texts: Identification of black growth on onion skin

texts:
I have encountered this black-colored growth on onion skins a lot. It seems to develop over the course of weeks and I have rarely, if ever, encountered the material on fresh ones. If I peel the onion and it streaks the onion flesh, it appears, dark blue-ish. It looks like a fungus, perhaps a bacterium, but I am unsure. It is often found 'hiding' under the outer layer of skin on the deeper skin layers. In the photo the outer layer of skin was peeled off. It never seems to invade the edible parts below, though.

The pictures below are standard white onions from the local supermarket in Canberra, Australia (Canberra [Australia's capitol yes!] lies between Sydney and Melbourne). I must admit, I don't know if they are imported. The pictures below were taken mid-winter. Temperatures in our kitchen plummet during the day because of bad insulation. In the evenings and weekends it's room temp with heating. The onions are stored in the dark, in a kitchen cabinet. Humidity is low and mostly the days are dry and sunny. However, we cook in the kitchen so at times there is plenty of moist.

Also, I wonder, would it be harmful? No self-help medical issues here, I always wash and fry/cook my stuff and no issues whatsoever, just curious.

I understand there is little to go with. However, a general genus or group of fungi would already be cool. I googled and sought for images to no avail.


texts: Why do marmosets have claws when most primates don't? What is the structure of their hands like?

texts: The majority of primates have really thick nails, though not as broad or flat as humans'. However, marmosets have 18 claws, and only their big toes have nails. What differences in evolutionary pressures caused this? And how does the structural relationship between marmosets' germinal matrices and their distal phalanxes differ from other primates, so they can grow claws?


texts: Why are these trees leaning, but no trees around them are?

texts:
This was observed in Florida.The trees on the left have a distinct lean to them, but none of the other trees in the area are leaning, why is this?

I'm not sure what other information is pertinent or what else I should look for.


texts: What metabolically happens when an egg fuses with the nucleus of a somatic cell

texts: In stem cell biology, it is recognized that embryonic stem cells are transcriptionally inactive for the first 3 days of development. However, during somatic cell nuclear transfer, the nucleus is likely to include various polymerases and RNA both coding and non-coding. Does this affect the success rates of cloning?


texts: Validation of houskeeping genes in a mixture of cDNAs of two species

texts: I have a parasite sample (mixed with host blood) and I need to check gene expressions of parasite using relative quantification (RT_qPCR). For this, I need a good housekeeping gene. I chose 10 genes (suggested as housekeeping) that I need to validate and after choose the most stable one(s). My problem is that my parasite cDNA is mixed with host cDNA and it is impossible to separate them or count the parasite. I do not know how I could choose the best housekeeping gene in this case? I do not have the real amount of parasite cDNA used for qPCR, and I do not have any good internal control. Basically, it is circular problem: In order to validate my target gene I need a good housekeeping gene for internal control, but I do not have an internal control to make relative quantification of my housekeeping genes and to chose the best one. Could you please suggest any study or method that deals with such a case?


texts: Correlation of non-coding DNA with coding DNA

texts: I sequenced the first exon of the MC1R gene of 15 labradors (genomic DNA) to look for the loss-of-function mutation (C.916C>T) and as expected, it was where it should have been (916th base pair). As i compared the SNPs with the phenotype of the dogs i found a second mutation that also correlated 100% with the phenotype of the dogs. The mutation is located 45 base pairs before the start codon of the first exon. As far as i'm concerned the region that lies right before the first exon should not be part of the coding DNA. If so, why could this mutation have been evolutionary conserved? Or am i simply mistaken in that the mutation before the first exon could also be part of the gene for MC1R (meaning there would be an intron before the first exon which i'm not sure if that's possible)?


texts:
I assume that all carcinogens must be mutagens, but I've read that this is not the case. However, I can't find any good examples or an explanation of why it is not the case.

How can a non-mutagenic agent be carcinogenic?

How can something lead to uncontrolled division of abnormal cells without changing the genetic material of the organism?

The only explanation I've found is that normal replication of genetic material during normal cell division includes occasional errors, so any physical or chemical agent that simply speeds up cell division will increase the number of errors per time and can therefore be considered a potential carcinogen even though it is not directly mutagenic.

But that example doesn't satisfy me because such a compound would not increase the number of errors created per cell division, but is that the only way something non-mutagenic can be "carcinogenic"?

I've also read in This Question that Alcohol is an example of a non-mutagenic carcinogen because Alcohol does not damage DNA, but I think that's not accurate because I've also read that Ethanol is mutagenic via its first metabolite, acetaldehyde, or are they just using wordplay to say that Alcohol is not mutagenic because only its first metabolite is?


texts: In Japan, the official average body temperature is 36.0 °C. Why so different from that of Europe?

texts:
The Japanese Wikipedia states that the average human body temperature is 36.0 °C (here,"ヒト").
The statement references the data from the Japanese government.

Actually all of my Japanese friends think the same.
A body temperature of 37.5 °C is considered a serious illness in Japan, justifying absence from work.

Most other countries' sources cite 37.0 °C as an average.
Is there a biological explanation for this apparent discrepancy?


texts: Is there a homeostatic setpoint for number of hours of sleep required by a human?

texts:
I've heard this TED.com talk about dieting and it mentions that there's a very definitive setpoint within the human brain about how much a human should weight. The speaker mentions that after as much as 7 years, the body returns to that homeostatic weight setpoing.

I'm interested if there's something similar for sleep - is there a homeostatic setpoint that says that a human should sleep X hours out of 24?

In this example by homeostatic I mean:
If the sleep setpoint is at 9 hours, the human can sleep for 8 hours for some time, but when the artificial sleep restriction is removed, the human would return to 9 hours of sleep naturally.


texts: Is there any convincing evidence for the existence of nanobacteria?

texts:
The existence of nanometer scale microorganisms has been proposed and used explain several phenomena  including morphological structures in a martian meteorite (ALH 84001) and implication in the formation of kidney stones (1).

Is there now any consensus in the biology community whether these are biotic or abiotic in nature?

(1) Kajander EO, Ciftcioglu N (1998) Nanobacteria: An alternative mechanism for pathogenic intra- and extracellular calcification and stone formation. Proc Natl Acad Sci U S A 95: 8274–8279


texts: Compare and contrast "Rubisco activity" and "assimilation rate" (is there a difference, and if so, what is it)?

texts:
I am confused about the variable "RuBisCO activity". How is it measured, and is it any different from the net assimilation rate?

Based on some background reading (e.g. Kling, 2008; Lambers et al 2011)  the only difference that I can find is the units. Both would have "carbon fixed per unit time", but RuBisCO activity is expressed per unit mass of the enzyme, while assimilation rate is per unit leaf area (or less commonly, leaf mass).


texts: Are olfactive indicators always the result of inadequacy in sanitation?

texts:
Question

If you can smell the scent of food in a thoroughly cleaned container, does that imply trace amounts of food particles remain?

Scope

It goes without saying that our sense of smell is commonly used in helping identify undesirables in day-to-day life, and as such it's understandable to correlate certain smells to hygiene effectiveness.  However, I'd like to definitively understand whether or not the presence of odorants unequivocally indicates ineffective or insufficient sanitation (in particular, on direct food-contact processing utensils and containers in a commercial/industrial environment).  E.g., coffee mugs with lingering scent of coffee despite repeated washing.

From the standpoint of HACCP/HARPC, I've always been slightly curious about the absence of "smell" as a modus operandi for pre-operational inspection (visual is the go-to).  I've always made the assumption that it simply isn't a reliable sensory indicator (despite visual being the same, in that sense), but I'm not fond of assuming.  I have a physics background, but I am unfortunately a bit lacking in biology / chemistry knowledge (beyond food safety-related microbiology).

Parameters

I'd like to understand from a scientific stand-point: is there an exclusively causal relationship between the two?  Are there possible scenarios where we can detect odorants despite having met sanitation performance standards?  For the sake of this question, I'd like to preclude the hypothetical possibility that "there were traces of debris/microbiological activity/etc., only they were within the tolerable limit defined".

I'm sure there might be a lot of complexities I am glossing over in my question, for which I apologize; e.g., I am aware in the framing of my question, I am holding some prejudice that the hazards of concern are microbiological -- whether pathogenic or not -- wherein the results from an adenosine triphosphate swab may be used as a quantified measure for overall activity.  For the sake of keeping this question from becoming too technical and convoluted to answer, and to also simplify and make measurable the criteria for "sufficient sanitation", please advise from the microbiological stand-point, but if relevant please advise from other standpoints as well (under HACCP/HARPC, the remaining potential hazard categories would be physical and chemical [includes radiological]).

Thank you!


texts: How is (Insect) population control through male sterilization effective

texts:
This is no doubt a simple question.

I was reading about Sterile Insect Technique where sterile males out-compete non-sterile ones to mate with females and thus reduce the population.

My question is - why don't the females just re-mate after they don't reproduce?

I'm assuming that the number of sterile males will be much less than the existing male population.

Is it because my assumption is incorrect and there are more sterile males?  Or my assumption is correct and given the life-cycle of the organism, the females have only once chance to mate?  Or something else?


texts: Why does underwinding create topological strain of DNA?

texts: I am currently studying the supercoiling of DNA. I understand why overwinding would create additional strain for two attached strands of DNA, but I really don't get why underwinding would create strain and thus supercoiling. If anything it seems that the strands would just separate and strain would be relieved from any DNA helix. If someone would care to explain, that would be great!


texts: CNS lymphatic vessels around ventricles lat et 4th?

texts:
I am searching for precise locations of the lymphatic vessels of the CNS based on the applications of the article here.
However, I did not find any when having a focus on the immediate region around ventricles (lateral and fourth).
I know this 2D visualization of the lymphatic vessels:

and this visualization at perivascular lobes

I am interested in how much the lymphatic vessels cover the lateral sides and ventricles.
I know this Blender application here where I consider Full hemispheres, each as a single mesh most useful.
However, I have a problem in adding those small membranes on top of each hemispheres and there lymphatic vessels because I do not know how evenly I should put those in the model.
I am particularly interested in the ventricles and how lymphatic vessels are around them.

