Identification of Bird feather, probably from a predatory bird Found in Berlin,Germany
Area of Charlottenburg
I want to know the species of this bird, someone please tell me.
Approximate size 19 cm

This is a Common Kestrel (Falco tinnunculus) primary wing feather, so it is indeed from a predatory bird. The orange hue suggests that this came from a juvenile and/or female individual. Featherbase provides a good reference here.
For future feather identification questions, you may wish to post them to the Found Feathers project on iNaturalist.


Does our immune system react on all bacteria? In our body we carry a lot of bacteria. Some of them are bad for our health, but others are beneficial. For example bacteria may protect us against other pathogenic bacteria.

But is our immune system reacting to all bacteria, i.e. the good and the bad, or does it selectively target the bad? If yes, how does it differentiate between beneficial and pathogenic bacteria?

The immune system is capable of recognizing pathogenic ("bad") bacteria, either by components of the innate (non-specific) or adaptive (specific) immune system. Pathogenic bacteria will have antigen on their surface that mark them as 'foreign', leading to an immune response targeted to the bacteria. In contrast, the immune system tolerates the normal flora of the body. The precise role that the human immune system takes in tolerating and regulating the populations of the normal flora is not known, it is currently a hot area of research.

Current research suggests that microbiota induces host immune tolerance to commensal bacteria directly via a microbe-associated molecular pattern (MAMP) and polysaccharide (PSA) signalling. The immune system continuously monitors the resident microbiota, and certain antimicrobial mechanisms are constitutively engaged to prevent overgrowth of the colonizing microbes: this maintains what is loosely called immune homeostasis. The mechanisms that control (intestinal) tolerance include those that:

1) minimize exposure to and 2) immune recognition of intestinal microbiota, and 3) those that down-regulate immune responses through intra-cellular and inter-cellular mechanisms.

Research has shown that he tolerance of the normal microbiota of the gut seems to require an extensive network of regulatory immune cells including Tregs and (tolerogenic) dendritic cells.
Thymus-derived Tregs were discovered by Dr. Leszek Ignatowicz to be a crucial  player involved in "educating" the immune system about the diverse bacterial colonies in the intestinal flora of mice. In response to the diversity of gut bacteria found in the gut, the Tregs express a 'repertoire T cell receptors' (TCR) that recognize the antigens characteristic of individual bacterial colonies in the gut. Upon engagement of these receptors, Tregs suppresses the adaptive immune response, specifically through the release of immune-modulatory cytokines such as interleukin-2. Moreover, it was found that gut bacteria can also be recognized and protected by a distinct innate lymphoid cell population (ILC) in the intestinal lining of mice. These cells behave like antigen presenting cells, and can recognize and present antigens from gut bacteria through the major histocompatibility complex class II (MHCII). But rather than activating CD4+ T lymphocytes through MHCII engagement, these ILC works by suppressing CD4+ T lymphocytes through MHCII engagement. CD4+ T lymphocytes are involved in clearing pathogen/bacteria, and thus the suppression of CD4+ T lymphocytes is involved in the immune-tolerance of normal flora.

http://www.sciencedirect.com/science/article/pii/S2352345X14000083

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4007055/


Computational/mathematical models for predicting phenotype from genotype Karr, Sanghvi, et al. (2012) propose a whole-cell computational model for predicting phenotype from genotype in Mycoplasma genitalium. Their model simulates myriad cell processes such as DNA replication, RNA transcription and regulation, protein synthesis, metabolism and cell division at the molecular level over the life-cycle of the organism.

They achieve this by combining many existing mathematical and computational models into one piece of software. The article suggests that this is the first comprehensive whole-cell model at the molecular level in detail. They cite previous molecular-level models for their sub-modules, but don't go on to discuss more coarse-grained genotype-to-phenotype models. Their model is exciting, but the 10 hours of simulation on a top-end computer cluster to follow the life-cycle of a single organism is unreasonable for someone who wants to study evolutionary processes.

Are there prior reasonably accurate computational (or even better, analytic) genotype-to-phenotype models? If there are, what are some of the best coarse-grained genotype-to-phenotype models for commonly studied organisms such as E.Coli?

The Karr et al. paper attempts to capture most of the details in their model by combining features from the genome, transcriptome, proteome, and metabolome. This work heavily builds off of the coarse-grained models that you ask of especially on the work from Bernhard Palsson from which Markus Covert did his training. The answer to your question rests entirely on the type of question that you seek and what you want the model to do.

For the most part, most of your questions can be answered using COBRA, the COnstratins Based Reconstruction and Analysis Toolbox. You can get a good idea of what genotypes can be knocked out and see how it affects the phenotype as long as the phenotype is a known pathway that gets affected by that gene and you don't care about temporal and dynamic information.

There is also the E-Cell Project for E. coli. I personally don't know much about it but it has created some basic models for E. coli and that may be good enough.

If you want to build your own models, you should check out BiGG where all of the large-scale reconstructions exists. A good chunk of the code is stored at the Palsson lab website where you can attempt to use COBRA and start generating your own hypotheses.


Request for an ID of two spider species found in Australia, NT These two spiders were found in the Northern Territory in Australia in July (winter time). Both arachnids were shot during the night (I suspect them to be nocturnal), and both were found close to the ground. They do not build webs I think (way too big).

The upper spider is quite big, pretty much hand-sized, and about as big as a bird-eating spider. I think the guy with us told us it was a species of wolf spider (if I recall correctly - I'm unsure). The bottom hairy spider with its nice camouflage is somewhat smaller (if I recall correctly), but still well sized.

I have been searching for their names, but the amount of spider species is overwhelming and Australians tend to focus online resources on the poisonous ones. I'm fairly sure these two are harmless.

