'm working on a research proposal for a certain course. I need help or guide on cell proliferation assays. I have a target gene , recent papers show that this gene's haploinsufficiency increases cell proliferation. However the most recent paper (published in 2020) showed that haploinsufficency decreases cell proliferation instead. I want to investigate this discrepancy but I don't know what methods should I use. In both papers they used immunostaining with Ki67 antibodies and SOX2 and TRB2 markers and in 2020 they also tested cyclin D levels. I'm not an expert at this field and I want to know what methods I can use for my experiment.
Thank You

There's no discrepancy between those results. Haploinsufficiency means only the gene on one chromosome is producing functional protein, not both chromosomes. Due to this lack of the protein, the cells increase their proliferation. However, in normal cells with both copies of the gene producing functional protein, cell proliferation decreases. That means this protein is a negative regulator of proliferation - if there's not enough of it, proliferation increases; if there's enough of the protein around, proliferation decreases. No discrepancy at all.

Sorry I didnt write my question right.. I meant that in one paper haploinsufficiency causes increased proliferation and in the other haplo causes decreased prliferation. In the last paper published they said that there is a discrepnacy and it needs to be further investigated

OK, that makes more sense. Can you please [edit] your question to clarify that?

It will also help if you can link the specific papers so that one can suggest a good experiment.


text:
How do cilia beat?
From what I have learnt, the mechanism of the beating of cilia is: movement of dynein towards the (-)-end i.e. towards the microtubule-organizing center (MTOC), causing the 2 pairs of microtubules to (supposedly) slide. This is prevented by linker proteins anchored in the adjacent pairs of microtubules. Therefore, when dyneins move, the linker proteins become skewed hence and bending of cilia.
My question is: As far as I know, dynein can only move in one direction (towards (-)-end) i.e. the cilia can only move in one direction, which is forward beating action. I would like to ask how can the cilia move back to the original position (backward movement) and initiate the next beating?
Edit: I have checked Wikipedia, it says there is a process called intraflagellar transport (IFT), which is bi-directional and allows the retrograde transport of cilia (backward movement?) by dyneins, which seems contradictory to what I have learnt, so how can this process actually happen?


text:
Introns and miRNA
From this paper, it is stated that some introns may contain genes coding for miRNA, miRNA is essential in regulating gene expression by pairing with RNA, hence disrupting regular translation.
From this answer, it is stated that introns are broken down and the nucleotides will be recycled by ribonucleases.
Question:

How do ribonucleases sense the presence of miRNA genes in introns, hence not breaking them down, what is the mechanism for that?
How to 'extract' the miRNA present in the introns? (My thought is by a mechanism which is similar to splicing, but we are extracting the DNA sequences in between i.e. switched the positions of introns and exons than regular splicing)

Thank you.

The answer to Question 1 is:

The ribonucleases responsible for digesting removed intron RNA do not recognize the miRNA as such. They are unable to digest it because (or to the extent that) it assumes a double-stranded structure, as they are specific for single-stranded RNA.

The answer to Question 2 is briefly:

By the same mechanism as the many microRNAs transcribed from the DNA using their own promoters rather than from the promoters of the genes containing the introns in which some occur. (And some intronic microRNAs have separate promoters.) This involves a different enzyme that does recognize the microRNA region.

The mechanism of generation of microRNAs from their precursors
This is shown in the diagram below adapted from a review by Lucas et al. of the situation in Drosophila. It is initiated by the recognition by Drosha of the double-stranded RNA formed by the self-complementary miRNA sequences in whatever single-stranded RNA.

The pre-miRNA moves to the cytoplasm where it is further processed to the single-stranded active form.

But in general…
…it’s not quite so simple. MicroRNAs are not the only small RNAs found within introns. It is quite common to find small nucleolar RNAs (snoRNAs), which function to recognize methylation and pseudo-uridylation sites on rRNA; and although these snoRNAs have double-stranded regions, these are less extensive than in microRNAs (see e.g. this review). Our knowledge of the details of digestion of excised introns by RNase is sketchy, but it may be better to consider the situation in terms of competition between two types of RNA-binding proteins for the small RNAs (and even mRNA). On the one hand there are the RNases that will digest the RNA completely — on the other hand there are proteins (like Drosha in this case) that recognize some feature of the RNA and bind to it. Once the latter bind, the 5′-end of the RNA would be protected from digestion by exo-ribonucleases. So it would not be a question of all or nothing, but a balance, which has the advantage that it can be regulated — tipped one way or another — depending on the relative proportions and activities of competing proteins.

That same review also mentions mirtrons.

@canadianer — I have amplified my answer. I don't think it helpful at this level to go into details of which intronic microRNAs have their own promoters or not, unless someone requests it.

I have now added a rider to my answer, discussing the situation with other intronic small RNAs.


text:
How many giant kelp are there per square meter?
In a high-density giant kelp (Macrocystis pyrifera) bed how many "holdfasts" or roots would there be per square meter of seafloor on average?

Welcome to Biology.SE! Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, we expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For example, please add in the species of "giant kelp" for which you want a density. Have you done any research to try to answer this yourself? Please summarize what you found (and where) and what  you still wish to know. Thanks!

The density of Macrocystis pyrifera is pretty variable. According to Dayton et al. 1984 off of the Southern California coast it can range from less than 0.1 to to 1.0 $individuals/m^2$. The variation depends on the location, where there are different exposure levels to high energy waves, upwellings containing nutrients, and predation by sea urchin.
Dayton, P. K., Currie, V., Gerrodette, T., Keller, B. D., Rosenthal, R., & Tresca, D. V. (1984). Patch dynamics and stability of some California kelp communities. Ecological monographs, 54(3), 253-289. https://doi.org/10.2307/1942498


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What are these tiny, bouncy balls I found in my Calathea substrate?
I found two of these small eggs/seeds (?) in the substrate of the Calathea plant I just bought from a botany store. I cut one of them open to make sure it's not just plastics or similar.

About 4 mm across
Quite bouncy
It looks like they have something a little darker on the one side of the sphere, and the other side seems a little bit transparent
When cutting it open it was a little "crusty"

I looked up what Calathea seeds look like, definitely not like this. Any idea what this could be?

Since these are the non-organic fertiliser beads used when filling the pot (a few are sprinkled in before selling to slow-release nutrients) and not something biological such as snail-eggs, this question would be off-topic here. If you're interested in knowing more about them, check-out the [gardening.se] site which specialises in related stuff.


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Where can I find DNA decryption research?
What is the name of the science that studies the mathematics of DNA?
Where can I learn about maths, statistics, types of code, numbers, patterns and graphs for genes and information found in DNA?

There isn't one, because I've never seen it regarded as a science per se, but you are free to invent one. In the meantime you could look up articles in what has been termed "Theoretical Biology", although this encompasses other areas. "Bioinformatics" analyses DNA (and other things) in the way you may be thinking, and appropriate books in that field may give you a start. Try browsing in your university library or bookshop (if you have access to these).