How can you visualize the CNS lymphatic vessels around the immediate neighbourhood of ventricles (lateral and fourth) in 3D?


texts: Need help identifying what looks to be a skull

texts:
( BOTTOM VIEW )I was given this skull(?) by someone a few years ago, it was found washed up on a beach in Panama. I collect bones so usually I’m really good at IDing skulls and I’ve spent some time trying to just generally research skulls that look the same. I’ve looked at snake, fish, mammal, and bird skulls but none of them seem to match, it’s just a very odd shape. I researched on animals that live in the water in Panama but none of them matched up. I could just not be looking hard enough or looking at the wrong things. It doesn’t have a lower jaw and the eye sockets or at least I think they are, are very deep inside the skull. It does seem to have a base for vertebrae. Which is why I assume it’s a skull along with the general structure. The top part of the piece is completely flat with a small incline.
This is my first question so please tell me if I’m missing anything.


texts:
Many slow-growth pathogens (e.g. Mycobacterium tuberculosis, lentivirus, Rhabdovirus, Leptospira spp) are difficult to treat. In addition, a review of 61 pathogens found that

  slower growing pathogens are significantly more virulent than faster growing pathogens

I was wondering why this may be the case. Is slow growth a virulence factor? How does slow growth benefit a pathogen?


texts:
Are there substances that can promote TIMP enzyme production, or MMP enzyme production or supression in tendons?

Are there medical tests that measure quantities of MMP and TIMP enzymes in tendons?


texts:
Does anyone know which direction the nucleosomes are wrapped? I wonder:

Relative to the B-DNA double helix twist direction (right-hand)
Relative to the neighbor nucleosomes. Do they alternate to prevent supercoiling?


texts: Many times I have heard someone having to pull the plug because the patient was declared brain dead before the body healed fully? Why do they pull the plug without first waiting till the body/brain has a full recovery? What situations if not recoverable would they allow the body to fully heal before pulling the plug?


texts: Are erythrocytes lysed during alpha hemolysis?

texts:
Wikipedia says:

  When alpha hemolysis (α-hemolysis) is present, the agar under the colony is dark and greenish. Streptococcus pneumoniae and a group of oral streptococci (Streptococcus viridans or viridans streptococci) display alpha hemolysis. This is sometimes called green hemolysis because of the color change in the agar. Other synonymous terms are incomplete hemolysis and partial hemolysis. Alpha hemolysis is caused by hydrogen peroxide produced by the bacterium, oxidizing hemoglobin to green methemoglobin.

From this it seems that in alpha hemolysis , it's not the lysis that's the defining event rather the chemical change of the hemoglobin molecule.

Wikipedia states:

  Beta hemolysis (β-hemolysis), sometimes called complete hemolysis, is a complete lysis of red cells in the media around and under the colonies: the area appears lightened (yellow) and transparent.

I am unsure of the reason for color change (blood agar plate) in beta hemolysis, my guess it's due to diffusion as I have found no mention of chemical change in hemoglobin molecule anywhere (yet).
So far my position is chemical change in hemoglobin without lysis is alpha hemolysis and lysis followed by diffusion of the hemoglobin molecule is beta hemolysis. Problem is my support is shaky at best.


texts:
In 2015 many sources, including USA TODAY, Discover Magazine, and National Geographic, ran stories about the Opah fish (Lampris guttatus) being warm blooded.

Image Source: http://discovermagazine.com/2016/janfeb/58-meet-the-first-warmblooded-fish

Headline from USA TODAY 5/14/2015:  First warm-blooded fish identified

  In a discovery that defies conventional biology, a big fish that lives
  deep in the Pacific Ocean has been found to be warm blooded, like
  humans, other mammals and birds.

Article from National Geographic 5/14/2015: Meet the Comical Opah, the Only Truly Warm-Blooded Fish

  The opah’s wonderful nets are in its gills, and that makes all the
  difference. The blood vessels carrying warm blood from heart to gills
  flows next to those carrying cold blood from the gills to the rest of
  the body, warming them up. So, while a tuna or shark might isolate its
  warm muscles from the rest of its cold body, the opah flips this
  arrangement. It isolates the cold bits—the gills—from everything else.

  This allows its huge pectoral muscles, which generate most of its
  heat, to continuously warm the rest of its body. It also keeps that
  heat with the help of thick layers of fat, which insulate the heart
  from the gills, and the pectoral muscles (which produce most of the
  animal’s heat) from the surrounding water.

According to the Merriam-Webster Dictionary warm blooded is defined as:

  having warm blood; specifically : having a relatively high and
  constant internally regulated body temperature relatively independent
  of the surroundings

This definition seems to agree with the stories about the Opah fish being warm-blooded.  However, it seems different from humans, mammals, and birds which generate and maintain body heat when muscles are at rest too.  Are there different definitions of warm-bloodedness that would fit the Opah fish that is different from humans, mammals, and birds?


texts: Are there any anatomy books focusing on etymology?

texts:
I noticed that I can remember names for a very long time if I now their etymological background, the reason is easy I love etymology, especially when it is connected to mythology. However when I learn anatomy searching for the etymological background consumes too much time.

Are there any books or even preferably searchable online materials focusing of the etymology of anatomical nomenclature?


texts: I have read in books that Proteins and Peptides are fundamental components of cells which carryout important biological functions.Can any one explain me the structural difference between Proteins and Peptides?


texts: Significance of basal lamina for outer layers of epithelium

texts:
In stratified (not pseudostratified) epithelia such as the epidermis, what purpose does the basal lamina serve for the outer layer cells which do not even stand in contact with it?

Also, how do these cells attach, all just through tight junctions to lower layers?


texts: How important is the womb's environment?

texts:
- Background -

Talking about one phenotypic trait, the total phenotypic variance $V_p$ is decomposed into genetic and environmental variance for this trait, represented by the symbols $V_G$ and $V_E$ respectively. Also the covariance between genes and environment affect $V_p$ but we'll ignore it for the purpose of this question.

$$V_p = V_E + V_G + O(Cov(E,G))$$

The genetic variance $V_G$ can be further decomposed into dominance and additive variance. Similarly the environmental variance can be further decomposed into for example, for the mammals, the variance in the womb $V_W$ and the other environmental variance $V_{OE}$.

$$V_p = V_w + V_{OE} + V_A + V_D$$

$$h_N^2 = \frac{V_A}{V_p} = \frac{V_A}{V_w + V_{OE}}$$

One could measure $V_W$ by looking at correlation between dizygotic twins.

- Question -

What part of the environmental variance in phenotype is explained by the variance in wombs' environments? i.e. what are the estimates of $\frac{V_w}{V_e}$ or what are the estimates of $\frac{V_w}{V_p} = \frac{V_w}{V_w + V_{OE}}$?

Of course the answer will depends on the trait and on the species. I welcome either a general idea/estimation or any such measure for any specific trait.


texts: If dinosaurs could have feathers, would they still be reptiles?

texts:
I just finished watching a video where it was mentioned that nowadays birds are dinosaurs and non-avians dinosaurs could have feathers.

I confirmed this from wikipedia:

  Birds are highly advanced theropod dinosaurs, characterised
  by feathers, a beak with no teeth, the laying of hard-shelled eggs, a
  high metabolic rate, a four-chambered heart, and a lightweight but
  strong skeleton.

And:

  Direct fossil evidence of feathers or feather-like structures has
  been discovered in a diverse array of species in many non-avian
  dinosaur groups, both among saurischians and ornithischians.

And this family tree of reptiles mentions:

  Archosauriformes (crocodiles, birds, dinosaurs and extinct relatives)

And later in the Mesozoic era:

  The dinosaurs also developed smaller forms, including the feather-bearing smaller theropods.

So, were these non-avian dinosaurs with feathers actually reptiles?


texts: How does Mupirocin affect in staphylococcal infection?

texts:
I found this sentence confusing

Transitor carriers of staphylococcal infections 70% because of mupirocin i/n.

Mupirocin is drug which affects some way.
I am not sure if the statement means inner neuronal.

I am little confused by the abbreviation i/n.
What is the point of the sentence?


texts:
http://www.scientificamerican.com/article.cfm?id=identical-twins-genes-are-not-identical

According to this article some identical twins show differences with respect to their copy number variants. How is this possible? If mitosis of an egg can lead to this difference, why can't mitosis of any cell in our body?

If we assume that identical twins are exactly identical, then if we make a clone of a twin will all three be exactly identical?


texts: Can the body always find the right antibodies?

texts:
If the body produces random antibodies in order to fight a virus, is there a small chance that the specific antibody needed to fight the virus just won't be randomly generated? Even though it is a common virus that normally doesn't kill people?

For example if you have a common cold, is there a small chance that you could die from this just by probability? Whereas someone else won't because they randomly produced the right antibody?


texts: To my knowledge plants do not have an uncontrolled growth disease similar to cancer. Is the function by which they avoid uncontrolled growth related to their cell wall and preventing damage to DNA/RNA? Is their telomerase special in some way in that it does not indefinitely replicate?


texts:
You know how your cells die all the time and new ones are made to replace them, so you practically have a new body every maybe 5 years?

Many people say you become a completely different person every several years, but what about neural cells, do they get replaced?
I believe it would cause a lot of information to get lost if this happened.


texts:
Cells of a triple-mutant yeast strain (leu- his- trp-) were spread
either on minimal medium or on minimal medium supplemented with
various combinations of histidine, leucine, or tryptophan. The
cultures were grown at either 25C or 37C for 3 days. Colony numbers
in each plate were counted, and the data are listed in the following
table.

What kind of mutation most probably causes the his- phenotype?What
kind of mutation most probably causes the leu- phenotype?
A.Point mutation
B.missense mutation
c.nonsense mutation
d.conditional mutation
e.deletion mutation

My questions : What is the meaning of confluent in this context ? Can anyone give me a hint to solve this question ? I have no clue how to solve this.


texts: Will ants arriving with travel luggage form a new colony?

texts: I have found a few dozens of ants in my luggage after arriving back from holiday. Am I at the risk that they will form a colony in my home? Are those ants able to form colonies that are normally gathering food? Will any other kinds of ants be present in the luggage? What will happen to these ants after they start exploring my flat (which is distant from their original colony)?


texts: How do large herbivores get enough protein?

texts: The food they eat seem extremely low on protein. Do they need less protein per mass unit than carnivores? Most of them grow quite a lot in the first year, is most of that from the mothers milk?


texts: How does sucrose protect bacterial cells in lysozyme solutions?

texts:
I have a microbiology question.