The bottom one is most certainly a Huntsman. Something akin to a Holconia immanis, aka the Sydney Huntsman. The picture is difficult but a characteristic Huntsman typically has 2 front legs that are longer than the back legs. And of course they tend to be larger spiders.

 Holconia immanis. source: Wikipedia

The top one looks like a type of brushed trapdoor spider (family Barychelidae), typically composed of such species as Idiommata scintillans, which are known as silverbacks or goldbacks depending on the color of the hair on their head (ref).

Idiommata sp., the 'Silverback'. source: Archne.org.au


How is each region of the DNA replicated only once? In "Molecular Biology of THE CELL" 3rd Edition, 1994, by Alberts, Et al. (Yes I know there is a newer edition)

the question is posed on page 362

  How is each region of the DNA replicated only once?

Two suggestions are offered:

Inhibitor-addition model
Initiation-removal model

Since the 3rd edition of the book is now 24 years old, has the answer been discovered and if so what is it?

I am reading the 3rd edition now because that is what I have and plan to buy the newer 6th edition if a 7th edition will not be out in the next few months. This is for self-study so no need for me to rush or have the latest and greatest info for the first pass of learning as I am only reading.

DNA Replication ensures it only occurs once by the use of licensing factors. These factors are released and bind to the origins of replication during one distinct phase. After the factors have been released and the first phase has ended, the actual replication initiates.

Information on the licensing factors:

The licensing factors used to create the pre-replication complex is the Minichromosome Maintenance (Mcm2-7) protein, Cdc6, and Cdt1. The Cdc6 and Cdt1 are required to load the Mcm’s onto the DNA and therefore, are highly controlled during the cell cycle. The Mcm2-7 hexamer is the actual DNA helicase that is used during DNA replication.

The way that the re-replication of DNA is prevented is that when the DNA replication starts, the Mcm helicase moves away from the ORC and the newly replicated DNA, meaning it then cannot be reinitiated. Along with the physical moving of the helicase, Cdt1’s activity is suppressed by the protein Geminin, which prevents the licensing of the helicase during times of non-replication.

Image from the article on the licensing.

More information on this topic:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688777/#!po=21.8085


Is it possible for two brown-eyed parents to have blue-eyed child? Here's the (real) story: A young man has stunning blue eyes. On his mother's side are lots of instances of blue eyes, but on his father's side is no history of blue eyes. Both parents have brown eyes.

When he was born, with these bright blue eyes, it was considered a "miracle". As an adult, he still has these potent blue eyes.

How is this possible?

I obviously understand the popular science behind dominant and recessive genes. The mother could be Bb, but if the father was BB, it doesn't seem possible that he could have blue eyes... but I've read more on eye colour recently, and it appears to be a lot more complicated than I initially thought.

For example, this article goes into some detail explaining How Blue Eyed Parents Can Have Brown Eyed Children, but I've not seen anything that talks about it being the other way around: Could a BB parent have a bb child?

If so, how? And what is the rough probability of such a thing?

Possible, yes but probable, no. (I assume that the history of the parental family as you mention is important)

Let us first consider HERC2 (H=brown, h=blue) and OCA2 (O=brown, o=blue) as per the names mentioned in the reference you cite, to be completely unlinked, such that they are independently assorted. Since the father's lineage has no history of the recessive phenotype(blue), and the genes segregate independently (our assumption), we can conclude that the father is homozygous for the dominant allele in both the genes(HHOO). In this scenario, it is very unlikely to get blue eyed children, but is still possible in the following two ways:-

The father's lineage does have a recessive gene (which probably entered his family gene pool due to non-consanguineous mates carrying a heterozygous phenotype in either of the gene pair HERC2 or OCA2), and has evaded expression by pure chance or because the recessive gene carrier entered into the family very close to the father,i.e. probably just one or two generations above the father(so that not enough generations have passed to allow the homozygous recessive trait to develop). In each of these cases, one or both the gene loci in the father might be heterozygous(HhOO or HHOo or HhOo) and coupled with the mother's heterozygous genotype(a good guess considering the history of many recessive phenotypes), might produce a blue-eyed child due to homozygosity in any one of the gene.
There is a mutation in the germinal cells of the father which creates a non-functional mutant allele and thus can give a blue-eyed child with a heterozygous mother.
But in either case, considering independent assortment, the chances are very bleak.

But if we also take into account the linkage of the two genes, then the probability rises significantly. Now there is a good chance that the father's lineage might contain a heterozygous (or homozygous recessive) allele pair on a single chromosome, which due to their tight linkage, might pass on without any recombinations and therefore might evade phenotypic expression more efficiently(although, since a dominant allele in both the genes is required for the dominant phenotype, the extra evasion efficiency due to linkage is less). As given at the end of your reference, suppose there is one chromosome in the parental ancestry that carries both the recessive genes. If they are linked, the chances of brown eyed parents to have blue eyed children decreases (and the chance of being heterozygous also decreases) thus making it more likely that the father's lineage could have a recessive allele in spite of there being no significant expression in his family history. Therefore, more tightly they are linked, greater is the probability that the father is heterozygous. Linkage does not significantly lessen the possibility for the father to have a blue-eyed child since the mother does contain a recessive linked- phenotypic pair in all probability. (Actually, the probability is also based on which combinations are linked, but the possibility of there being a heterozygous allele remains positive with most combinations).This again gives some chance for brown eyed parents with the history you mention, to have a blue eyed child.

In any case, there is a chance but the probabilities depend a lot on the linkage, the linked combinations, and the actual genotypes of the parents but there is always a possibility.

ADDITION

Just to add a bit of information, the kind of recessive epistasis we described here, where the homozygous recessive (at the hypostatic,HERC2, loci) phenotype resembles the phenotype for the recessive condition at the modifier pair (OAC1), is only a part of the story. Actually, certain polygenic influences further complicate the situation by introducing a variety of phenotypes.