Are you asking about DNA in biology or DNA as a data store for non-biological data? "DNA decryption" mostly returns results for what I would see as a presently silly use of DNA in cryptography.

Yes, to know about all the codes and maths that have been found in Biological DNA, gene lengths, variations, duplicates, randomness of loci, types of markers, to see many graphs that represent what DNA is in numbers, lots of statistics and functional maths... I also only found silly pages about data security keys using  DNA.

You are probably looking for mathematical biology as a whole. Your question is very broad because it is unclear to me if you are talking about genetics in general or if you just want summary statistics for genes in particular organisms. From a mathematical perspective, there is also DNA topology (structural features of the DNA), the field of quantitative genetics (linking phenotypes and genotypes) and the entire field of population genetics (inheritance within populations).

Also "DNA decryption" isn't descriptive enough. There is an emerging field called DNA computing (or nucleic acid computing when including RNA as well) that uses DNA or RNA to perform computation tasks, as well as ongoing efforts to use DNA as a storage medium for information (DNA digital data storage).

I can think of several possible terms for what you could mean (with my interpretation of what people in those fields do):

Computational biology (the study of biological topics using computation)
Bioinformatics (the study of biological topics using computation)
Mathematical biology (the study of biological topics using mathematics)
Sequence analysis (the study of patterns in nucleotide [DNA] and protein sequences)
Genomics (the study of genomes or more generally large quantities of nucleotide sequence)

These all bleed into each other and doubtless other people have different interpretations.
There has been a ton of work in these areas, so they probably cover what you mean, but without some more concrete examples it's a little hard to say which is most appropriate.
As an aside, "DNA decryption" will be interpreted by most people in light of attempts to encode non-biological data in DNA and then decode it (see e.g. george church's stunts). However, based on what you say I think this is not really what you are interested in.
If you are looking for the technical literature for such fields, you could see the following journals, which are some of the better-known peer-reviewed journals focusing on these areas:

Bioinformatics
PLOS Computational Biology
Genome Research
BMC Bioinformatics
Molecular Biology and Evolution

Thanks! awesome answer. When I check what kinds of hackers and computer scientists have used numeric science knowledge to research, decode and classify DNA, only find dna being used for non-biological codes. I want to know, if you gave the DNA code to an elite hacker, who can get into the pentagon... What would he find?

@com.prehensible Just to be clear, this "DNA code" being given to a hacker is a naturally occurring DNA sequence, e.g. human genome or E. coli genome or whatever? Or a random DNA sequence, or something else? Naturally occurring sequences are usually assessed on the basis of deviations from random or comparisons between biological genomes, which have somewhat different "rules", so I'm just trying to understand what your baseline is here.


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What percentage of Americans have Native Indian ancestry?
What percentage of americans have native indian ancestry?
I tried to find the answer online and it's difficult to search for.

Probably unknowable unless you find genetic markers, and do genetic studies on a statistically significant fraction of the population.  And of course you have sub-populations with greater or lesser percentages.

I found some averages from 23andme on sciencemag. It doesn't state the figures for all americans, although it says that 8 percent of white americans have some native american ancestry, afro-americans have on average 0.8%, and latino have 18% native american ancestry.


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Bug identification: Striped grub/worm, 5mm long, indoor highrise 9th floor, Ottawa, Canada
I've seen two worms like the one below tonight, but none before.  A neighbour with a dog moved in next door 2 days ago, and it is close to our wall that I've seen them.  However, she hasn't seen the bug.  I saw one on the kitchen tile floor and one on the kitchen counter.  I'm in Ottawa, Canada, in a 9th floor apartment of a highrise.  I have no pets.
Not sure if it's relevant, but it also got very cold in the last 2 days (negative teens in terms of celsius) -- never seen these grubs in previous years when it got this cold.  It's mid-December.  The grub is about 5mm long.

Does this look similar? https://biology.stackexchange.com/q/74209/16866

It might be, but I have a bit of doubt.  It's not as big (5mm vs.  18mm).  The answer in the page you cited hypothesize a dermestid carpet beetle, which seems hairier and plumper.

The larvae size information is spotty, but sizes seem varied, so the above 5mm vs. 8mm discrepancy might not mean anything.  The stripes of a dermistid beetle seem to be due in part to its segments of its body, and my bug was too small to see this, but the stripes seemed to be due to actual colour.  But if that's what it is, I'm not liking what I find about dealing with it, nor about what it can eat.

I offered the carpet beetle as an option b/c your image isn't very clear. However, after reading your description and comments with less tired eyes, I can see that even lacking a clearer image that the carpet beetle larvae is probably not the most likely candidate. Let me ask you these: did you notice any "projections" from either end of the specimen? Or does the thicker end have a broadened body segment (i.e., one that is "thicker" than the others?) Are there any type of leg-like appendages anywhere along the length? Lastly, notice any flying insects in your home lately?

Thanks for reconsidering.  I can't answer the questions beyond what I can discern from the photo because the photo is actually better than what I could see with my bare eyes (which aren't great).  So even though it may not mean much, I didn't notice any hair-like projections at the ends, and the photo shows one end thicker than the other.  I did not see any legs, and there have been no flying insects in my home.  It's beginning to look like it might not be a dermestid beetle, which I appreciate.


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Questions on mid-2019 Covid-19 Spread in Spain
I recently read in the news from Reuters that Covid-19 was already present in the Europe in March 2019 as reported by the study by Chavarria-Miró et al (2020). According to  Chavarria-Miró et al they found traces of SARS-CoV-2 in March 12, 2019 sewage samples from Barcelona.
I am interested in this news because I do research on effects of covid-19 pandemic and government responses to covid-19 on macreconomic indicators. In macroeconomcis we are unable to run randomized control trials but sometimes nature can create natural experiments or situations that allow for use of quasi-experimental statistical techniques, and I think I can use the situation above in such way.
Consequently, I have the following questions:

How conclusive is that  Chavarria-Miró et al study? Are there any red flags that would indicate the conclusion drawn from the study should not be taken at face value? Essentially, I am interested in knowing if the study is reliable or if there are possibly other corroborating studies.

Is the SARS-CoV-2 found in march 12 the same SARS-CoV-2 that was circulating in 2020? Or we can't tell? Or to what degree it is similar if it is possible to know (in terms of infectiveness and mortality/morbidity)? If it is not possible to answer this empirically, is it at least possible to answer it theoretically based on how similar viruses mutate? (Here I would also appreciate some references to literature/data if possible).

The reason why I ask this second question is that given how dangerous and infectious is Covid-19 considered, I am surprised that there weren't spikes in deaths in Spain. In fact, according to statistics provided by Statista the number of deaths in 2019 was highest in January and even declined after March. When the number of death is totaled across whole year 2019, and compared to years prior years in data from Statista here, again the number of deaths was comparable to 2018. I realize that just looking at a crude naïve statistics like this is not rigorous but I would expect at least some visible effect if Covid-19 was already spreading in March 2019.