When we put bacterial cells in sucrose solution with concentration higher than 0.5M we observe plasmolysis - the cytoplasmic membrane detaches from the cell wall due to water loss in order to balance the osmotic gradient.

If after that we put some lysozyme in the solution, the cells become spherical as they turn into spheroplasts, but they are still alive.

If we put lysozyme in a solution that contains bacterial cells, but no sucrose, they die. So my question is how does sucrose protect cells from lysis?


texts: How much of the genotype-phenotype map do we understand in HIV?

texts:
From what I understand, viruses have very small genomes relative to those of standard model organisms used in biological research. For example, according to Wikipedia, "the HIV genome contains nine genes that encode fifteen viral proteins". This is several orders of magnitude below the complexity of the mouse genome for example, with over 20,000 genes encoding over 50,000 proteins.

As a bioinformatics student (from a non-biological background) working with mammalian genomes, I often find the link between genotype and phenotype quite abstract and I'm unable to fully get an intuition for concretely how genomes can encode the instructions (or recipe using Dawkins' analogy) for creating complex phenotypes.

With this in mind, I wondered whether viruses, in particular HIV, which I know has been well studied, provide the simplest models for understanding the principles of how genes can encode the complete phenotypes of a functioning biological entity. Having such a small number of genes, I assume it is feasible to follow the transcription, translation and interaction of all genes and proteins? If so, is it the case that we understand how all of the genes and proteins work in HIV? If not, what is the main barrier in our understanding?

Apologies for this poorly-defined question. I am having a hard time getting my head around how molecular/cellular biology fits in with the complex phenotypes I've been studying in developmental biology/physiology and hoped that a simpler species/biological system could help to illuminate how it all comes together! Any pointers to further resources would be much appreciated.


texts: What is the difference between a spore and a cyst?

texts:
Last year I read a course in biology. During that course I learnt that Protozoa like Lamblia intestinalis or Entamoeba hystolitica form cysts in unfavourable conditions.

This year I read a course in microbiology. I learnt that bacteria like Clostridium perfringens or Bacillus anthracis form spores in unfavourable conditions. So far so good. But then I learnt that prokaryotic Borrelia burgdorferi can form a cyst, not a spore.

Firstly, I would highly appreciate any comments that would cast some light on these terms.

Secondly, I would also like to know if the spore inside, say, B.anthracis is the same organism as B.anthracis that produced the spore. Does a spore and the bacteria that produced it have the same DNA sequence? In other words, if I were a sporeforming bacteria, would my spore be myself, my bodypart or my child?


texts: Why social animals attack odd members of their own group?

texts:
Some social animals are known for attacking odd members of their own group, for example, chicken:

  If you have a large group of one type of chicken, they will usually gang up on the one or two others that do not look like they do. They recognize color differences the most and will beat up on the odd chickens in a group.

Of course the same behavior is most commonly observed in humans, where any difference can be a reason for aggressiveness.

Why this behavior developed and still exists and how it is called?


texts:
In [1] it is written that:

  Whole-genome and RNA sequencing identified recurrent in-frame activating FGFR3–TACC3 fusions

What is a recurrent in-frame activating fusion?

[1]   Cancer Genome Atlas Research Network, “Comprehensive molecular characterization of urothelial bladder carcinoma.,” Nature, vol. 507, no. 7492, pp. 315–322, Mar. 2014.


texts: Why would eating the meat of cows fed with antibiotics trigger an immune response to the antibiotics?

texts:
The document "Antibiotics and Antibiotic resistance" contains the following paragraph:

  The indiscriminate use of antibiotics in feed stuffs means that humans
  may receive unwanted doses of antibiotics in meats, eggs and milk.
  This exposure may cause the development of an immune or inflammatory
  response to the antibiotic so that the human cannot be treated with
  the drug at a later date. The practice has also resulted in the
  development of antibiotic-resistant strains of bacteria.

Here are my two questions that test general biology principles:

How can there be an immune response to an antibiotic?
I think that the answer to the first question will answer this one anyways, but for the sake of completeness: why would the immune response to an antibiotic prevent the antibiotic from being used again? (I may know how to answer this once I actually know what an immune response to an antibiotic looks like.)


texts: Dimethyltryptamine and Sigma 1-type opioid receptor interaction

texts: Where exactly do dimethyltryptamine and sigma 1-type opioid receptor interact? I read in this When the Endogenous Hallucinogenic Trace Amine N,N-Dimethyltryptamine Meets the Sigma-1 Receptor but it does not say where exactly they interact only that they do.


texts: What color is the hemolymph of the Japanese giant hornet?

texts: This is a random and very specific question that's been nagging me for quite some time. I've tried asking on other websites with no luck, and am hoping that somebody here can either give me an answer or redirect me to somebody/somewhere where I can get my answer. I guess it isn't required but I'd also prefer to know, if you can give me an answer, how you got your knowledge on it. Thank you in advanced!


texts:
I am trying to narrow down the possible search criteria from an RNASeq experiment. I already have the cds sequences so I took these and used Blast+ program to blast the data against itself to find sequences that were the same.

From what I have read the E Value is based on the database size. My database only has ~27,000 sequences in it, does this mean that only exceptionally low E values will be relevant to me? Are there any other criteria I should search for before writing the program to eliminate similar sequences?


texts: Why is dsDNA nuclease activity by CRISPR/Cas9 only shown indirectly?

texts:
In Jinek et al., the authors show nuclease activity of their CRISPR/Cas9 system using the so-called Surveyor assay method. This assay recognizes small mismatches in dsDNA which are introduced by error prone non-homologuous end-joining after dsDNA breaks have been introduced by some foreign agent (such as Cas9).
The Surveyor assay then -again- breaks the DNA at those points where it recognizes mismatches. The newly broken DNA fragments can be assayed and so one can identify the position of the initial, Cas9 dependent breakage.

My question is: for direct demonstration of Cas9 activity at the programmed position, why not first silence non-homolguous end-joining repair mechanisms in the cell and then directly analyse the lysate? Is this technically not feasible? Or is it not done in order to not introduce another change in the cell for which there would be no control?


texts: Can we make a rough estimate of the number of generations since the origin of life?

texts:
According to what we've learnt :

we can approximate the number of generations since the first human pretty much like us (depending what / who we talk about).
we have an idea of the series of life forms we come from.

So is it possible to give it a very rough number ? Or it's not, because of some issues - but which ones ? (I only think about the many, short generations of the first forms, which moreover we don't really know about, as a limit to counting)

What if we stop counting at "unicellular" (or else) ?


texts: If I have bacteria diluted in water and I centrifuge at max speed for 15-30 min, it is possible that I break the walls so the DNA can scape and I do not get any DNA pellet? or should I get it as a pellet everything togheter (lipids, proteins..) even if the mixure is just bacteria diluted in water?


texts: How does latency in carcinogenisis differ from the effect of chance?

texts:
Most chemically induced cancers seem to have a long latency between exposure to the carcinogen and expression of the disease. Mesothelioma typically 30-40 years, bladder cancer about 20 years, for example.

Most carcinogens also seem to have a dose-response relationship, with both tumour formation andlatency.

The only way I've ever heard latency explained, however, is the number of cell activities in the presence of the mutagen which are required to give reasonable accumulation of errors, but this seems like the same level of variation as dose. The higher the dose the more likely an error so the fewer iterations required before such an error might reasonably occur.

Yet this doesn't seem to be how latency manifests in epidemiology at all. For a start it seem an absolute value - no one no matter how unlucky, gets cancer five minutes after exposure to the carcinogen, it's seems to take some absolute length of time no matter what. Also, whilst latency is dose dependent it seems much less so. Risk can vary between 1 in a few hundred at high exposures, to 1 in a few million at low exposures, yet latency varies hardly at all despite massive variation in dose.

So basically, what causes latency in carcinogenisis, what is happening in the body for those decades, and how does this differ from the randomness of simple dose-response carcinogenicity?


texts: How well supported is the hypothesis that aging is mainly caused by the number of mutations in tissues?

texts:
I heard the hypothesis, that the (main) reason of aging is the increasing number of mutations in body tissues. The higher the number of mutations is, the older tissue is.

Is this true? And how well supported is the idea?

Have somebody measured the numbers of mutations in different tissues at different ages, and if so, where I can get these numbers?


texts: I took this photo on Madeira, in a botanical garden.


texts: How do sarcomeres coordinate contraction?

texts:
As can be seen from the figure

if myosins from both sides apply equal force then how does muscle contract? And also how do actins resist tearing?
Is there any kind of  coordination between different sarcomeres? How does they achieve it? I know that acetylcholine is released in response to action potential so does the release of acetylcholine controlled in each individual sarcomere?
Or simply there is an increase in the number of myosins as the distance of each sarcomere increases from the neuromuscular junction?


texts: I'm learning about development via the example of Drosophila embryogenesis. I understand that bicoid regulates hunchback, among other genes. My question whether the regulation is direct or indirect? In other words, does the level of bicoid directly govern the expression of hunchback, or are there steps in between?


texts: From which end of mRNA does transcription start?

texts:
The book "Understanding bioinformatics", says that "RNA polymerase transcribes the anticoding strand in the direction from 3' to 5', so that the mRNA strand is produced from the 5' to the 3' end".

But from Khan Academy's article, I got "RNA polymerase builds an RNA strand in the 5' to 3' direction, adding each new nucleotide to the 3' end of the strand". Also "the codons of an mRNA are read in order (from the 5' end to the 3' end)". Which one is correct?


texts:
Sulci and gyri are complementary views on the very same brain-anatomical phenomenon

(Note that there is the named concept of gyrification, but not of sulcification, but it's the very same process.)

As the main evolutionary advantage of sulci/gyri stands the enlargement of the surface of the brain, i.e. the neocortex.

As another evolutionary advantage of gyri (not sulci) Wikipedia mentions "increased speed of brain cell communication".