Which strains of C. diphteria are causing Diphteria toxin? I got this question:

Diphteria toxin is produced only by those strains of C. diphtheria that have which of the following characteristics?

Encapsulated
glucose fermenters
lysogenic for b-prophage
only mitis-strains
sucrose fermenters

I think the right answer is lysogenic for b-prophage, since Freeman found out that toxic gene is encoded by lysogenic phage infecting all toxigenic strains in 1951.
However, I am not sure what "b-" means in "b-prophage".

Which part is "b-" in Prophage?

Real simple: Beta!  Often called "phage beta" b-prophage is a more modern way to write it.  I knew that one off the top of my head, but I like to refer the general public interested in bacteriology to Tadar's online text.

It's nicely done, and I wish that it had been around when I was studying bacteriology.

Specific to your question:

  Hence, Corynebacterium diphtheriae can only produce the toxin
  responsible for the disease if it carries a temperate virus called
  phage beta. Only lysogenized streptococci  produce the erythrogenic
  toxin (pyrogenic exotoxin) which causes the skin rash of scarlet
  fever; and some  botulinum toxins are synthesized only by lysogenized
  strains of C. botulinum.


Is lemon water an alkalizing agent in the body? I was recently having a discussion with someone about whether lemon water actually increases the pH of your body (by which I assume they mean the blood); their claim was that once Citric acid was metabolised it results in an increase in pH due to the "anionic properties of citric acid".

I looked around on the internet at it would seem that this is a common claim circulating around health forums: Example 1, Example 2, etc.

Now to me this sounds like something which cannot possibly be true and appears to be a crazy health fad (they seem to spuriously appear and gain popularity now and again), and I cannot find any scientific papers or articles to support or refute their claim.

Can anyone provide a reliable scientific reference or provide a reasonable scientific explanation (preferably accessible to a layman with only A-level (college level) understanding of chemistry and biochemistry) which either supports or refute the claim that drinking lemon water (citric acid) increases the pH of the blood?

I have crossposted this to Chemistry.SE as well, as it is a crossover between chemistry and biochemistry.

The blood pH is tightly controlled since variations are quite dangerous for us. Under normal circumstances the pH is 7.4 (with a normal range between 7.35 and 7.45). Below that we are talking about acidosis, above it about alkalosis. If the blood pH goes about 7.8 or below 6.8, death will occur. This pH is maintained by the Bicarbonate-buffering system, for details see here and here.
Food that we take up does not directly influence the blood pH (and there is also no reason for us to do so, since this is tightly controlled and regulated), so this is a health fad. Details that debunk this myth about it can be found here, here and here.


Which human cell lines do not express the GLP-1 receptor? I need a human cell line that does not express the GLP-1 (glucagon like peptide-1) receptor.

I'm working with HeLa cells, do those express the GLP-1 receptor? Which other cell lines exist that don't express this specific receptor?

Are there any general resources where I could find this kind of information?

AbCam suggests HeLa cells as positive controls for their antibody to GLP1R. They provide the following pictures of HeLa cells labeled with their antibody:

(The image of the right is treated with synthesized peptide.)

According to Wikipedia, GLP1R is also expressed in pancreatic beta cells and the brain.


Creating ideal conditions for life Suppose some scientists built a large vat, sterilised it and filled it with distilled water. Then they start dissolving compounds into the water such as amino acids or what ever they deem conducive to life. They can also control temperature, radiation and other environmental factors.

They periodically capture a sample of the water and examine the results.

Would they be able to inadvertently create self replicating molecules and the precursors to life?

Would this kind of experiment be worth attempting?

That question was asked in 1953 by a classic experiment by Miller and his mentor Urey. You can find it on Wikipedia under "Miller_Urey_experiment"
Basically they zapped basic molecular building blocks to life with electricity and more complex molecules (amino acids) formed.
The experiment, with updates is nicely discussed here.
The experiment showed that the molecules required for life could be formed spontaneously on Earth from lightning. You would need amino acids, but also bipolar lipids, which can spontaneously form compartments. However, attempting to create life this way would not be worth attempting for two reasons, relating to time and scale. First (time), life has evolved only one time on Earth over 4 billion years. Second the scale of the entire Earth over billions of years is a pretty big experimental "test tube". It happened once in all this time, over all that space. A small side-issue; the fact that the codon table is optimized (and pretty universal, with only small differences), such that common amino acids have more ways to make them (more codons), and codons close to stop codons are for rare amino acids. This indicates that some early life experimented with alternative suboptimal codes that didn't make it.


How does a glucose molecule enter the cell from blood vessel? The transporters in the plasma membrane of the cells promote the entry of glucose molecules from the extracellular matrix to the cytosol of the cell. Could someone explain how does the nutrient molecule enter the extracellular space from the blood vessel?

For instance, in the context of the pancreas, the walls of the blood vessel is fenestrated. The literature also provides evidence for the presence of connexon in the endothelium of the capillaries.

My doubt is, the nutrient molecule that diffuses from the blood vessel reaches the cytosol of the cell through

Diffusing through connexon ?(or)
Does it reach the interstitial matrix(the fluid surrounding the cells) and then uptaken by the transporters present in the plasma membrane of the cell?

I think I understand your question, Natasha. In short, your own answer #2 is correct.
There are 3 spaces, and 2 pathways for glucose to pass from one to the next:

intracapillary plasma
extracellular fluid
the cytosol.

Ways glucose gets into the cell:

(2->3) To get from the ECF to the cytosol , glucose always needs a transport protein. These are the GLUTs. In two cases, the small intestine and kidney, these are part of a secondary active transport system based on the Na/K-ATPase. In the pancreas, it's GLUT2.