Do you maybe have your years mixed up? 2019 vs 2020? It's 2021 now, last year was 2020.

@BryanKrause no actually no, as the Reuters reports "Spanish virologists have found traces of the novel coronavirus in a sample of Barcelona waste water collected in March 2019". Although I was surprised as well and thought it was mistake initially but apparently it is so

Ah; that's definitely a false-positive then. This is probably a better question for Skeptics.SE, there isn't much if any actual biology in your question.

@BryanKrause but the paper is from actual biologists - and I am interested in reliability of the paper. As far as I understand skeptics site is more for credibility of general claims not research papers. Also why about my second question? Isn’t that biology question?

@BryanKrause just to clarify because maybe this was not clear - I learned about the information in Reuters but then I actually went and searched up the study on Google scholar and the chavarria-miro et al study also states it was March 12, 19. I mean of course it could be false positive but is there anything in the study that would indicate that their method is not rigorous (in the study they mention multiple samples in March 12) and I am not familiar with what’s the proper procedure but I would assume the such tests are on samples multiple times to reduce chance it’s false positives

Especially before publishing research. But that publication might of course also be of low quality- it is hard for me to judge without formal training in biology. I don’t think it belongs to skeptics since their site is according to their help center for “for challenging unreferenced notable claims” and this claim has whole study behind it - it is just difficult for me to judge the results of the study.

It's a preprint, not a publication. Regardless of the publication quality, it makes zero sense. We have seen what happens clinically with COVID-19: respiratory distress in a sizeable fraction of infections, a pandemic lasting several months. It isn't feasible that the virus was somehow present in one place in Spain and yet resulted in no broader spread and no clinical notice.

@BryanKrause sorry you are correct about it but still most scientists don’t put up preprints if they are not confident in their paper (at least in my field that is usually the last step to gather some extra comments before sending it out to journals - not sure if biology works differently in this regard)

@BryanKrause well if it is impossible or very improbable given the general consensus of epidemiologists that actually answers my question as well, so if you would consider expanding that into an answer that would support that with some references I would be willing to accept it after letting the question to sit for while to potentially collect more answers. The paper itself tries to claim that early 2019 cases were probably misdiagnosed as influenza - maybe that is just handwaving claim - this is why I came here to see what experts have to say about such claims

This seems unlikely given most phylogenetic studies estimate the emergence of SARS-CoV-2 in China somewhere between October and November 2019, e.g. this study.

@user438383 fair enough but then there are also reports of covid spreading in Italy in September 2019 in a study that was looking at covid antibodies which is still month before October  see here - this one is not even preprint but published in journal, I mean  perhaps its another false positive and publication bias, could you maybe consider expanding your comment into an answer providing more complete explanation?

@1muflon1 Consider that it is much more likely that a PCR artefact (like Chris described in his answer) can give a one-off false positive results, such as the Italian or Spanish study, than 1000s of SARS-CoV-2 genomes all happen to coalesce to the wrong date, which also happens to be just before the first recorded case occured. The two studies aren't an equal weight of evidence.

Related q on Skeptics: https://skeptics.stackexchange.com/questions/47583/did-europe-have-a-covid-19-case-in-december-2019 Note that someone tried to give that Bacelona study as answer but it ended up negatively scored... On the other hand (and this is why I'm linking) you can see there what water analysis looks like in other less controversial instances (Italy, later in 2019); there's a continuous series of positive results... By the way, China could have published such studies too, but they seem very skittish to do so...

To judge about this assay, it is important to see how they worked. They used different sets of primers to analyze for SARS-CoV-2. Namely targets IP2 und IP4 from Institute Pasteur in Paris (see reference 1) and to validate results also primers targeting the "E" sequence (reference 2) and two against the nucleoproteins N1 and N2 (reference 3).
Then they tested frozen samples taken between January 2018 and December 19. Of those, only the sample from March 2019 come back positive for 2 out of 5 primer pairs, none of the samples before and after tested positive, despite mentioning that samples where already positive as early as January 2020 again.
If you look at the published amplification curve you see a very late Ct value for the sample (I would eyeball it somewhere between 39 and 40), which is basically in the area of non-specific amplification. Running the PCR another 10 cycles until 50 is highly unusual in my experience.

Conclusion: I see this result as a PCR artefact and I doubt, this will be published (at least I hope it will not). The reasons for it are:

only two of five sets of primers is positive. Since these are highly specific, I would expect all five of them positive.
the Ct value is very high, around the usual endpoint of qPCR. If you let PCR run long enough, it will eventually amplify something. The also show no melting curve to prove the have a good PCR product.
it is highly unlikely that the virus appears in March 2018 in the wastewater of Barcelona and then disappears again without leaving any trace. This is clearly not the experience we have been making throughout 2020.

References:

Protocol:Real-time RT-PCRassays forthe detection
ofSARS-CoV-2InstitutPasteur, Paris
Detection of 2019 novel coronavirus (2019-nCoV) by real-time RT-PCR
CDC 2019-Novel Coronavirus (2019-nCoV) Real-Time RT-PCR Diagnostic
Panel

Unfortunately the study has already been cited rather uncritically in the news section of Nature https://www.nature.com/articles/d41586-020-03165-9


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Why is the mRNA not damaged at -70 C temperature Corona vaccine?
Why is the mRNA not damaged at -70 C temperature Corona vaccine?
Need for -70 degree temperature for Corona vaccine
I assume that if I, for example, were to freeze, say, a chicken egg after heating to room temperature, the protein binding would be destroyed.
What mechanism, process or substance ensures that at -70 C mRNA is not damaged? Or is this a natural property of the mRNA itself?
As I understand it, random errors in the conformation of DNA, RNA and proteins often lead to information distortion.
https://translate.google.com/translate?sl=pl&tl=en&u=https://pl.wikipedia.org/wiki/Konformacja
Sorry for My English.

An egg is an egg. A molecule is a molecule. If you ask this sort of question you need to set out a chemical reason why a molecule should be harmed by freezing. Do you have one?

Yes I have one: https://translate.google.com/translate?sl=pl&tl=en&u=https://pl.wikipedia.org/wiki/Konformacja
Auto translated from polish.

Maybe you want to ask here or chem SE a simple q like "how do cryoprotectants work for preserving RNA?" instead of offering your theories. Conformational isomerism (which you've linked to in Polish) doesn't seem to have anything to do with that... (I should also say here that the vaccine is not just mRNA, but mRNA contained in lipid nano-particles [LNPs], so some of the freeze-thaw effects on cell-like structures may matter too. But as far as I can tell cryoprotectants are used even for "unwrapped" RNA preservation, so you may start with asking about that.)