But there seems to be another (as usual: unintended) evolutionary advantage of gyri (not sulci) which I could not find discussed/investigated/analysed in detail: being prerequisite of internal long-range connections of the neocortex in a somehow systematic way (which goes beyond mere "increased speed"):

I am looking for references where this - possible - evolutionary advantage is discussed.

Addendum: In the above mentioned Wikipedia article on gyrification one reads

  that axonal tension forces between highly interconnected
  cortical areas pull local cortical areas towards each other, inducing
  folds.

If this was true (it's only stated as a hypothesis), it would suggest that folds are a consequence of such connections, not their prerequisite.

Addendum: In Gray's Anatomy I read:

I wonder why fibers passing the walls of a sulcus and fibers connecting adjacent gyri are explicitely mentioned (BTW: Isn't a fiber passing the wall of a sulcus connecting two adjacent gyri? Don't both of them must have U-shape? Is being intracortical vs. subcortical their only difference?) but not the ones connecting the walls of a gyrus (which would be straight, see above)? Aren't there such fibers?


texts: How many plants or trees should one plant to take carbon dioxide from atmosphere?

texts:
I'm interested on computing things. I know that some biologists have done mathematical modelling. Has anyone took any calculations on the following?

How many trees or plants should one plant such that those plants takes more $CO_2$ from atmosphere than human uses in his or her life? Feel free to make reasonable assumptions.


texts: Why is methylcellulose used in pharmaceuticals?

texts: Why is methyl cellulose used as a pharmaceutical excipient? Is it due to certain chemical properties? What are the reasons for relying on the chemical properties of methyl cellulose?


texts: Find the probability of Filium (child) that are dark (and) heterozygote

texts:
Two mice are crossed and both are dark and heterozygote. Find the probability of their filium(children) dark (and) heterozygote in F1.

Here's what our teacher explained:

I don't understand. I thought it would be 1/2.


texts: Maximum parsimony tree - Am I right, or is the correction model right?

texts:
Alright. Monday we have a test, and now I was making a practise test.

We have to make a maximum parsimony tree. We must do that monday again, so I want to know if I am thinking wrong, or if the answer model is incorrect.

The sequences are:

Seq     1    2    3    4    5    6    7
1       A    T    A    A    G    C    C
2       T    C    A    C    C    T    G
3       A    T    C    C    G    A    C
4       T    G    C    A    C    T    G

This results in:

          1    2    3    4
----------------------------
   1  |
   2  |   6
   3  |   3    6
   4  |   6    3    6

And eventually, this results in:

          1,3     2,4
-----------------------------
1,3  |
2,4  |    6

This is the tree in the correction model:

My tree has two 1,5's instead of the two 3's at the root of the tree. Because 6 is the last distance. 6/2 = 3, so both branches should get a distance of 3. But, according to some examples I saw on the internet, it's a distance of 3 to the end of tree then, and not 3 to the next node. And there is already a distance of 1,5 in further benches at both sides, so only 1,5 remains (because 3 - 1.5 = 1.5).

So, am I wrong, or is the correction model wrong? Then I know how I must do it at the real test.

Sorry if my English is bad, and it's a little hard to explain because English is not my native language, but if I am right, you should know what I mean.


texts: Why do people have antibodies against other blood types?

texts:
The ABO blood type divides each blood type according to whether they have the "A" and "B" antigen(s) (AB has both, O has none). People also have antibodies against the antigens they don't have (AB has none, O has both), even before they have ever come in contact with those antigens.

Why do people have antibodies against these antigens they have never come in contact with? This isn't the normal situation for the immune system (e.g. for a virus or the blood type rhesus factor)


texts: Relationship of RNA-binding proteins to peptidyl-prolyl cis-trans isomerase

texts: I am studying a Plasmodium gene, known to encode an RNA-binding protein. However a BLAST search brings up mainly peptidyl-prolyl cis-trans isomerases from other species. Why would this be so?


texts:
What causes tooth decay bacteria or acids?

I've been told that it is a combination of both but why would bacteria eat enamel?  There are much easier supplies of protein for bacteria to munch through (such as gums) and many of the elements within enamel are not needed for bacteria to respire. Is bacteria eating enamel a myth and if not why do they do it?


texts: Immune response to IgA positive bacteria

texts:
If certain bacteria can be coated with IgA in vitro, does that mean they are likely to elicit an IgA immune response?

Edit
I'm working on a project that involves IgA-Seq analysis. Bacteria are coated with IgA and then sorted for how much IgA they actually ended up having on them. I'm a biostatistician, so I don't know the biochemical details. But I'm assuming that the IgA binds to receptors on the surface of some bacterial more than others. I was wondering if that was related to immune response. I tried googling, but couldn't find much.


texts: What is the overall end result of proteins and enzymes binding together?

texts:
My rudimentary understanding is...

a gene gets transcribed to mRNA
that mRNA is sent off to the ribosome
that ribosome pumps out whatever proteins are coded by that gene
each protein floats around in the cell until it encounters an enzyme that it fits into, and along with other molecules that may have floated into the same enzyme a chemical reaction occurs and one or more products are formed.

I'm assuming "products" are either new protein molecules or maybe the amino acids that made up the original input proteins. What I don't understand is what the overall end result of these reactions are. So there's a reaction, but what does that mean? How does that reaction, lets say, result in some physical attribute of the organism?

Any examples would be helpful.


texts:
I am a data scientist with really next to no training in microbiology.  I hope you'll all forgive my ignorance to entertain these questions.  The attention COVID-19 has gotten recently got me thinking:  What is the fundamental difference between viral RNA and the RNA native to a particular cell?

What I mean is, we are often told in school that viruses hijack the cell's protein manufacturing facilities to express their own genetic material.  The cell produces so much of the viral protein that it eventually lyses (for example).  But what is it that makes the cell produce so much of the viral proteins?  How does the cell not produce too many proteins from the cell's own DNA?

I suspect the answer comes down to the lack of gene regulation for the viral RNA.  But is every gene that is native to the cell really subject to some sort of regulation?  If so, is the real danger of viruses that they lack any kind of regulation?  Then that seems to be a fairly easy thing to detect- at least theoretically.  In other words, a cell, or a scientist could label a sequence of RNA as dangerous simply because it is unregulated, regardless of whether it came from a virus.

A second question is, we are told that the viral proteins self-assemble and encapsulate copies of the viral RNA just by chance.  Doesn't this seem unlikely?  Are the virus's components really so ubiquitous in the cell that the virus will self-assemble including all its necessary components a significant portion of the time?  I suspect for this to happen, the virus's RNA would need to be copied many times so that it would be plentifully available.  Then it comes back to the same question as above.  Is viral RNA unique in that it gets copied indefinitely?


texts: What are the major differences between them, apart from one being in humans and other in Drosophilla?


texts: Are all Autoreceptors Downregulated by their Respective Endogenous Ligands?

texts: I know that the 5-HT1A and $\alpha$2 adrenoreceptors receptors serve as autoreceptors for serotonin (5-HT) and norepinephrine respectively and are down-regulated by repeat exposure to their respective ligands, it's believed that this is likely the cause for the therapeutic delay in the actions of antidepressants that target the serotonergic and noradrenergic systems.  My question is this: "Is this the case for all autoreceptors? Are all autoreceptors down-regulated by the actions of their respective ligands?"


texts: Short-term Lamarckism in asexual single cell organisms

texts:
I was reading through the Karr et al. (2012) whole-cell computational model. One of the things they did was to induce single-gene disruptions in their model. They observed several to be fatal, but:

In some cases (Figure 6B, fifth column), the time required for the levels of specific proteins to fall to lethal levels was greater than one generation (Figures 6C and 6D).

As far as I understand this is because when a single-cell divides, daughters get not only get a copy of the mother DNA, but also have their initial levels of proteins and RNA set to those of their mother (or similar, with some statistical fluctuation).
To me this screams of Lamarkism: if an organism during its lifetime came in contact with an environment that caused a greater expression of some protein that in had at birth, its children will also have a higher initial expression of the same protein. In other words, the trait of "level of this protein" seems to be being passed down in a Lamarkian way. Is my understanding correct, or am I missing the point?
If my understanding is correct, then what are some standard methods to account for this short-term Lamarkism in mathematical models of evolution?

Notes

I am primarily interested in mathematical (or other formal) treatments of this. I have a background in mathematics and some work in mathematical modeling for population biology and evolutionary game theory. I have no background in biochemistry or microbiology. I would appreciate answers or references that cater to this awkward background but I am not adverse to plowing through some microbio if it is for something awesome.

Similar partial arguments can be made for non-single-cell and sexual organism by considering hormone expressions of the mother during pregnancy, as in this answer. I am satisfied with an explanation for asexual single-cell organisms, but bonus points if it can also say something about non-single-cell and/or sexual organisms.

Follow up question on modeling the mechanism behind this: Macromolecule levels in daughter cells after fission


texts: Why is mRNA used as a biomarker for cancer over tRNA or rRNA?

texts: I cannot find a clear explanation for why mRNA is used as cancer biomarker and not tRNA or rRNA. Is there something peculiar about mRNA which cannot be fulfilled by tRNA or rRNA?


texts: Mammal size and capillary wall thickness

texts:
How does capillary wall thickness vary with the size of the animal?

Background/context of question:

Of the following, Figure 1 is most consistent with the fact that, in general, smaller mammals have:

A] thicker capillary walls than do larger mammals.

B] a more rapid metabolic rate than do larger mammals.

C] smaller surface area/volume ratios than do larger mammals.

D] capillaries of more variable cross-section area than do larger mammal

My working:

Of the following, Figure 1 is most consistent with the fact that, in general, smaller mammals have:

A] thicker capillary walls than do larger mammals.

B] (correct answer) a more rapid metabolic rate than do larger mammals. This is correct because a smaller animal has a higher surface area to volume ratio and hence radiates/loses heat quicker, and so must metabolise food quicker to keep their temperature up.

C] smaller surface area/volume ratios than do larger mammals. This is wrong as a smaller object has a higher surface area per volume

D] capillaries of more variable cross-section area than do larger mammal

My issue: I am trying to work out why A and D are wrong.

I can't find anything on the Internet about how capillary wall thickness (Answer choice A) or capillary cross sectionn (Answer choice D) vary with animal size.