(1->2) To get from the capillary plasma to the ECF requires filtration, the process of applying hydrostatic pressure to the plasma and literally squeezing it like a sponge. The boundary of the "blood sponge" is the basement membrane. The membrane holds in the proteins, and lets anything dissolved in the watery serum (like glucose) through.

The Filtration Constant Kf is proportional to the percentage of the BM that is exposed in a given capillary, which varies by the type and other factors like histamine release.

Type 1 (continuous) has the lowest exposure of the BM (only the intercellular clefts). Type 2 (fenestrated)has the clefts and the fenestrations to expose the BM. Type 3 (sinusoids) have huge gaps between the cells, and importantly, an incompetent BM that allows proteins and cells through along with the watery serum.
Dynamic factors that change filtration rates:

Histamine causes the post-capillary venule's endothelial cells to contract, and exposes more of the BM allowing more serum filtration, but it also allows neutrophil extravasation, during which the neutrophils punch holes in the BM through which white cells can squeeze, which is why you get a proteinaceous exudate in Type I hypersensitivity.

Increase in blood flow Like a water balloon increasing its surface area with more blood flow, skeletal muscle capillary beds (Type I) increase their volume and surface area when engorged with blood during exercise. This doesn't change the Kf (the only exit for serum is still the intercellular clefts, but they're bigger now).

P.S. A 1985 morphometric study of pancreatic capillaries shows that the idea that endocrine glands need a boatload of bloodflow (high serum filtration) is valid. Even within a single capillary that feeds both an exocrine acinus and and endocrine islet, the side facing the endocrine islet had more fenestrae.


How can grass-fed livestock generate fat? How can herbivorous cattle get fat? These animals eat only grassy substances, think of cattle, buffalo, goats etc. For example, wheat grass contains 0% fat, and its nutritional value is limited to carbohydrates and fibers. Still, livestock can have substantial (10%) fat content and give milk with lots of fat on top of it.

Where does that fat come from?

Short answer
Plants typically store energy in the form of starch. Animals, including livestock and humans for that matter, can digest starch, metabolize it into acetyl-CoA and turn it into fat.

Background
Plants contain sugars, formed by photosynthesis. Plants generally do not store energy in the form of fats, but in the form of starch, a glucose polysaccharide*. Animals digest this starch through hydrolysis catalyzed by the enzyme amylase back into glucose (Fig. 1). Cellulose is another polysaccharide. In grass-fed cattle, it is mainly cellulose that forms their source of energy. Cellulose cannot be digested by ruminants (cattle, goats, sheep) as they are unable to synthesise the enzymes needed to digest cellulose and other plant compounds. Cellulose can be hydrolyzed by cellulase enzymes in e.g. Ruminococcus species present in the ruminant tract in the guts of these animals. The cellulase enzyme endoglycosidase cleaves the disaccharide cellobiose from cellulose, and another type of enzyme, β-glucosidase hydrolyzes cellobiose into glucose monomers (sources: Microbe Wiki, University of Waikato).

Glucose is then degraded to pyruvate by aerobic glycolysis in the cytoplasm of the cell. Pyruvate is then transported into the mitochondria, where pyruvate dehydrogenase oxidatively decarboxylates pyruvate, forming acetyl-CoA and other products (Fig. 2).

Acetyl CoA can then serve as a substrate for citrate synthesis. Citrate, in turn, can be transported out of the mitochondria to the cytoplasm. There it can be split to generate cytoplasmic acetyl-CoA for fatty acid synthesis under the influence of anabolic factors like insulin in times of plenty (Fig. 3), referred to as lipogenesis.

Fig. 1. Starch is hydrolyzed by amylase. source: Biotek

Fig. 2. Acetyl-CoA formation. source: University of Utah

Fig. 3. Lipogenesis. source: Sharing in Health

*: Although plants usually store their energy reserves in the form of starch, there are important exceptions to this. Most notably certain seed pods, like peanuts and walnuts, contain substantial amounts of fat. Further, cell membranes and other components will add traces of fatty substances even in grassy plants. With credits to Marzipanherz.


How does one identify a seed's species & variety? How does one identify a seed's species & variety, could it be done by some means of DNA or by use of a microscope?
Say for example, I had a pumpkin seed, I knew that it was a "small sugar pumpkin" variety, but how would one scientifically identify it to know that it was infact a small sugar pumpkin as well as a pumpkin without going through the process of planting it. Is there some kind of indicator on a DNA level that shows "This is what I am?"

My knowledge regarding biology is extremely basic, but I am very interested in knowing the full process of how this would work.

Yes, their name are "molecular marker". Every gene carrying a phenotype, quantitative or qualitative, is identified as an allele of every gene encoding for proteins.
In order to identify a phenotype using just infos gained from DNA, you'll need a previous library made by these gene regions, were every polymorphism between them is associated with a phenotype. For example, a kind of marker used for this kind of work is SSR , or "Simple sequence repeats" : it is made by a simple sequence of DNA interspaced between two other region. The number of repeats of the internal sequence could be associated with a phenotype.

So, by a simple PCR you could amplify this regions:

And by a electrophoresis you could see how much repetitions are in your band, using just the molecular weight.
Here is an example of SSR used for phenotype/genotype screening


Which wavelength to use to determine algae using a colorimeter? I am doing a Biology project involving the measurements of the density of algae (Nannochloropsis) using absorbance colorimetry. What wavelength should I set my colorimeter to?

The issue is that there are two types of chlorophyll, each with a different absorbance optimum, there is spectral scatter to consider, as well as UV absorption when going to low wavelengths. What to do?