Why is the mRNA not damaged at -70 C temperature Corona vaccine?

Actually they use Sucrose as cryoprotectant.
https://medicalsciences.stackexchange.com/questions/25289/why-use-sucrose-rather-than-glucose-in-an-injectable-vaccine/25290


text:
How is the GenBank used in typical biological research?
How is the GenBank used in typical biological research? According to the GenBank statistics, the database contains about 100 million sequences. I find it difficult to understand why is all that data needed. To make the question less broad, what are the most common use-cases? Check if someone already sequenced DNA of some plant or animal?

Can you please specify your question? At the moment its quite broad...

Any better now? I would be interested what are for example the three to five most common use-cases.

This is a bit like asking what are the top uses of a library. The reasons are myriad.

You need to do some basic research on Genbank.

Go to Google Scholar. Enter "Genbank" into the search field and press return. Limit the results to 2013 and later (left side of the results).  Skip the few entries that say only "GenBank." Browse through the pages and pages of search results to get a feel for the many ways that GenBank is used in scientific research. It's used from everything for phylogenetic analysis (relationships among organisms) to determining protein structure and so much more.


text:
Organisms in food deposits
I have just discovered that my kitchen sink pipe has been leaking for quite some time (possibly months) which has resulted in water and food deposits collecting in my cupboard.
I smeared some of the residue onto a slide and looked at it under my microscope. I could see a large number of translucent organisms (visible at 40x magnification, they are roughly 100 µm in length). They all appeared to be of the same species although they varied in size and developmental stage. The 'adults' are quite long and look similar to maggots; they scrunch their bodies into balls and then stretch out in order to propel themselves.
Unfortunately I lack the equipment to take a photo of it but here's a rough sketch of what it looks like moving to the right:

Don't take the features too literally.
Can anyone hazard a guess as to what it might be?

Can you make an image of this organisms?

@Chris I have updated my question.

http://www.colorado.edu/eeb/EEBprojects/FiererLab/Flores_etal_2012_kitchens.pdf

I cannot help to answer your question, but I admire your action of taking swabs instead of freaking out after discovering this fact.

It seems like Euglena but I need more parameters than what you have provided.

(source: eastmarinedrive.com)
https://www.youtube.com/watch?v=ZHZZKwrYm4g
you can narrow it down by this:
http://goo.gl/XTEZ7S
Or
You can find them in commonly found microorganism in kitchen:
http://www.colorado.edu/eeb/EEBprojects/FiererLab/Flores_etal_2012_kitchens.pdf
Or
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0078866.t001/largerimage
Source: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0078866

Euglena are certainly very similar! Although they don't scrunch up and move like those that I observed. I will look through this list when I get some spare time, thank you.


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What regulates the timing of the motion of molecular machines during DNA Replication?
This question is about this video I found on Youtube. I just want to know what is the mechanism which regulates the timing of motion of the parts of these molecular machines.
I know that those big molecules moves using mechanical energy from ATP molecules and take advantage of the electric forces specially the hydrogen bonds, they also take advantage of the Brownian motion of water molecules around them.
From what is see, the green floating molecule triggers the whole process by attaching the purple one, then some electric equilibrium is disturbed so the {purple+green} molecule is attracted by the horizontal cyan molecule...etc.
But the problem is: does the green molecule attaches to this group in a periodic timing ? or in other words does the Okazaki fragments have the same lenght evertytime ?
Thank you in advance !

http://www.singlemolecule.nl/publications/vanOijen_AnnuRevBiophys_2010.pdf

That's a pretty neat video, I'll just give you some background information first. It's an illustration of the "trombone model" of DNA replication. The darker blue molecule is helicase, it unwinds the DNA and facilitates translocation (this is an ATP dependent process). The dark purple molecules are DNA polymerase, they catalyze DNA strand synthesis (an NTP dependent process) using an ssDNA template and 3'-OH primer (the primer:template junction). The green circular molecules are sliding clamps, they increase the processivity of DNA polymerase. The light purple molecule is the sliding clamp loader, unsurprisingly it loads the sliding clamp onto the DNA (ATP dependent). The light blue molecule is a flexible linker that connects everything together. The other green molecule (the one that contacts helicase) is primase, it synthesizes RNA primers (which contains the 3'-OH initially used by DNA polymerase).
Certainly intermolecular forces play a significant role in this (and every) biochemical process, but I'm not really sure what you're talking about when you're describing electric forces and Brownian motion.

Anyways, the answer to your question is no, Okazaki fragments do not have a fixed length. DNA synthesis, as mentioned above, occurs only by adding NTPs to a 3'-OH primer. Thus the length of Okazaki fragments is dependent on the spacing between primers on the lagging strand. This is dependent on when primase binds which in turn is dependent on primase concentration as well as its binding affinity with DNA and other replication fork proteins (especially helicase). High concentration and/or high affinity leads to a higher binding frequency and therefore shorter Okazaki fragments. The opposite is true for low concentration and/or low affinity. Note that most (or all?) primases have some degree of sequence specificity which means that specific DNA motifs will increase binding affinity. For example, Escherichia coli primase (DnaG) recognizes the trimer GTA.
This process also requires some degree of coordination between leading and lagging strand synthesis. Primer synthesis and DNA polymerase recycling on the lagging strand is much slower than the continuous synthesis on the leading strand. It has been suggested that primase acts as a "molecular brake" by halting the replication fork during primer synthesis to prevent the leading strand polymerase from rapidly outpacing those on the lagging strand (Lee JB, Hite RK, Hamdan SM, Xie XS, Richardson CC, van Oijen AM. 2006. DNA primase actas as a molecular brake in DNA replication. Nature. 439(7076):621-624.).

Thanks !! That makes sense. I mean by electric forces the forces between molecules because molecules contain electrons and protons. This is interseting because if you know the electric structure of a protein very well you can know how its shape will change after a protein or even an electron attaches to it. I mean by the Brownian motion, the motion of water molecules which constantly collide with the protein, I think it plays a role in the stability of the movement of molecular motors. Thank you again !!


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Is this description of etiology of celiac disease correct?
There is a detailed and, to my inexpert eyes, plausible description of the etiology of celiac disease and other autoimmune disorders posted here: http://no-gluten.org/CeliacDisease.htm
Is it is at all accurate? If any of it is speculative or incorrect, which parts are those? Red flags to me are that it cites no sources and is much more detailed than any other description of celiac that I've seen. But, again, it does coincide with what little I do know of human immune biology.