If I was going to have a guess based on the stimulus:

For Answer choice A : From the graph, we know smaller animals have less oxygen partial pressure (as they lie to the right) and less HB saturation (as their curves lie to the bottom). If capillary walls were thicker, I would think this means that the oxygen partial pressure would be GREATER. I.e. if I think of a really thick walled balloon, it would be more difficult to blow up and increase in volume (and hence, have a higher pressure) than a thin walled balloon. However, as I know C is the correct answer, A (and my reasoning above) must both be wrong.

For Answer choice D: I don't really know how variation in cross section would have an effect. Maybe by providing a bottle-neck and increasing pressure in that way?


texts: Is there "stem" organelles in plant meristems?

texts: Two cytoplasmic genomes exist in plant in addition to the nuclear one. As far as I understand, they divide more or less during the entire life of the plant along with cell proliferation/growth in meristem. That means that somatic mutations arise. Can this variation accumulate and be passed on to offsprings? Let's say there is a mutation in plastid DNA that spread in a meristem before flower formation, will you find these mutation in the pollen/ovule plastid ? Or is there a way to keep the original genome intact for germinal cell? e.g: stock of proplastid/mitochondria in meristems that doesn't divide before reproductive tissue formation?


texts: List of np-hard problems in biology/bioinformatics

texts:
I'm not sure if this is the right place for this but...

I am looking for a list of computationally "hard" problems such that if a problem from this list could be solved effectively, it would be (significantly, or otherwise) beneficial in some form or another to the biology community.

Some examples I have found (or atleast were tagged as "np-hard" problems):

Multiple sequence alignment problem
Protein threading / design problem
Map / sequence assembly problem

The list does not have to be extensive, but hopefully more than a few.

Thank you!

(Also, I couldn't think of any more tags to add so feel free to help out there as well.)

Note:
Same question at biostars: https://www.biostars.org/p/98112/


texts: Why does the root of a plant go away from the sun? The shoot goes towards the sun, why does the root go away from it?


texts: Is alternative splicing possible in the same cell?

texts: I know alternative splicing is possible in different cell types of an organism, or within the same cell at different developmental stages. There are several examples like this. But are there any instances of alternative splicing within the same cell at the same time? Perhaps some melanin variants producing shades of different color for example. Normal cells, not cancerous.


texts:
Does the venom of the Sydney funnel web spider have to be injected into the bloodstream to have an effect? If the venom was swallowed (e.g. if a spider was eaten), would it still have an effect? Or wouldn't it be able to pass through the gut lining, or be broken down in the gut?

I understand that the funnel web's venom is different to most spiders', but would this answer apply to spider venom in general?


texts: Why oldest trees are all around 4k years old?

texts:
In christianity stackexchange I saw someone discussing young earth creationism.

One of the evidence they show is that the oldest tree, if measured by ring counts, are around 4k years.

Which, according to YEC, correspond to the Noah's flood.

Yes there are trees that are 10k years old. However, YEC doesn't believe in carbon dating. I wonder what ring counts do those tree have.

Is there any other reasonable explanation why oldest trees are 4k years old besides some massive catastrophe to all trees 4k years ago?


texts: How do I efficiently grow bioluminescent algae?

texts: I have 6 vials of Pyrocystis lunula that I would like to grow. What would be a more suitable container, a tank or a clear jar? Also, I would like to know what kind of nutrient solution to use. Is it possible to get them to reproduce at a rate that eventually there can be a whole tank full of them?


texts: Most optically transparent muscle phantom?

texts:
I am trying to use Schlieren imaging techniques to visualize how a sound wave propagates through muscle tissue.
In the past, when needing to experiment with muscle we would use an agar based muscle phantom but they diffuse light. Might anyone have experience with making tissue phantoms that have similar clarity to something like PDMS for example?


texts:
When I opened my front door, there were five of this type of spider sitting on the door. I can't quite find anything online matching the two black stripes on it's back.

I vacummed them up before I realized I should identify them, so the above picture is the only one I have available. (I like spiders, but there were too many.) I'd feel more comfortable if someone could identify the spider and determine it's threat level.

Details:

Inch or so longer
Brown
North East Wisconsin
Wooded Area with little to no grass
Mile away from lake Michigan
Jumpers
Party of about 5
Door was in direct sunlight


texts: What are the different types of helices in protein secondary structures and how do they differ?

texts:
What are the different types of helices in protein secondary structures and how are they differentiated?

In the DSSP docs, types of helices mentioned are: Alpha-Helix, Helix-3, and Helix-5.

In the STRIDE docs, types of helices mentioned are: Alpha-Helix, 3-10 Helix, PI-Helix.

Why does DSSP have Helix-3 and Helix-5, while STRIDE has 3-10 Helix and PI-Helix - are they different expressions for the same thing?

What are the differences between these types of helices, what are their full scientific names so that I could read more about them, and are there any other types of helices not mentioned here?


texts: I see in databases "curated" or "not curated" for genes. What does that mean?


texts: Common Ancestry of ETCs and ATP Synthase complexes

texts:
Rickettsiales are widely regarded as the ancestor of eukaryotic mitochondria through endosymbiosis.
Cyanobacteria are widely regarded as the ancestor of eukaryotic chloroplasts through endosymbiosis.

These two organelles bear striking similarities in terms of structure and mechanics. There seems to be plenty of information regarding speculation on the endosymbiosis that led from these free-living organims to the organelles. However I can't seem to find much on speculated relationships between these organisms in terms of common structures.

My Quesions : Are the electron transport systems and chemiosmosis simply ubiquitous phenomena in prokaryotes, or are these similarities evidence of highly conserved common ancestry? Or is there another answer?
Is there any information regarding the phylogenetics of Rickettsiales and Cyanobacteria. Do these two organisms belong to a single small clade or were these biochemistries (ETCs, ATP Synthases, etc) ubiquitous at some point and have simply been preserved in these two organisms today?


texts: I know one of the main reason why our muscles get tired is because there is too much lactic acid, but how does this lactic acid negatively affect the action of myosin on actin?


texts:
.

South India
Arm to arm about 3 inch in length. Day time. was hiding inside a cardboard storage box.


texts: Why does ampicillin in solution turn yellow?

texts:
I have a universal tube with 10 mg mL-1 ampicillin. When I got it, it was supposed to be sterile. It was opened for approximately 20 minutes for an experiment and has since been standing around sealed for a good month now.

Within the last couple weeks, it has gradually turned yellow. Right now the colour is faint, with a green-ish tint.

Why would it turn yellow? I know NADH is yellow, so that was my first guess. But I couldn't exaplain why ampicillin would cause NADH to accumulate, so I discarded that.

Side info: Ampicillin acts on bacterial cell walls, maybe that might help.


texts:
I am in search of a term that describes movement, or practice of motor skills, as a factor of laterality. Would "kinesiological" be appropriate? I'll leave my two previous questions down below; hopefully it can shed more light. Thank you so much!
What type of factor is practice of motor skills?
What causes motor laterality/ side dominance?


texts: Is ATP Synthase a channel or an enzymatic protein?

texts:
Today in a biology lecture about plasma membranes and functions of proteins, we learned about channel and enzymatic proteins along other kinds of proteins. ATP synthase is considered an enzyme that synthesizes ATP, but it also creates a channel for H+ ions to pass through into a lower concentration area.

My question is could ATP synthase be considered a channel protein as well as enzymatic protein? Or no since the ion channeling is part of the enzymatic reaction? Also are there more examples were some proteins could have more than one kind of protein to them?


texts: Do butterflies pass over migration patterns to their offspring?

texts: So, earlier, I read online (http://io9.com/butterflies-remember-a-mountain-that-hasnt-existed-for-509321799) that Monarch butterflies veer east during their southward migration to avoid a mountain that no longer exists. If this is true, how do butterflies know to continue avoiding the "mountain" after countless generations, and does it have to do with evolution? Do other animals have similar abnormalities in their migration routes?


texts: Anomaly in growth of fungus in Potato dextrose broth.. turbidity is not seen in one flask

texts:
I have inoculated six flasks of 200 ml potato dextrose broth, one of which does not show any turbidity and the medium is clear with a fungal disc in it.

All were inoculated at the same time and from the same pure fungus culture.

What might be the reason for this anomaly?


texts: What animal / bird can be heard in this evening sound recording from Western Washington, USA?

texts:
We heard this animal outside in Western Washington (Port Townsend area) during the late evening. I think it is a bird, but it honestly sounds sort of like some creepy woman singing or something. The audio is linked below. The sound (in the audio) was repeated for a long time at random intervals averaging probably every ten seconds.

https://clyp.it/tzybty1w

Anyone know for certain?


texts: Why is the ribonucleoside derived from thymine, 5-Methyluridine, abbreviated m5U and not T?

texts:
The wikipedia article about Nucleosides presents a table in which there are three columns — Base, Ribonucleoside and Deoxyribonucleoside — and structures, names and abbreviations for the nucleosides corresponding to the five bases, adenine, guanine, thymine, uracil and cytosine.

The abbreviation pattern for the deoxyribonucleosides is quite regular — they are all termed dN, where N is the first letter of the name of the base and ‘d’ indicates ‘deoxy’ (i.e. dA, dG, dT, dU, dC).

In the case of ribonucleosides, apart from one exception, the pattern is similar — they are all termed N, where N is the first letter of the name of the base (i.e. A, G, U, C). The exception is the ribonucleoside related to the base, thymine, which is not abbreviated T — as one might expect, but as m5U, from its name 5-methyluridine.

What is the reason for this? Why does the abbreviation for ribonucleoside derived from thymine deviate from that for the other bases?
Do people distinguish between m5U and U when referring to RNA, or is the letter U used for both?


texts: Does covariance and phenotypic variance have to be for the same trait to calculate narrow-sense heritability?

texts:
I'm working on a problem where I'm given that the phenotypic variance of the parent, $p$, for trait $A$ is $175.2$ and the phenotypic variance of the offspring, $o$, for trait $A$ is $146.1$. However, I'm also given that the covariance between parent and offspring of a different trait, $B$, is $14.6$.