From Biotek I learned the following:

  Spectral scans of algae cultures demonstrate significant absorbance below 400 nm as well as two distinct absorbance peaks at 440 nm and 675 nm (Figure 1). Cell number determination is most consistent when light scatter is used rather than absorbance by cellular constituents. In order to avoid influence from absorbing material 600 nm [is best] to monitor growth.

Figure 1. Absorbance spectral curve of Microcystis aeruginosa suspension cultures.Source: Biotek


What makes us "tired" in the gym that forces us to rest? If I'm doing push ups or any other of gym exercise, I can do 10 in a row, but each one I do I feel more "tired", but if I rest for 5 minutes, I'm much "full of energy". Please explain me exactly what is different in my muscles chemistry.

I read that lactic acid overproduction is possibly linked.

I think you refer to the Muscle fatigue:

  A state of exhaustion or loss of strength and/or muscle endurance following strenuous activity associated with the accumulation of lactic acid in muscles. (Source)

So yeah, you're right about the lactic acid overproduction :)

How Muscle Fatigue Works ?

During short term (anaerobic) exercise, ATP and creatine phosphate (CP) are used up within the first 7 seconds of training. This signals the metabolism of glycogen to produce energy for your body. This process is known as glycolysis.

During glycolysis, glycogen (muscle sugar) is broken down to produce more CP. The breakdown of CP releases energy, which catalyzes a reaction to produce ATP. The production of more ATP allows movement of the muscle to continue.
Lactic acid is a product of glycolysis created by the breaking down of pyruvate.

Lactic acid is then disassociated to produce lactate. When lactic acid (C3H6O3) releases a hydrogen ion (H+), the remaining compound binds to a sodium ion (Na+) or a potassium ion (K+) to form a salt. It is this salt that is lactate.

Now the cell contains a lactate compound and a free H+ for each compound of lactic acid that is produced. It is this increase in cellular H+ that causes the pH to decrease, becoming more acidic. The acid in the muscle causes the fibers' calcium-binding capacity to decrease, thus limiting muscle contraction. This is the cause of muscle fatigue.

So the muscle Fatigue occurs when the muscle experiences a reduction in its ability to produce force and accomplish the desired movement.

Short term fatigue (failure to lift a heavy weight, do more push-ups, etc.) is different than long term fatigue such as as a marathon run, a 100 mile bicycle ride, or a full-day hike through the Rocky Mountains of Colorado.

Muscles become fatigued during high intensity exercise, most notably that the demand for oxygen can be greater than the supply. The blood flow to the muscle can be reduced because of :

muscles intensely contracting can reduce blood flow and thus oxygen availability, or
the muscle is simply working so intensely that there literally is not enough oxygen to meet demand (a sprint at top speed).

The factors that explain fatigue are complex and after more than 100 years of investigation are still a topic of active research, you can check those articles for more informatoins :

Experiment: EMGs during Muscle Fatigue
All About Muscle Fatigue
Skeletal Muscle Fatigue: Cellular Mechanisms


What is the trigger of pollen tube formation when the pollen is on the stigma? What is the mechanism of pollen tube formation when the pollen is close to the stigma ?

Is it because of chemotaxis? In other words, is the growth triggered by some chemical substance that is released by the stigma?

We have learnt that on a stigma of a flower, you can sometimes find pollen of other plant species. Would these pollen grains also form tubes in response to a possible signal from the stigma of a different species?

EDIT :

So in this experiment we put pollen grains in 2 bottles which contained all chemical substance required for the formation of pollen tube.

In bottle 2 we observe that all pollen tubes are oriented to the stigma! If it really is some kind of chemotaxis then what is the chemical substance that causes this?

Germination of the pollen tube begins when the pollen grain becomes hydrated on the tip of the stigma. The pollen grain absorbs water and also exchanges signals with the stigma. Microchannels form between the pollen grain and the tip of the stigma papillae and water is transferred from the stigma to the pollen grain (Taylor 1997). cAMP, which is produced by the protein PSiP, and cytosolic free calcium can be used as signals to orient the pollen tube to grow in the proper direction (Moutinho et al 2001).

Pollen tubes can also germinate in vitro even without contacting a stigma. If you place a pollen grain in germination medium, which contains calcium and boron, among other things, the tube will germinate but it will not grow to its full length.

Often when pollen of a different species lands on the stigma, the pollen will germinate but the pollen tube growth will stop before it reaches the ovary (Ascher and Peloquin 1968). Mating barriers are very complicated, however, and there are many different mechanisms for species recognition and arrest of pollen tube growth. In some cases, the tube is halted in the style while in other cases the tube grows, but slowly and inefficiently (Swanson et al. 2004). Species recognition in some species (for example, tobacco) is related to self-incompatibility and the S-locus. Species recognition can also be unilateral: that is, the pollen of species A can fertilize the ovule of species B, but the pollen of species B cannot fertilize the ovule of species A.

I would recommend that Swanson paper if you want to read more.


What advantages could there be for using the unseen variant chosen by He Jiankui instead of the naturally occurring CCR5-∆ 32 mutation? Jennifer Doudna mentioned in https://youtu.be/9Yblg9wDHZA?t=2566 on 2019-02-21 that  He Jiankui introduced an unseen variant of the CCR5 gene when gene editing the twin humans Lulu and Nana. What advantage might there be for using that unseen variant instead of the naturally occurring CCR5-∆ 32 mutation?

Figure from the above-mentioned YouTube presentation showing the CCR5 gene and some variants:

I have crossposted the question at:

https://qr.ae/TWtxdj
https://www.youtube.com/watch?v=9Yblg9wDHZA&lc=UgwInhQJsw8lhfQBVlJ4AaABAg

Possibly He Jiankui was using Cas9 without a template DNA.  If so, this generates double-stranded breaks that are repaired through processes such as non-homologous end joining (NHEJ) that often produce small indels (deletions and insertions) 1.