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How can I easily distinguish between eukaryotic and prokaryotic cells using flow cytometry?
I am trying to count populations of cells in a co-culture. One organism is Pichia pastoris and the other organism is a gram-negative bacterium. Pichia stains gram-positive using crystal violet and the bacterium is negative. These two populations are reasonably distinct in front and side scatter but not so much that I can gate the entire population. I can pick a region in FSC-SCC for each organism that I know will only include that organism, which is 'good enough' for my purposes, but I'd love to know if there is a quick, easy, cheap way to distinguish these two populations more decisively. To clarify my requirements:

Cheap: Ideally something widely available in the price range of <$1/sample e.g. Hoechst/Van-Bodipy/WGA-647
No processing steps: I just want to add the dye/stain to my sample automatically using the flow cytometer before running the samples

Things I have considered but have ruled out:

Antibodies: They are too expensive for my case. I would need a custom conjugated antibody or to add processing steps between primary and secondary antibody that is too complicated.
Tracker/tracer dyes (add to one cell population before mixing the co-culture together): Also expensive, and I will probably want to track my population over more generations than most of these dyes work for.
Intracellular markers that require permeabilisation: I don't want to do any processing

Things I'm considering and would welcome input on:

Conjugated lectins, specific to glycoproteins on Pichia pastoris
DNA dyes, using the fact that Pichia genome is approx 2x larger than the bacterial genome
Differing autofluorescence: There's nothing obviously different here from my data so far, but I will go back and tweak the voltages etc. if this is a very promising avenue
Any combination of stains/techniques that are not specific alone, but then the populations can be separated using e.g. PCA

Is there anything out there that will work for me? It seems to me that the cell types are so different there must be an easier solution here than expensive antibodies etc. An answer of "No" would be just as valid as yes! I can continue just using front and side scatter if the only solutions are going to be too complicated.

Acridine orange might work for nucleic acid content. You might want to check out the Molecular Probes Handbook for some options Ch8 and 15.

Ok to kill the cells you are counting?

@PolypipeWrangler Sure, but only if it's not too complicated/doesn't involve too much waiting

What about using cell size? The prokaryotes should be much smaller.

@Chris Yes, I do see a difference in forward scatter on the flow cytometer, which correlates with cell size, and it's 'good enough' when combined with a difference in side scatter. I'm wondering if there's a third dimension that I can separate them on that will make it totally unambiguous.

If you kill one population, the dead cells will be easily permeable to various dyes.


text:
Is the molecule nitric oxide responsible for healing blood vessels?

Is the molecule nitric oxide responsible for healing blood vessels?
How does nitric oxide heal the blood vessels?

I watched a documentary about the healing effects of nitric oxide. In the video I saw a cardiologist show an X-ray picture of one of his damaged heart blood vessels, and then another X-ray picture showing the same heart blood vessel completely healed. He claimed it was due to a radical change in his diet of consuming lots of nitrogen rich vegetables which the body in turn converted to nitric oxide. Is this possible?
Sources :
The original source was the youtube video Forks Over Knifes, however it was recently taken down. I have provide the following links which provide a little bit of information :
http://www.happyhealthylonglife.com/happy_healthy_long_life/2010/06/esselstyn-session.html
http://www.happyhealthylonglife.com/happy_healthy_long_life/2010/12/no.html
Dr. Caldwell Esselstyn was the one who made the statement about heart health and nitric oxide, also showing the xray pictures of one of his colleague cardiologists in the documentary.

Can you provide a link to that documentary? NO causes vasodilation, I have not heard of its role in regeneration. And simply eating nitrogen-rich food will also not increase NO (its synthesis is not limited by the availability of nitrogen)

@WYSIWYG The documentary is called Forks Over Knives. Thanks for the response.

Here's a review published in Nature, about the regenerative role of NO, followed by an application in 2012 to wound healing.
http://www.nature.com/aps/journal/v26/n3/full/aps200541a.html
http://www.nanomedjournal.com/article/S1549-9634%2812%2900090-1/abstract


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Do Parasaurolophus have hands with fingers to grab?
http://en.wikipedia.org/wiki/Parasaurolophus#mediaviewer/File:Parasaurolophus_cyrtocristatus.jpg
I cannot tell if the hands have fingers strung together to form a hove, or fingers to grab. I have seen so many pictures of Parasaurolophus standing up, suggesting possible other functions of the arms and hands. I think their arms are long enough to reach their mouth. Ironically, I have yet to find any literature talking about their hands, but lots of literature talking about their resonating chamber. Do Parasaurolophus have hands with fingers to grab?


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In our 23 chromosome pairs, do the 2 members of the pair have distinct or virtually identical sequences?
I understand that we have 46 DNA molecules in the nucleus of our cells, arranged in 23 pairs: 22 autosomal and 1 sex chromosome pairs.
I have read in different sources that the pairs contain nearly identical members, excluding any mutations. I have also read that the pairs contain 1 member we inherited from our mothers and 1 we inherited from our fathers, which are different due to inheritance.
This seems contradictory, given that genealogical companies match up on the differences on these chromosomes.
My understanding was that meiosis creates sperm and egg cells that each carry 23 chromosomes - they are haploids. During the first steps of meiosis that creates the reproductive cells we have a combining of the parent's chromosome pair from their parents to create 4 daughter cells, each independently viable, where the recombination of the chromosome pair has occurred at somewhat predictable spots (for you perhaps :-) ) and that these spots can be related to genes. It is this step that give us our genetic variation between siblings for example. A new person's DNA is partially formed from any one of these highly varied daughter cell possibilities.
Fertilization combines the reproductive cells to produce the 46 chromosome zygote with is again diploid.
I think this understanding supports the second interpretation that our chromosome pairs are not 2 nearly identical DNA molecules but are distinct.
Have I got this right? Is there a missing process or a misunderstanding in my interpretation?

I think there is a bit of confusion about what is meant by identical/distinct.  Two genes could appear identical, or nearly so, yet have different functions, say by just swapping a couple of nucleotides.

I am referring to the sequencing of SNPs, not to the function or expression of those sequences. Do both chromosomes in a chromosome pair have nearly identical sequences of ACTG excluding differences due to sequencing techniques and/or trivial transpositions of the sequence number up or down.

Could you elaborate on why you think the two sentences are contradictory? Nearly identical does not mean completly identical. SNPs are real single letter diferences between individual chromosomes - and not just differences due to sequencing technique. Genes are just small functional sections of the long chromosome sequence. What has been explained to you about sequences of genes does directly apply to sequence of chromosomes. The diferences are small and yet very important.

@BagiM One source stated that the two chromosomes in a pair will be identical except for the possibility of a very small number of snp differences could be due to mutation only. I believe this to be contradictory to the statement that within a pair one chromosome comes from the maternal source and one from the paternal source as there is no reason to think the donors would contribute identical dna.  I suppose what I am trying to ascertain is if there is a process somewhere in the fertilization steps where the donor chromosomes recombine, e.g. mix, before they form the new individual's dna.