Can I still calculate the narrow-sense heritability of $A$ using
$$\begin{eqnarray}
\frac{h^2(A)}{2}&=&\frac{\text{Cov}(p,o)}{\text{Var}(p)}=\frac{14.6}{175.2}\approx0.0833 \\
h^2(A)&=&2\times0.0833\approx0.167
\end{eqnarray}
$$
even though they're different traits?

I'm also told that any resemblance between parents and offspring is completely due to genetics, ie. without environmental effects. I've read that if this is the case, then $h^2$ is $0.50$, but I'm a little confused with it.


texts: What alternatives are there to the amyloid hypothesis?

texts:
Given the recent failure of the Bapi clinical trial, there is a lot of questions that have arised from he amyloid hypothesis. However, I can't really think of many other mechanisms that don't involved plaque formation via protein aggregation.

What are the other dominant proposed mechanisms for the biochemistry of Alzheimers?

Reference: Alzheimer’s Drug Fails Its First Big Clinical Trial. Unfortunately, the results of the study have yet to be presented at a medical conference but will be in September.


texts: How do substances for gene expression work?

texts:
How does amplification of gene expression work?
I often find in various articles expressions like "Using substance X or peptide X, we enhanced the expression of gene Z, which led to a certain therapeutic effect.

How to find out which substance enhances the expression of a particular gene? Is there a law, a pattern for this, or, if all this is found out empirically, a summary table of expressing substances?


texts: In cancer, why do cells duplicate themselves?

texts: In regards to cancer why do cells replicate themselves? If it's a mutation, what kind of mutation would this be classified as?


texts: Where does the additional 1 proton cost of oxidative phosphorylation come from?

texts:
I've been quite confused by the source of the additional 1H+ cost right now. I know it costs the F1Fo-ATP synthase 3H+  to produce an ATP, and it is also stated that:

  ADP3−cytoplasm + ATP4−matrix → ADP3−matrix + ATP4−cytoplasm //
  ADP/ATP exchange is energetically expensive: about 25% of the energy yielded from electron transfer by aerobic respiration, or one hydrogen ion, is consumed to regenerate the membrane potential that is tapped by ADP/ATP translocase.(Wikipedia/ADP/ATP Translocase)

So in some books I find out that they regard the net cost of producing an ATP as 4H+. Here is another statement:

  The phosphate carrier, which works in concert with ATP-ADP translocase, mediates the electroneutral exchange of H2PO4-for OH- (or, indistinguishably, the electroneutral symport of H2PO4- and H+). The combined action of these two transporters leads to the exchange of cytosolic ADP and Pi for matrix ATP at the cost of an influx of one H+. (Berg JM, Tymoczko JL, Stryer L. Biochemistry. 5th edition. New York: W H Freeman; 2002. Section 18.5, Many Shuttles Allow Movement Across the Mitochondrial Membranes.)

And my question comes here. Why do we not consider the effect of the process of ADP + Pi → ATP on the membrane potential? It also produces a net cost of 2e-. Putting these together, this will lead to 0, i.e. no additional net cost. Or should I only consider H+ but not e-?
(This might lead to another problem about H2PO4-'s breakup.)


texts:
Two years later, there is a follow up question to the one asked here: How do we know if the folding@home project results are right?
Since we are quite sure F@H is working right and following this article's statement:

  Similar techniques could be applied to protein folding, reducing energy consumption, or searching for revolutionary new drugs and materials.

...I would like to ask if AI stuff, like deep learning, neural networks and the rest of today's buzz words could be applied to molecular dynamics, especially in the protein folding field?


texts: What happens if both forward and reverse primers have same Tm?

texts:
One of the key rules in primer designing is that Tm (melting temperature) of forward and reverse primers should be in the range of ±5°C. For example, if Tm of forward primer is 62°C, then reverse primer should be either 67°C or 57°C.

What happens if both the primers are having same Tm?

Is this to be considered as perfect score of finding correct primers set?

Thanks


texts: What are the main mechanisms of interaction between the nervous and immune systems?

texts:
We know from pop science that our psychological states have an effect on our immune systems ("worrying ourselves sick", etc.), but what are the actual mechanisms through which our nervous systems pass information to the immune system?

Cell mediators come to mind, but where in the body would a nerve cell release an interleukin or other factor? (Put another way, are neurons releasing these factors as a part of their normal cell metabolism and the side effect is a communicative effect with the immune system?)


texts: Somatic Mutations in meristem tissue in plants

texts:
In angiosperm, in which layer of the meristem does a new mitotic mutation occurring has chance to be found in a pollen grain or in an ovule?

I also welcome some insights about non-angiosperm plants.


texts: BLAST, using Smith-Waterman in the last step and S-score

texts:
In my bioinformatics course we studied the BLAST agorithm. After finding the HSP's and joining the HSPs together that are close enough and in a correct diagonal trend, we perform a next step: namely a Smith-Waterman alignment. Why do we do this? Didn't BLAST already find the alignment by joinging the HSPs?

I also have a second question about BLAST. When calculating the E-value with the formula:

$E=K \times m \times n \times e ^{\lambda S}$

Which score is this S exactly? Is it the score found for the HSP with the used substitution matrix? What is the score if we have multiple HSPs in one database entry? Is the E-value, and thus the S-score, calculated seperatly for every HSP or is it a value for the entry in total?


texts: Are there inherent problems in simulating marine environments, as compared to terrestrial systems?

texts:
We cultivate a number of terrestrial organisms in greenhouses and stables where they live in completely artificial environments. This seems to extend far less to marine organisms, such as fish. Aquariums (especially the salt water variety) seem to be quite unstable and require a lot of maintenance, and commercial scale installations, like salmon farms, are set up in the ocean, rather than in a separate tank.

Are there inherent difficulties in cultivating marine organisms, or is it just that mankind has not tried as hard as with land species?


texts: Book Recommendation: Complex Traits and Complex Genetic Architecture

texts:
I am looking for a book (or any good source of information) that offers an in-depth discussion and models about the evolution and analysis of complex traits and complex genetic architecture. Do you have any suggestions?

I'd define complex traits as those traits whose variance in the population is explained by quite a lot of various genetic loci and environmental factors.


texts:
When an intermediate is formed between a substrate and an enzyme, this is called an enzyme-substrate complex.

When a molecule is bound to its respective transfer protein, (the molecule being transported is unchanged when released from the protein at the destination) would this be called a complex? If not, what would this be called?


texts: Species identification - greenish blue ocean worm (nudibranch?) in Perhentian Islands, Malaysia

texts:
We found this on a beach at the Perhentian Islands, Malaysia in March, 2016 and cannot identify it.  It's some sort of worm-type creature with many legs and bluish back about 15cm long.  The legs undulated along the body as it swam.

back:

belly side:


texts: Why do asparagine and glutamine have two different abbreviations?

texts:
I'm looking at amino acid abbreviations and on every site I visit, asparagine and glutamine have two different abbreviations. Is there a reason for this? Do they represent different forms of the amino acid that may have different properties?

I'm looking at the abbreviations on this site as an example:
http://www.hgmd.cf.ac.uk/docs/cd_amino.html

On the page, asparagine has an abbreviation of 'N' and an abbreviation of 'B'. The abbreviation 'B' doesn't correspond to a codon so why is it there?

Glutamine also has two abbreviations ('Q' and 'Z'). The abbreviation 'Z' doesn't correspond to a codon either.


texts: Where can I find a full genealogy of human cell types?

texts:
It is said on Wikipedia, that the precursor of blastocyst is a morula, and that the precursor of morula is a zygote. This gives us the part of genealogy tree of cell types. Unfortunately, no full genealogy can be found in Wikipedia.

Where can I find a more complete picture, preferably a full tree of cell types including information about each type?


texts: How do seagulls know it is the 9th inning at a baseball game?

texts: Multiple times that I’ve gone to San Francisco Giants games, the seagulls sensed when the game was ending so they could pick up food. https://youtu.be/LPra_ZfwanU


texts: Are there any evolutionary reasons for the different tree shapes? If so, What are they?

texts:
So we know there are a thousand types of trees with different shapes.
We have Columnar shaped trees:

Pyramidal or Conical shaped trees:

Weeping shaped trees:

And we also have Round, Vased, Open-Shaped, and Umbrella shaped trees. So im not really into botany so forgive me if I butchered some phrases. But I got into a conversation about evolution at school and we switched the conversation to plants this time.
We got into the photosynthesizing cycles of leaves, Like of course we know green is the leftover color from the light spectrum, Orange and yellow colors means the plant is utilizing Carotenoids as it ages, And Anthocyanins for pink to red leaves to protect it from intense sunlight.
But we got into the topic of the different tree shapes. Since plants are living things and goes through the same process of natural selection, Is there any evolutionary reasons for their different shapes? What made some trees that way and how do they fare differently from one another?


texts:
Found this mushroom today. It's a kind of puffball mushroom and I think pestle puffball but I hope someone can confirm that/point me to other likely species.

It was in Central Eastern Sweden (Uppsala) in a pine and birch forest. Autumn has been quite dry so the season may be a bit delayed. They were in bunches of 2-5 mushrooms, they are about 1-4cm across the ball and the stem is quite fat plus about 1-3cm long. They are white through the middle.


texts: Why are sea dwelling mammals less aggressive than land dwelling mammals?

texts: Many mammals on land seem to be quite dangerous to humans: e.g., tigers, lions, elephants, hypos etc. However, their sea-dwelling counterparts (e.g., orcas, dolphins, sea lions, whales etc.) are relatively friendly to humans (and in contrast to say sharks). Is there a simple reason for this?


texts: Behaviour of neuron when membrane potential is maintained at threshold potential or more

texts: Via an external electrode the membrane potential of a neuron or group of neurons can be increased from resting potential of -70 mV to -50 mV or more. This will cause them to fire an action potential. What happens if the electrode maintains the membrane potential at -50 mV or more for say 1 minute? Initially it should fire once, but then it will not reach the resting potential, will it stop firing or keep on firing continuously since it is above threshold potential? Will this kill the neuron or make it malfunction permanently?


texts: What is a normal healthy amount of Titratable acid in a person's blood?

texts:
A person's normal pH for arterial blood is 7.41 and venous blood is 7.36.
But I am curious to what is a normal amount of Titratable Acid in someone's blood?


texts: Does increasing contractility increase LV ESP?

texts: I see many PV diagrams showing a negligible difference in the ESP when contractility increases. I'm wondering why this is the case, because if more blood is being pumped out into the aorta, the MAP should increase, which should subsequently increase the ESP.


texts: Is it possible to Clone a Dinosaur with a full strand of their DNA?

texts: If you have a full strand of Dinosaur DNA would it be possible to make it living and hatch a dinosaur? Or would it be a failure? Could you use a bird or alligator, for replacein


texts: What is the pBR322 convention? For example in the description of the pET28a vector we can find information that the sequence is numbered by the pBR322 convention, so the T7 expression region is reversed on the circular map.


texts: How do cells figure out the big-picture shape?

texts: I'm wondering what makes cells to divide (and stop) in such a way that they make our hands the shape that our hands are...


texts: How do antibiotics create drug-resistant strains

texts:
I've heard for years that low-level use of antibiotics causes the spread of drug-resistant strains of bacteria, but the explanations always fall short.  I understand mutations and natural selection, and that a bacterium can randomly mutate into one that is more resistant to the antibiotic than the wild-type.  I understand that the antibiotics kill off the less resistant strains and leave the more resistant ones, but those more resistant strains would be there even without the antibiotic use, right?