This is consistent with the apparently random small deletions and insertions around the cut site seen in both girls.

An additional, unflattering possibility is that this way he could prove that these were his edits and didn't happen spontaneously.

Useful starting points for understanding how Cas9 works can be found at the Addgene website and on Wikipedia.

Reference:
1: Brinkman, Eva K et al. “Kinetics and Fidelity of the Repair of Cas9-Induced Double-Strand DNA Breaks.” Molecular cell vol. 70,5 (2018): 801-813.e6. doi:10.1016/j.molcel.2018.04.016


Is the mesenterium a synonym for the mesocolon? On biodigital anatomy browser I found a structure called the mesocolon. I didn't find the term in Uberon and I'm unclear whether it's simply a synonym for mesenterium or whether it's a separate concept.

Mesentery is the name of a whole set of tissues attaching the intestines to the abdominal wall.

In human anatomy, there are three different portions of the mesentery:

Mesenterium sensu strictu, also called Meso
Mesocolon transversum
Mesocolon sigmoideum, also called Mesosigmoideum

Two smaller mesenteries can be found at the appendix (Mesoappendix), and at the cranial part of the rectum (Mesorectum)

So... Mesocolon is a part of the mesentery, but no synonym.


Is severe but short-term pain worse than moderate but prolonged pain for the body? I'm wondering about the effects of different durations and intensities of pain on the body. So the two can be compared, let's say that the cause of pain is the same in both cases, but in one the duration is shorter although the pain is more severe, and vice versa. Also, by effects, I mean biological but also psychological (which is probably more interesting), but the latter might be out of the scope of this site, so forgive me if it is.

For the sake of a (rather grim) example, if someone is exposed to a painful stimulus such as a mid-voltage shock for a long duration, and if someone else is exposed to a much higher voltage shock for a much shorter duration of time, which would produce worse effects on the body's normal functioning? (Somewhat morbidly, I should say to assume that they both live and do not die on the spot.) Since the answer very well might depend on the type of harmful stimulus, I'll give another example of a burn. If one is repeatedly subjected to a first-degree burn for a while and another is subjected to a third-degree burn only once, which is worse?

Upon pondering the question, it seems that the psychological effects would be more interesting since they should be roughly the same regardless of the type of stimulus, but biologically the effects obviously differ.

Thank you for your time, and any responses or thoughts on this would be greatly appreciated.

Edit: Obviously most experiments to test this would be subjective and unethical, especially in the case of psychological effects, so just an opinion from someone more knowledgeable in biology is more than fine.

The biological part of the answer to your question depends on the thing causing the pain. Burning for example, a large burn can be very life threatening biologically but small burns are not as harmful comparatively. But the psychological harm they would cause is phenomenal. This is because large burns open up the body to infections, dehydration and a lot of other harm.

Let's take stabbing as another cause of pain. One stab in a less dangerous place missing all important structures may be not that harmful but may be painful. However multiple small stabs into important structures like arteries or spinal cord could be horribly destructive.

Then let's look at headaches or nerve pain. Here it is only the pain and usually there isn't any destructive or harmful process. Most individuals would take one really, really bad headache followed by never having a headache then chronic daily "tension" headaches.
Psychologically though usually the chronic daily pain is the worst. Particularly as without adequate pain management from the start, it is less responsive to painkillers (analgesia). It frequently adds to depression if it does not cause it itself and can lead to suicide. Also painkillers themselves may cause chronic pain which does not help.

In summary, acute severe pain suggests something is seriously wrong and needs to be dealt with immediately biologically as there is likely a damaging process underlying it. However if this event is survived, it may be linked with high disability from any biological process that underpinned the pain. Chronic daily pain suggests a long continuing process. The cause of this may be life threatening, such as cancers, but is usually less dangerous at least compared to acute severe pain biologically. However the psychological aspects of this pain are seriously important as they can be particularly detrimental.


An unexpected mushroom in my garden My grandma is a great fan of mushrooms and knows quite a lot about them. About 10 years ago, she started throwing out mushroom remnants in one special place, in order to grow her own mushrooms. In fact, for last three years we found some parasol mushrooms (Macrolepiota procera).

Today she found something, that nobody at home can classify. From what I searched, it might be  Cortinarius privignoides, but it is marked as almost extinct here in Poland, so I doubt this classification. Maybe you have seen this or know what it really is:

The hat is light brown with faint violet shades, the leg on the outside is partly violet too, but the inside is all white.

Some more photos:

All three

The gills are lighter brown, also with a violet tone

The cut through the leg

The cut through the hat

At my parents' house I found one more mushroom atlas, and a new candidate: Cortinarius traganus, but one thing is not right - the ones that I have don't have a smell and gassy webcap should smell and taste bad.

Thanks to MCM's advice I know for almost-certain that this is Lepista personata.


How to learn biomathematics? I'm currently an undergraduate math student and researching on the internet I discover that exists an area called "biomathematics". Looks so interesting. They use the graph theory and topology to describe the cells and DNA structure. Was love at first sight, because I really love maths and biology.

I'm reading the book "Clinically Oriented Anatomy" of Keith L. Moore and "Essential Cells Biology" of Bruce Alberts, but I don't know if I'm doing right. If anyone know how to start to learn this science I would really appreciate it.

MathsBio is quite a large field. It is an interdisciplinary branch having utility in a lot of branches in biology like biophysics, biomedical, genetics and molecular biology. Applied  Mathematics is generally used in modelling and understanding biological phenomena where we have to deal with large amount of data, for example the use of graph theory for analysing biochemical networks. Systems biology is an emerging field which uses a lot of mathematics.