Homologous chromosomes (those that are paired up), excluding the sex pair are almost identical in size, shape and genes (members as you called them) present in them.
Genes determine traits and each homologous chromosome controls the same traits. The level of identity of a gene inside a population varies between genes. There are very conserved ones that do not change even between humans and yeast and others that vary alot event inside a species. This changes can be small in sequence length, a simple base (letter) swap or one deletion, and have a huge effect on the traits. This is how chimps and humans are very different but share 98.6% of their genome and humans are very similar and share 99.9% of their genome.
In summary, on the bigger scale homologous chromosomes are very similar (size, shape, traits inside), on the smaller scale homologous chromosomes have small changes that affect greatly.
EDIT: elaborating on when recombination occurs.
The zygote do not recombine the chromosomes it gets from it's parents. Each parent chromosomes recombine in the first step of meiosis. We do not expect them to be identifcal on the gene level (or the SNPs level). Each chromosome represent each paren't genetic material.
Lets look at parents A chromosomes
parent a Paternal: a-b-c-d-e                       parent b Paternal: a-B-c-D-e
parent a Maternal: a-B-C-D-e                   parent b Maternal: a-b-C-D-e
possible recombination  (a)                       possible recombination (b)
(a-I) a-B-C-d-e                                         (b-I) a-B-C-D-e
(a-II) a-b-c-D-e                                         (b-II) a-b-c-D-e
Now the child can be any of the 4 possible combinations (and obviously all other not shown). Let's say (a-I) and (b-II). This chromosomes do not recombine until they get to the meiosis stage.

I am asking about an individual, not a population. I do not use members to refer to genes, I use members to refer to the individual chromosomes within a pair. I am also not asking about the impact of a mutation of a gene's base pairs.

@Stephen  Is your question "In each pair of chromosomes, are the parental and maternal chromosomes nearly identical or very distinct?". If you want an answer about an individual we need background about him, otherwise he is merely a random sample from population with every possible pairs of parents. I think my answer shows that chromosomes are almost identical on the macro scale and slightly distinct (but not much) on the micro scale. If you elaborate more I could expand my answer

I think that if you need to know specifics about an individual to answer this question then the question is not clear as I am asking about the typical results of the general reproductive cycle.

This is an attempt to understand at very high level what the strands of DNA in each chromosome of a pair are expected to be. To reword it, looking at the sequences of SNPs of an individual's DNA do we expect the sequences of the 2 chromosomes of a pair to be (nearly) identical, e.g. because the maternal and paternal donor DNA was combined and then duplicated, or do they remain distinctly identifiable as maternal and paternal complete, undivided chromosomes?

I think you may have been trying to answer "in a chromosome pair is the location and function of genes identical on each of the 2 chromosomes", which I understand to be "yes".

@Stephen I expanded my answer, maybe know it is clearer

Between what you have added, and what was posted by swbarnes2 in their answer, I believe I now understand my confusion. The overall number of differences between the two donors of chromosomes will be small compared to the overall size of the chromosome. Enough to be distinguishable for genealogical purposes, and to affect the expression of particular traits, but ultimately small in number, thus the "nearly identical" comment is in fact correct and not in contradiction with the other interpretation. Thank you for your effort in making this clearer.

I have read in different sources that the pairs contain nearly
identical members, excluding any mutations

"Nearly" is doing a lot of work there.
You have a copy of Chr 1 from your father and a copy from your mother.  Your copies might have mutations as compared to your parents that happened either in you as you were developing, or in the gametes as compared to the stem cells they originated from, but most of the differences between your maternal copy and your parental copy were caused by long ago mutations that have been in your parents' families for generations, (we'd be more likely to call those polymorphisms, rather than mutations) not mutations that just happened.
Even with those differences, your two copies of Chr 1 are at least 99% identical.

I think now that you've hit on what I needed to understand. Although there likely are differences caused by who we inherited the chromosome from, which are useful to understand from a genealogical point of view, these sequence differences are derived from, to use your number, about 1% of the matches, thus, "nearly" could be considered accurate, "from a certain point of view".

Two major resources of genetic variation between siblings:
1- Random segregation of chromosomes during meiosis I. consider only mother: the mother has 46 chromosomes, 23 from grandmother and 23 from grandfather. during meiosis anaphase I, pairs of similar (homologous) chromosomes are segregated randomly. finally you have  egg cells with 23 chromosomes, some from grandfather and some from grandmother. this can make 2^23 (8 millions) different combination of chromosomes for egg, and 2^23 for sperm and 2^46 (7000 billions) different combinations totally.
2- Recombination of homologous chromosomes during meiosis I. which is exchange of chromosome pieces during meiosis I metaphase, and I see you know enough about it.
Also, there are other resources of variation which are out of the level of this question.

Hello and thanks for answering. I do understand the points you've made in point 1. I am curious about the other sources of variation if you care to leave a reference. I think my confusion arises in the fertilization step - whether or not the donor chromosomes "pair up" but remain intact as one source indicated, or if the donor chromosomes undergo random segregation and combination akin to point 1, and then replicate before forming the chromosome pair of the new individual. My original understanding had been the former.


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With an mRNA-vaccine, would it hypothetically be possible to get that sequence transcribed into their genome for people who suffer from a retrovirus?
I recently read a bit about the mRNA-vaccines for COVID-2019. I fully understand that mRNA cannot enter the genome of a healthy person as they lack the required reverse transcriptase to transcribe RNA back into DNA. This made one question pop up in my head, though:
What about the people who do have reverse transcriptase in their body? As far as I understand it, a retrovirus like HIV does express the required proteins to form reverse transcriptase as it's part of the virus strategy to integrate itself into the human genome.
Wouldn't that mean that an HIV-positive person, upon being vaccinated using an mRNA-vaccine, could theoretically end up having the RNA-Sequence of the vaccine transcribed into their genome if reverse transcriptase is present in their cells at the right moment? Or am I missing something? Would that mean that the COVID-vaccine could essentially become the artificial equivalent of an endogenous retrovirus, even possibly immunizing future generations?

It’s relevant to note that all humans have reverse transcriptase from retrotransposons and mRNA can be reverse transcribed and integrated into the genome (this the mechanism by which processed pseudogenes arise).

https://medicalsciences.stackexchange.com/questions/25392/why-is-the-new-mrna-vaccine-unable-to-modify-human-dna

https://skeptics.stackexchange.com/a/53027/155

"if reverse transcriptase is present" - Case is use of rev. transcr. from HIV virus by CoV. There lies some analogy in  the fact that LINE1  which is a retrotransposon mentioned by canadianer above is being used by ALU elements to have themselves integrated.

Interestingly, there's recent news we may all have some reverse transcriptase activity and in some people it leads to serious disease.  The specificity of that reverse transcription is not yet known, but HIV reverse transcriptase is going to require a primer binding site - basically some lysine tRNA sequence - to get started.  Of course, with low odds, there may be some conceivable way to get around that by mutation, template switching, etc., but I don't know of evidence it happens.
Reverse transcription of random RNA transcripts (including the genomes of mRNA viruses that infect us) is surely a theoretical possibility, but we should bear in mind how rarely this must occur (otherwise, our genome would be even more overflowing with spam than it is).