Do the more resistant bacteria compete somehow with the less resistant ones and the antibiotics kill off the competition?

(Edited: previously used the terms "strong" and "weak" which apparently have unintended connotations, and was unclear about the role of mutation).


texts: What is this Sacrificial Reproductive Strategy Called?

texts:
The reproductive strategy of salmon is 'suicidal'. Before breeding the males metamorph permanently into a form suited for the breeding season but unsuited for survival. The females devote so much of their biomass to producing eggs that they do not survive long after spawning.

Does such a breeding strategy have a name? Where the parents die shortly after breeding, or indeed during the mating process. I'm sure the latter, more specialised, case could only occur in particularly simple organisms (think polyps, think deep sea). But does there exist an organism which as part of its reproductive strategy, after breeding, devote such a portion of its biomass into the production of eggs that it literally dissolves into  cloud of spawn?


texts: Cell-type specific methylation profiles: original reference finding?

texts:
This is a general question, and a specific question. I'm looking for the original reference that first talked about how DNA methylation profiles are cell-type specific.  This is specific, because I care about this specific reference paper, but it is general because I don't know how to go about finding original reference papers to begin with.

Any help would be super appreciated!


texts:
Found them in Gujarat, India.
Found growing among potted plants


texts: why did capacity of regeneration decreased in evolution?

texts:
When we consider trend of evolution the ability of organisms to regenerate decreased as the complexity of body structure increased.

acetabularia-can regenerate whole body even if 1/100th part of body is left
small pieces of sponges can grow complete individual.
hydra-interstitial cells are totipotent.
planarians-neoblasts are omnipotent
crustaceans-heteromorphosis.
lizard-regenaratetail..........what is the reason you expect for this ?


texts: Determine which gene is in the middle complementation

texts:
Possible Duplicate:
  Crossing mutant strains on minimal media problem

I'm studying this problem for my genetics final:

My Attempt:   The answer for part B is met2 and the answer for part C is Df1.  Met2 and met 1 both have 1 no so i'm not sure how met2 is in the middle.  I didn't even know complementation tests could tell gene location. I think the answer to part C is because df1 has the most NOs, which means it's missing the most DNA.  (If it had that DNA, it would complement).


texts: I'm in Western Arkansas, and these are red, hollow mushrooms with a brown slimy coating that popped up in our mulch, roughly a half an inch in diameter and they have grown several inches tall. Is there anything specific that I can/should do to these things? I have young kids and pets that I assume I don't want eating these things.


texts: Is the tensing of muscles equivalent to stretching them? I am trying to understand what tensing of the muscles means.


texts: Are there genes in sex chromosomes that determine facial features?

texts:
My friends and I were bored enough to try out this activity.

Picture a teenage boy in your mind.
From this picture, remove any accessories (glasses, piercings, etc.), moustache or beard, then replace the hairstyle with that of a stereotypical teenage girl.
Are you possibly convinced if someone tells you that, this picture was originally of a teenage girl?

I tried it by picturing a few boys who are my friends, but still, I was never convinced because I feel that there's something inherent about the facial features of these boys that made them appear boyish rather than girlish.
If this is not some psychological effect caused by my acquaintance with the boys I pictured (as I know them well so I cannot accept the mapping of their faces to the opposite gender), then are there really biological factors, genes in sex chromosomes in particular, that result in differences in the development of facial features between males and females?
Apparently, "facial hair" isn't an acceptable answer...


texts: In metabolic control analysis, a number of coefficients are defined, including the flux control coefficients. How is this coefficient defined and what does it measure?


texts:
I attended a seminar about neurogenesis that presented results for PAX6 as an important TF that contains 3 domains with very distinct patterns of downstream expression. The speaker ended up saying that PAX6 can be considered as 3 TFs in one protein, acting independently in different situations:

Relative roles of the different Pax6 domains for pancreatic alpha cell development

Does anybody know of more examples like this?


texts: Which proteins are most sensitive to electric fields?

texts:
Many Proteins have ionic charges that can attract each other (e.g. Formation of salt bridges) or repel each other. On the other Hand, Proteins are mostly immersed in water that screens most of the Electric charges of the proteins. The reason is that water is a dielectric, the H2O-molecules can be polarized easily. So the Electrostatic Forces are reduced in aqueous solution.

Now I am asking which Proteins can be easily affected when applying an Electric field? That means which Proteins will Change their conformation substantially even when weak Electric fields are applied?

Can some proteins immersed in water also be dependent on external Electric fields?


texts: What is the symbiotic relationship between truffle fungi and their host trees?

texts: I understand that truffles share a symbiotic relationship as they reside among the root systems of host trees, but I cannot find any material that specifies the details of such a relationship. In other words, what exactly do truffles get from their host trees, and what do they provide in turn?


texts: Why humans have the temperature they have?

texts:
It is obviously very onerous to generate heat at all, although it has advantages. We don't have to lie on the sun like a crocodile to get warmer. And we avoid the freezing of our body water by out own means. But wouldn't just a little of heat be enough?

Why do humans go as far as 37 C? Couldn't we just have a temperature of 10 C to avoid freezing but stay at it?


texts: Does anybody know what strange plant this is?

texts: Can anyone try to help me identify this plant? Thanks!


texts: Bird species ID in the Northern Territory, Australia

texts:
I was visiting Darwin, NT, Australia a few years back and I encountered this bird. I must say it was in Darwin's Botanical Gardens, so I can't be absolutely positive the Northern Territory is its original habitat. However, I'm pretty sure it's a NT native, as the whole Gardens were packed with, and dedicated to NT's wildlife.

The photo is kind of dark and a bit fuzzy due to poor lighting conditions. I already tried to digitally enhance it by removing shadows and so forth.

I tried Google Images reverse search to ID this bird, but I'm not a hero with that tool. Although it looks a bit like it - it's definitely not a Jabiru.


texts: Why do parasites involved with malaria going into red blood cells?

texts: When someone is infected with the mosquito bug which has the parasite, this parasite will go into the liver to grow. Afterwards he goes in the red blood cells and blocking the vains of the brains. But why do they leave the liver and go into the red blood cells?


texts: How does CO₂ concentration affect photosynthesis?

texts:
I have heard the theory that with the increase of CO2 in the air, the speed of the photosynthesis would increase, thereby limiting the increase of CO2 levels.

What is currently the rate limiting factor of photosynthetic reactions in plants? Is it really CO2, or rather the limited energy that a plant can absorb from sunlight?


texts: "Imperviate" is it a word what can be substituted?

texts:
Sentence:

The aquaporins allow water to pass through the membrane and imperviate any solute molecules from diffusing across.

I'm looking for a word that pretty much is the opposite of perviate or to occlude.
http://www.etymonline.com/index.php?term=impervious


texts: If a human is stranded with beer but no water, should they drink it?

texts:
TL;DR: At what percent (if any) will alcohol dehydrate you more/faster than drinking nothing?

Let's contrive a situation for dramatic effect...

A human goes out on a boat for a nice sail in the sea. But oh, the sea was angry that day, my friends. The weather turns, and the sailboat is tossed asunder. Luckily, our survivor grabs hold of some debris and is washed onto a deserted island.

Lo and behold, the debris that floated with the survivor to the island is a cooler, and it is filled with beer! There are no other food or water sources on the island. What should our survivor do in regards to the beer to stay alive for as long as possible?

The crux of the situation and my question: will drinking the beer help hydrate the human, keeping them alive longer? Or would the effect of the alcohol as a diuretic actually dehydrate them, causing an earlier demise?

Details and follow up questions:
Let's assume this is an average beer ~4% alcohol. However, I know there must be a breaking point. Some kombucha or ginger beer with .5% alcohol should surely be imbibed. But should this beer still be drunk? What if instead it was a 7% IPA? Or a 14% quadruple IPA like I have in my fridge? What about wine, whiskey, or gin?

How would the situation change for a caffeinated beverage like coffee? Or what if the cooler was filled with energy drinks?

I look forward to your answers!

EDIT: The linked question, while similar, does not answer my question. It links to one 1996 study that talks about the effect of alcohol on rehydration, but not the specifics of yes, probably ok to drink at about this percent ABV, and no don't drink at above this percent. It also doesn't discuss rate of intake, changes based on body weight, etc. which are all things I would surmise have an impact on this. I understand there isn't going to be a hard and fast STOP percent level, but I would like to understand more about the underlying mechanisms and factors that change things.


texts: What is meant by nucleated in this context?

texts:
Hi I am little confused in one of my classes; because the teacher will say that " the actin is nucleated by the ARP 2/3 complex" or "microtubles are nucleated by the centrosome". Unless I am misunderstanding, I don't take this as having anything to do with the nucleus as in the nucleus inside a cell. ( or does it). so what does this really mean than?

Thank you


texts: Recent and good quality articles on systems biology

texts:
I'm a biotechnology student and I have to write a sort of non-experimental thesis (30 pages long) within the end of a three years study.

I'm very interested in the "systems biology" field and I'm searching good (innovative) and recent (max 3-4 years old) articles about this subject, but unfortunately I've found my research more difficult than I expected.