You should pick a book depending on the field in which you want to use mathematics, though having knowledge of elementary biology is necessary. I am suggesting some books which cover wide application of mathematics in biology.

Mathematical Biology: I. An Introduction by JD Murray

For systems biology:

Mathematical Modelling in Systems Biology: An Introduction by Brian Ingalls


Is there any database with RNA classification? I am looking for a database that would provide classification of various types of RNA - information about its structure, function, etc.

Rfam is a database about RNA families, similar to Pfam (wich is for proteins). I think it's what you're looking for.
http://rfam.sanger.ac.uk/search

You could also enjoy miRbase, a database for micro RNAs: http://www.mirbase.org/
There are tRNA databases, too, like this one: http://trnadb.bioinf.uni-leipzig.de/
And this tool for predict RNA secondary structure (However, this kind of tools aren't as good as they proteinic counterpart): http://mfold.rna.albany.edu/?q=mfold/RNA-Folding-Form


The pBR322 convention 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.

pBR322 is a distant ancestor of pET28a. If you compare the two maps below you will see that they have the same replicon labelled as ori or pBR322_origin.

The map of pBR322 is shown in the conventional orientation: the single EcoRI site is at coordinate 0/4359 and numbering proceeds in a clockwise direction through the BamHI site. The map of pET28a is presented with the pBR322-derived ori element in the same orientation (note the labelling of a pBRrevBam_primer also). Because of the way that the pET vectors were built, this means that in the conventional depiction the expression region runs counter-clockwise.


Inheritance simulator not working properly I created a python program to simulate inheritance (a simplified version of it) to better understand how it works. A person is represented by a class that contains a chromosome property, a method for reproducing with another person, a method for generating gametes (through recombination), and a method for calculating how similar a person is to another person (by comparing the chromosomes).
The problem with my program is that cousins are not as similar to each other as they are supposed to be. My program says that 2 cousins about 75% similar when they should be 12.5% similar. I don't understand why this is. I think it could be down to 2 things

My similarity function is wrong.
The way I am representing a chromosome is wrong.

Here is the code:
    import random

    CHROMOSONE_LENGTH = 1000
    NCHROMOSONES = 22

    class Person:
        def __init__(self, chromosones = None):
            self.chromosones = chromosones
            if  chromosones is None:
                self.chromosones = []
                for i in range(NCHROMOSONES):
                    self.chromosones.append ((self.get_random_dna(),self.get_random_dna()))

        def get_random_dna(self):
            #return [random.random() for x in range(CHROMOSONE_LENGTH)]
            return [random.choice(["0","1"]) for x in range(CHROMOSONE_LENGTH)]

        def get_gamete_meiosis(self):
            gamete = []
            for i in range(len(self.chromosones)):
                gamete.append([])
                for a,b in zip(self.chromosones[i][0],self.chromosones[i][1]):
                    gamete[i].append(random.choice([a,b]))
            return gamete

        def reproduce(self,mate):
            chromosones = []
            my_gamete = self.get_gamete_meiosis()
            mate_gamete = mate.get_gamete_meiosis()
            for i in range(NCHROMOSONES):
                chromosones.append((my_gamete[i],mate_gamete[i]))
            return Person(chromosones)

        def get_similarity(self,other):
            sim = 0
            for s,o in zip(self.chromosones,other.chromosones):
                for a,b,c,d in zip(s[0],s[1],o[0],o[1]):
                    if a == c or a == d:
                        sim += 0.5
                    if b == c or b == d:
                       sim += 0.5

            return sim/(CHROMOSONE_LENGTH*NCHROMOSONES)

    grandmother = Person()
    grandfather = Person()
    child1 = grandfather.reproduce(grandmother)
    child2 = grandfather.reproduce(grandmother)
    grandchild1 = child1.reproduce(Person())
    grandchild2 = child2.reproduce(Person())
    # Should be 12.5%
    print(grandchild1.get_similarity(grandchild2))

A chromosome is represented by an array of 2-tuples. Each tuple represents a chromosome pair. The number of pairs is set by the NCHROMOSONES variable. There are 22 pairs in the above code.
The actual genetic data is represented by an array of 0s and 1s. The number of 0s and 1s in a chromosome is set by the CHROMOSONE_LENGTH variable.
The similarity function takes two people and compares them at each position of each chromosome. If the two people have the same number at a given position, then it adds 0.5 to the sim variable. It then averages this across all positions. The reason I add 0.5 is because two people can either be 0%, 50% or 100% identical at a given position on a chromosome. 0% occurs when neither pair is identical, 50% occurs when 1 pair identical, and 100% occurs when both pairs are identical.
I noticed that as I use more symbols than just 0 and 1 to represent genetic data, the similarity actually approaches 12.5%. But I don't understand why this should be.
So my basic questions are:

Is my way of calculating the similarity correct.
Why can't I use just 0 and 1 to represent genetic data?

There are a couple of things going on here, I think. Let's start with simple conditional probability:
import random

sim1 = [random.choice([0, 1]) for x in range(1000)]
sim2 = [random.choice([0, 1]) for x in range(1000)]
for locus in range(1000):
   if sim1[locus] ==sim2[locus]:
     match+=1
print(match)
# prints 492