The scientific PNAS article underlying the reverse transcriptase press release is available here.

Reverse transcriptase is not the whole story as I learnt. There must be "integrase" or the like to put it in (so to say). What is known about "free floating" DNA - retrotranscribed or not - "going into" host cells DNA strains? Any idea? Maybe that is rather unknown, do you know? I refer to the mechanism of integration in a narrow sense; how is viral DNA being put into (so to say) host DNA, if there is no integrase?

@Peter Bernhard - getting the DNA into the cell is "transient transfection", while integrating it is "stable transfection".  See https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8067914/ .  I don't deny that, in the absence of a viral vector or some other trick, stable transfection of random DNA in any given cell is very rare.

"...how rarely this must occur..." If there were a working principle that integration kills the infected cells (e.g. not by apoptosis, not like cytotoxic t cells) integration might be more common, and the less searched for (as that would be a way to get back up again).

@Mike Serfas Thank you for providing the link. You name it:  "The specificity of that reverse transcription". I think it would be interesting to read more on that issue in your answer. Provided link refers to my comment above which refers to Canadianer's. That link refers to ALU as one, special specifity of LINE1, I think. Are there any others or pertaining sources you know of?

"Even in non-retroviruses that lack integrase, such as the adenoviruses, integrase may be expressed through genetic engineering technique", this struck me first in the link you, Mike, provided above. What is the natural mechanism for integration of DNA, that comes in as such, not as RNA? Counterintuitively, integration of DNA suddenly seems more intricate than "integration of m-RNA" (because the enzymes are combined or not?). From your paper: DNA viruses, how do they integrate, in case they do?

From first link in your answer: "The buildup of a certain type of DNA in the cytoplasm, Alu, contributes to macular degeneration, the researchers found. This buildup appears to kill off an important layer of cells that nourishes the retina's visual cells." - This seems higly relevant in the context of the question, but not only, as it leads to some hypothesis that "integration kills" infected cells: no need to inherit embedded vaccine... Again: if integration kills, that's good if it's infection?

The first link you give is good. You point at some issue you should elaborate on, as it's about "specifity" you speak of: They say, "Different retroviruses use different host tRNAs as primers. HIV-1 uses Lys3." How can specificity lie in such thing as  tRNA. t for trivial? Sure there is some basic knowledge underlying. - If possible, more on "promoting" integration specifically, but, even more so, more on unspecific integration and if it exists. Thank you.

Is, in your opinion, specificity of insertion, of integration in a narrow sense, no issue? The question refers to transcription "into" the genome. So even if by unspecific HIV-retro-transkriptase were produced CoV-DNA that couldn't be inserted because of lack of integrase? ("transient DNA")
The paper linked in your answer surprisingly does not tell how insertion by HIV is produced. There is no integrase. Thus, HIV looks like illustrating some paradigm unknown: specific DNA may integrate into host DNA because it's specific, No enzyme needed. That cannot possibly be? Some other answer on that?

I think your answer is way not explicit enough about the rather exciting "result" the study linked to in you first sentence offers. All this may go unnoticed to people like me who think they knew already. Please be more elaborate about the HIV enzyme being blocked, thus having blocked not insertion of HIV RNA/DNA, but of ALU RNA/DNA. Again, retro-transcriptase of HIV was found to work on something totally different? Thus, "...to get around that by mutation, template switching, etc.," seems obsolete, not necessary.


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Do species other than humans have distinct daily feeding patterns?
I have a general interest in complex adaptive systems and I have found that nature and the organisms within it is a perfect natural case of a rich adaptive system with a lot of possibilities for gaining insight in general about the nature of complex adaptive systems.
My mind accidentally started thinking about the common human feeding pattern breakfast-lunch-dinner and I sought reference points in nature, realizing that I'm not aware of any specific cases where the feeding pattern of animals other then humans follow a distinct pattern, in contrast to a constant, stochastic or mainly opportunistic search for food.
In the case of humans there is probably a very strong cultural cause for our very distinct feeding pattern, but that is not necessarily to say that these patterns only can occur in species with a highly developed culture.
How does the scientific body of observations look like here? Is there any research or empirical observations about the feeding pattern of animals?
For example, I would of the top of my head assume that some common reasons for these patterns to develop could be connected to e.g. the 24h circadian rhythm, dependencies to availability of food, or internal dependencies on behavioural organization in social species.
Of course it's likely that many organisms do not have the luxury of spending a significant time on other activities then acquiring food, but nevertheless we can see that some animals have evolved into a situation where they don't have to constantly be in the search for food, but instead can spend time on other activities increasing their fitness, like engaging in social interactions, searching for and seducing sexual mates, exploring their environment and migrating, building nests and so on.
To clarify what kind of observations I'm imagining could happen, take these speculative examples:

Some species of birds have a significantly higher feeding activity in the morning, where they after a night of inactivity have depleted their daily energy resource and when the insects, their main source of food, starts to activate after a cold night and are still cold and slower/easier prey. After this the birds only have an opportunistic approach to feeding which is enough to satisfy their energy need, and they spend more energy on pruning, calling for potential mates and engaging in territorial battles.

Many primates engage in collective feeding sessions where they as a group travel to a known area rich with food where they spend a couple of hours before they retreat back to a different location for socializing and digesting the food. One reason for this behaviour can be that there is a high risk of predation at these food-rich areas, as the predators learn that these places are frequently visited by prey.

Feline predators on the savannah are usually concentrating their hunting in the night as the darkness gives them an advantage of stealth and surprise. This is why they in daytime instead spend a considerable amount of time on resting, engaging in activities regarding social hierarchies, order and bonding with the pride, while most often only opportunistically engaging in hunting.

Do we have a body of knowledge here?
While it would be close to hand to start trying making lists of observations like this, which certainly would be interesting in itself, the intention of this question is to get a good overview on the subject. Are patterns like these common or uncommon? In the cases where they are found, what are the common factors and what can be identified as the underlying causes?

I'm not sure what you're asking here. Wild animals eat when they can secure food. Most of the time, the food supply is limited enough that they don't have the option of "breakfast, lunch and diner"; in that case, the predator population would increase to the point of making the prey relatively scarce once more. Many herbivorous animals spend most of their awake time eating (or traveling to where food can be found). Are Jane Goodall's decades in the Gombe Stream National Park empirical evidence? I'm just unsure of what you want here.

@anongoodnurse Yes, I know that this is the common view on animal feeding: They eat when they can. But I think that this is a too simplified view, and sometimes just wrong. Animals have to do other things than eating, like seducing potential mates (which can be a quite big thing, including very expensive fights), resting and sleeping, engage in social activities like play and bonding and so forth. And even when it comes to feeding, when looking at the big predators we know for sure that they can sustain quite a while on a big meal, leaving time to do other things.