I'd like to focus on not immediate/easy articles and possibly containing new and promising approaches.

Does anybody have suggestions?

PS: it all started from Uri Alon's great lessons on YouTube.


texts: Why do cockroaches flip over when they die?

texts:
This question has always mystified me since young. For beetles, I can reason that they flip over because they have a higher centre of gravity causing them to be in unstable equilibrium when they tuck in their legs when they are about to die. For cockroaches with a lower profile, I would expect them to stay upright. But why do they flip over? Is it more comfortable for them to die this way or is there a scientific explanation for this?

Edit:

As noted in some of the comments below, this is a general observation based on cockroaches being killed by insecticide. I haven't got the chance to observe (or notice) cockroaches that die in other ways and therefore do not want to limit the scope of my question to just insecticide poisoning.


texts: Human population growth - where can I find the data?

texts:
Out of curiosity, I'd like play around with data of human global demography.

Where can I find data that describe the "per region (per continent for example) population size" versus time since the "Out-of-Africa Event" or earlier?

Here is for example the kind of graph I'd like to reproduce but if possible in a region per region basis.


texts: How do dragonflies manage to fly at such high speeds without their wings collapsing? Their wings are thinner than paper, but they do not even flutter. What gives them their strength?


texts: Where do the antibodies that trigger the specific immune response come from?

texts:
In A level Biology, we are taught that in order to trigger the specific immune response of the body, antibodies must first attach to the pathogen. The macrophages contain antibody receptors, and this allows them to attach to the antibody carrying pathogen and subsequently engulf them by phagocytosis. This then triggers a certain pathway that involves T helper cells activation, which release cytokines to cause differentiation of B helper cells into plasma cells, and THESE release the antibodies.

The question is: where do the antibodies that start off the whole process even come from?


texts: Microbiome Context for Amino Acid Essentials and Non-Essentials

texts: Given what we are now learning about the diverse mix and variance of microbiomes (aka bacterias via human gut project), is it possible that synthesis of aminos can be done by specific bacteria and therefore provide the "essentials" if atomic ingredients are available in digestive tract?


texts:
I have raspberries growing in my garden.

One of the raspberry canes has some sort of growth on it.

Size: Approximately 2 inches long
Location: Zone 5; east of Toronto, Ontario, Canada
Date: April 4, 2019.

What is the growth? Is it insects, fungus, bacteria, a defect, or something else?


texts: Book recommendations for algorithms used in evolutionary biology

texts:
Do you have recommendations for a book that presents the different algorithm used in theoretical evolutionary biology?

I don't mean evolutionary or genetic algorithms (otherwise this question would not be a good fit for Biology.SE) but algorithms applied to evolutionary biology. I am not interested in statistical procedures and algorithms to reconstruct phylogenetic trees, to annotate DNA sequences or to find out synonymous changes by comparing sequences of closely related species. I am not interested in introductory book on programming.

I am interested to computational modeling applied population genetics, kin selection, game theory, population range expansion, simulating sexual reproduction, selection for different sex determination system, evolution for robustness/evolvability, evolution of codon usage, evolution of genetic code, evolution of cognition, evolution of multicellularity, …

I don't quite know if one book that encompass all these subjects exist. If not, I wold welcome suggestions of book that present the algorithmic used in some but not all of these subjects.

Searching a bit in amazon, I easily found tons of book but don't quite know if they fit my expectations. Below are some examples

Evolution as computation

Individual based modeling and ecology

Models and algorithm for genome evolution

modelling for field biologists

Practical computing for biologist

Evolution as computation

Genetic and evolutionary computation

Genetic algorithms+ data structures = evolution programs

The missing algorith

Cellular Model: Mathematical and theoretical biology, Algorithm, Data structure, Bioinformatics, Computational biology, Artificial life, Computer simulation

Natural-Artificial-Models-Computation-Biology

An-Introduction-Genetic-Algorithms-Paper


texts: Why are there different gene expressions that are refered to the same gene in microarray experiments results?

texts:
I am studying gene expression profiling considering a dataset available on NCBI website. I do not understand the following: why are there some genes that have different profile and different ID numbers but they refer to the same indentical gene ?
The dataset that I am analysing is here .
For instance, we have that ID-8938, ID-1870, ID-7323 and ID-15 refer to the same gene called RadA but the gene expression profiling is different for each ID. So I ask which is the difference between these ID if they represent the same gene ? Moreover, how can I understand which is the one that has to be chosen for the analysis ?


texts: Is DNA from more parents (than two) better for the fitness of the offspring?

texts:
I'm designing a system (a computer system actually) and (a whole while ago) I spoke with a friend about it and he had this opinion:

  If you combine DNA of more parents (than 2) it's better for the
  offspring.

It's a bit of a theoretical question but is this true?

I'm using genetic algorithms where you can choose the number of parents,
if this were to be true I'd take 4 parents, if not I'd stick to 2.

I saw here a question about the occurrence in nature but it remains unanswered.

(2 parents are easier - in this system - so maybe that's the reason it is not observed in nature)

About the system: it needs to produce 'fit' offspring (as fit as possible and as fast as possible), where fitness is measurable (this part is already covered...) and the most fit individuals in the population are selected to pair.

The only limitation set on this kind of systems is that the offspring has to have a chance to be fitter than the parents (so children are allowed to be less fit than parents (being it 4 or 2).

(Of course this lowers the importance of the question but still: does offspring of more than 2 parents have a higher chance to be fit? (my friend mentioned: the more diversity in the DNA the better...))

If you need more information about this bit I'll try to answer comments (if I do know the answer or can give more information about it).


texts: Why do human vaccines affect different animals differently?

texts:
Doubtless the simple answer is that these animals differ, and that the amino acids of their ACE2 receptors differ. Are there other reasons?

  Chan, working with his HKU colleague, microbiologist Kwok-Yung Yuen, and others, pinpointed the problem by doing a cross-species comparison of the segment of ACE2 to which SARS-CoV-2 first attaches. In the mouse, 11 of 29 amino acids of this critical domain differed from the human version. (Rats had 13 differences, but hamsters only had four.)

I quote p 738 of Y. W. Kam et al. Vaccine 25, 729–740; 2007.

        Vaccine-mediated protection against SARS-CoV infection
  in mice has been demonstrated using different vaccine
  approaches [19,20,65]. However, mice do not replicate
  SARS-CoV to high titers and do not showpronounced pathology
  in lungs [15]. On the contrary, ferrets [28], cynomolgus
  macaques [29] and hamsters [30] have been shown to support
  high titer replication of SARS-CoV in the respiratory tract
  associated with pneumonitis. In order to assess the respective
  role of neutralization or ADE in vivo we performed SARSCoVchallenge
  experiments in hamsters vaccinated with three
  doses of 2, 10 or 50 g of protein in alum adjuvant. All vaccinated
  groups showed a significant decrease of viral load at
  3 days post challenge by at least four orders of magnitude
  without signs of enhanced lung pathology. The rare foci of
  hepatocyte necrosis that we observed in these hamsters did
  not correlate with pre-challenge neutralizing antibody titers,
  liver enzyme levels (pre- or post-challenge), or immunohistochemical
  detection of SARS-CoV antigen suggesting that
  hepatic cellular necrosis is unrelated to SARS-CoV immunization
  or infection in Syrian golden hamsters. This contrasts
  with a report of hepatitis 28 days following challenge with
  SARS-CoV in ferrets vaccinated with a poorly immunogenic
  recombinantMVAvaccine expressing SARS-CoV spike protein
  [24].

Why will it take so long to develop a COVID-19 vaccine? - The Globe and Mail

  Another study revealed that some investigational SARS vaccines produced negative side effects in some types of animals (such as ferrets) but not in others (such as mice). For that reason, many researchers are convinced that a vaccine should be tested in two different types of animals, Kozak says.


texts: Why rabies virus has nearly 100% fatality rate in human (see this virology blog; thanks to @iayork for the link) if not vaccinated early, even some people have survived Ebola, then why does rabies doe not get extinct as its most virulent form will kill host and virus also?


texts: What's the max speed that humans could run?

texts: Assuming humans could use all of their muscle strength at once, with no need of cooling or energy, how fast could we theoretically run?


texts: Is water released when a phosphodiester bond is made between two nucleotides during DNA replication?

texts: I know that when two sugar molecules (like glucose) connect to each other, H2O is released because of the -OH and -H groups in both of the molecules. I want to know if the same thing happens when two nucleotides connect to each other during DNA replication.


texts: Why do some people have cold hands and some have warm?

texts: I've known people who have warm hands even in the most chilling weather and also those having cold hands in a relatively hot climate. Why does this happen?


texts: Clarification in the name "white cheeked barbet"

texts:
Everyday I was listening sound of the birs "white cheeked barbet". Then I was wondering how this name came to it? It should be by certain properties of them. In wikipedia it says

  Barbets are named for the bristles at the bases of their stout, sharp bills.

But this statement I couldn't believe from picture, since I couldn't see bristles. The words "white cheeked" can be understood from photo clearly.  I then thought this may be due to some change during the migration, or anything else.

Can one help how this bird gates named "white cheeked barbet"?


texts: How is protein cavity centre related to binding?

texts:
I am confused and I have the following questions:
1. What are (in the context of article below) protein cavity centres?
2. How are they related to binding?

(Automated identification of protein-ligand interaction features using Inductive Logic Programming: a hexose binding case study, Santos et a. 2012)


texts:
I am not a bio major but I have heard about Telomerese shortening in each cell division which leads aging and cellular death. I also read that Hayflick limit is about the number of divisions a cell can make before it dies.

So my question is, how is it possible for us to have constantly dividing cells such as in our hair or nails. They are also cells right? They constantly divide almost our entire life, so how come they do not die out of Hayflick limit?

Or is it like, when a cell divides for the first time, it loses one unit of Telomere but the second cell also have the same number of Telomeres as the first one? I mean if Hayflick limit is 50 for the first cell, is there like 49 and 49 for both cells after division? And when do they decide to divide, is the first cell waits its child to reach Hayflick limit before it divides again? Is this just too complicated to explain in layman terms or are we just not sure yet?

Please do not go hard on me if I have conceptual mistakes, I am just really curious about this.