@anongoodnurse So what I'm looking for is cases when we have a distinct daily feeding patterns in animals, like in the cases of humans and our breakfast, lunch and dinner, or something similar. Observations from Jane Goodall would surely be considered empirical data, if not evidence. And on noting that, great apes would probably be good candidates that might have developed distinct feeding patterns I assume since they are very social.

"But I think that this is a too simplified view, and sometimes just wrong." I can say that about climate change, but that wouldn't make me correct. "when looking at the big predators we know for sure that they can sustain quite a while on a big meal" - exactly. It takes a lot of effort and some luck (they are not 100% successful) to bring down a gnu/other, so that prevents them from a breakfast/lunch/dinner pattern, as does most of nature. Feeding is to a great degree dependent of the availability of food, which varies.

@anongoodnurse Your reference to climate change denials seems a little strange, maybe we misunderstood each others somewhere. What I meant was that it's clearly the case that many animals do other things than search for food, thus leaving the possibility that there in some cases might be the case that some animals develop an daily schedule or pattern in their feeding habits. Cases like that would be what I'm looking for here.

@anongoodnurse And I'm totally with you that many animals might not have the luxury of arranging their feeding behaviour like this, but I'm searching for those that do.

unclear? This is pretty clear!

Since it apparently was unclear enough to have it temporarily put on hold, I have now rewritten the question for extra clarity.

For me it was clear enough, but it needs some research to answer...

What makes you think humans have distinct feeding patterns, 3 meals a day is a cultural practice and in no way universal in humans.

Preamble
This is a very interesting question one which I don't immediately know an answer to. I think this overly succinct answer and the fact nobody else has answered highlights the degree to which the age old darwinian assumptions play a role in the field.
Zoological POV
I'm not an expert in this area so I went to a zoology lab technician and this is what they had to say (I'm paraphrasing here):

Most animals are opportunistic and can't afford the luxury of a late
  brunch... The only animals that spring to mind that appear to 'plan' for
  meals are the hoarders (squirrels for example). But they don't
  typically cache food in the same way we would for a weekly shop, but
  do so for fear of food scarcity (overwintering, rival competition);
  Not unlike the mad dash for bread and loo roll when it starts snowing
  slightly!

Maybe animals do have their diet set to a circadian rhythm, or maybe not. We can't say for sure. Darwin implied, even a peaceful meadow is full of starving ravenous animals clinging to survival. There is no real time for luxury. If food is there, they eat it. Many animals don't even get full the same way we do.
Scarcity of Literature
The problem lies in that there is no body of literature around animal eating times since animals seldom have enough food in their natural environment to monitor any regularity. If you want specific questions on a particular species for optimum feeding times, I would recommend opening another question as lab animals do have recommended diets. Many predators have optimum hunting times (for example nocturnal, or dusk). However one could argue this is to do with success rates/effective hunting strategy and not necessarily scheduled eating times.

In reading the reaction from your lab technician I'm thinking that maybe it was a bad choice of me to make a comparison with our human pattern in this question, risking the appearance of someone trying to apply human attributes to animals, and in putting focus on whether animals consciously "plan" their daily food intake accordingly to their personal preferences. I appreciate your answer even if it did not provide deeper insight, and I take the opportunity to once again suggest that food is a very important resource, but for some "lucky" species maybe not the only one worth spending time on.

And maybe one thing to consider here could be the possibility that in some cases for some species, focused and active search for food is much more efficient than a purely opportunistic approach. Thus again opening up the possibility for well partitioned activities and patterns therein, I presume.

Amended my question to highlight the scarcity of literature. As it stands, the question requires very specific knowledge over a vast range of zoological niches. If you need a specific species dietary requirements, I would ask in a separate question.

Of course there are nocturnal and diurnal feeders. Insectivorous bats get active during the dusk (as I have observed) but are not so active later in the night (perhaps because of fall in temperature and low insect activity).

@WYSIWYG Those daily patterns arise not out of choice, but out of an inability to hunt effectively at other times. A list of the species that behave like this might be what Alex wants to know, in which case the question is far too broad. Are you aware of any literature in the field that provides a concise review?

@GoodGravy Nope. I have not really studied animal behavior. But I had heard some talk about two kinds of feeding behavior- one is, as discussed in comments and your answer, the opportunistic: eat as much as you can when you have the chance. Other one is to have a fixed eating pattern (no overeating) and big herbivores like elephants do that; the term that the speaker used for this is "metabolically regulated" (if I am not mistaken). This I heard some 3 years back and I didn't read up much on it later.


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Why is graft-vs-host so selective against phylogenetically close cells?
Is there a well established explanation for the phenomena that graft-vs-host is so much more selective against phylogenetically close cells? See historically significant references below,
"This type of aggression of the immune system is thus particularly directed against allo-antigens and is much less in evidence across two animals species. “ - Jerne, 1971
"Normal lymphoid cells obtained from animals that are phylogenetically unrelated or only distantly related to the chicken do not initiate graft versus host reactions when introduced into chicken embryos. " - Lafferty, 1968
References
Lafferty, K., & Jones, M. (1969). REACTIONS OF THE GRAFT VERSUS HOST (GVH) TYPE. Australian Journal of Experimental Biology and Medical Science, 47(1), 17–54. https://doi.org/10.1038/icb.1969.3
Jerne, N. K. (1971). The somatic generation of immune recognition. European Journal of Immunology, 1(1), 1–9. https://doi.org/10.1002/eji.1830010102

Since this has gone unanswered, I'll give my best guess. My guess is that closely related MHC* can still be recognized by CD4/CD8 (while not in distant relatives phylogenetically), but, the MHC + eventual bound peptide will not be recognized as self (with or without bound peptide), since its structure may differ even when binding self-antigen peptides that were exposed to T-cells during central tolerance "traning".
I am very intersted in what the established explanation is including references, and invite better answers if there is competence to produce that.
*in the context of the question, i.e., at species level, within species sufficiently close MHC genes are not attacked at all and compatible.
I'll attach potential reference to my guess that ability to recognize MHC as... MHC, decreases with phylogenetic distance,
Vignali, D. A., Moreno, J., Schiller, D., & Hämmerling, G. J. (1992). Species-specific binding of CD4 to the beta 2 domain of major histocompatibility complex class II molecules. Journal of Experimental Medicine, 175(4), 925–932. https://doi.org/10.1084/jem.175.4.925
that references this,
Lamarre, D., Ashkenazi, A., Fleury, S., Smith, D., Sekaly, R., & Capon, D. (1989). The MHC-binding and gp120-binding functions of CD4 are separable. Science, 245(4919), 743–746. https://doi.org/10.1126/science.2549633
that says this,

"although human and mouse CD4 share a high degree of amino acid sequence identity (19), the murine homolog does not bind gpl20 (11) and does not interact with the human class II MHC molecule HLA-DP as assessed by functional and adhesion assays (20). "