In other words, even two completely independent samples from [0,1] with uniform probability are expected to match about half of the time (492 / 1000 ~ 50%).
So you are correct, the problem lies in your fashion of encoding the data. When you are talking about "similarity", what I think you mean is "identical by descent". This is distinct from "identical by state", meaning what actual alleles you have.
Two individuals can be identical by state at a large number of loci without any significantly close family relationship, if they are members of a population without a lot of common alleles. This is close to what we mean when we say that humans are all 99.9% identical to each other- this is because most of the positions in the genome have very little variation. So, if you choose two people who have no common ancestors in the last 1000 generations, they will still be identical by state for >99% of their loci. This is the real lesson that your simulation is showing you, I think!!
If you want to show identity by descent, you will have to choose a different encoding. Using e.g. nucleotides will still run into the problem that very frequently the nucleotides will be identical by state in unrelated individuals, whereas what you actually care about is "did this allele originate from the exact same ancestor". So you want some way of guaranteeing (or nearly so) that every ancestor contributes a distinctive, unique allele that you can always distinguish. For example, the following code will produce a "unique" identifier that could be used for each founder individual (e.g. every time you call Person():
import uuid
unique_id = uuid.uuid4()

So really, what your Person.get_random_dna() method should do is something like this (minimal modification to your code):
        def get_random_dna(self):
            unique_id = uuid.uuid4()
            return [unique_id for x in range(CHROMOSONE_LENGTH)]

You may need to fix something else as well, I have not actually run this.


Can an adult without genetic lactase persistence still develop a tolerance for dairy foods? While investigating the rise of adult lactose tolerance, I came across the news that China has been encouraging its citizens to drink more milk, even though most of the Asian population lacks the SNP (single-nucleotide polymorphism) which conveys lactase persistence.

Is it still possible for an adult without lactase persistence to build-up a tolerance for lactose over time? If so, what's the mechanism?

It seems that yes, it is possible to increase the tolerance for lactose over time, and it has to do with the adaptation of microbiota.

A simplistic explanation comes in the following article:
 Hertzler SR, Savaiano DA. 1996. Colonic adaptation to daily lactose feeding in lactose maldigesters reduces lactose intolerance. The American journal of clinical nutrition 64: 232–6.

In which the authors claim the following:

"Colonic adaptation appears to reduce the symptomatic response to lactose via several mechanisms. (...)
(...) increased β-galactosidase activity after regular lactose ingestion indicates that colonic bacteria are able to ferment lactose more rapidly. (...)
(...) This metabolic shift is thought to result from the proliferation of lactose-fermenting, non-hydrogen producing organisms such as Bifidobacteria."

This article makes reference to another one which supposedly explains the microbiota adaptation:
Hill Mi. Bacterial adaptation to lactase deficiency. In: Delmont J, ed. 1983. Milk intolerances and rejection. New York: Karger: 22–6.

But unfortunately I could not find the full text. I hope you are luckier than me.


Why does exhaled air still contain oxygen? I am a high school student and I am a little confused in the concept of breathing:
My confusion is that, when we talk of exchange of gases we say that gases always diffuse from their high "PARTIAL PRESSURE" to their "LOW PARTIAL PRESSURE" and we know that partial pressure of oxygen in our alveoli is about 104mmHg and in our blood vessels it is about 95mmHg ,so we can see that this statement sounds true.
But partial pressure of oxygen in atmospheric air is about 159mmHg and in alveoli it is about 104mmHg then why the air that we exhale also have about 16% of oxygen in it? I think this statement is not correct oxygen don't have brain it will always move from the higher PRESSURE OF TOTAL MIXTURE TOWARDS THE LOWER PRESSURE OF TOTAL MIXTURE, e.g assume a balloon filled with different gases in it and total pressure of gases inside the balloon in much higher than the surrounding, but balloon has very less amount of Oxygen in it as compared to other gases so, its partial pressure is less then the surrounding so of course when you let it go all the air from balloon rushes out even oxygen, and its seems logical as oxygen doesn't know how is it different from other gases , how only oxygen can left inside the balloon?
I think beside this In exchange of gases we would talk in terms of partial pressure because we have to talk only about oxygen and carbon-dioxide ,not all gases, so just to represent their concentrations we talk in terms of partial pressures? But saying this statement that gases always diffuse from their high partial pressure to their low partial pressure this is wrong ,please correct me If I am going wrong somewhere and please give a logical explanation to it.
human-biology

You seem to be confused about diffusion versus bulk flow of fluid (air/gas).
In the lungs, there is diffusion between blood and the gas in the lungs. There is sufficient surface area that these equilibrate fairly quickly, and the partial pressure of oxygen in blood leaving the lungs is very similar to the gas in the lungs. Partial pressures are the best way to understand and explain diffusion of gases.
When you breathe out, a fraction of the bulk air moves out and mixes with outside gas. The partial pressures don't matter for this part, however, all that matters is that you have a big opening (as far as a gas is concerned) through the mouth/nose. Then again, when you breathe in, a fraction of bulk external air moves in and mixes with gas that remained in the lungs (you never completely breathe it out). This mixture will initially have more oxygen in it than the mixture that was exhaled, but it again quickly equilibrates with the blood via diffusion.
If you were to breathe in and wait long enough, eventually the partial pressure of oxygen in the blood would drop (used up in metabolism), and the concentration in the lung gas would also drop to match. However, you would lose consciousness far far before this would ever approach "zero".
The lungs are not a machine to pull all the oxygen molecules out of the air and provide it to the body. They are a gas-exchange surface to provide a massive surface area to help make the internal oxygen concentration as close as is possible to the external oxygen concentration. It never quite gets there, of course, but it gets relatively close.


Confirmation for a picidea I am sorting some pictures and found this one taken from Swiss Jura Mountains (North part, alt ~700m) in March 2013.

The day before I saw a Dendrocopos major (Great spotted woodpecker) and without looking thoroughly before I though it would be a young one.

Now when I examine in more details the picture it seems to be a Dendrocopos medius (Middle spotted woodpecker).

Am I right? Can someone confirm this?

You are right, this must be a Middle spotted woodpecker Dendrocopos medius. It has clear stripes on its belly, and the black stripe on its cheek does not reach the beak. The beak is also  smaller, but size is always hard to judge.


Can the RNA in the HIV virus make viral enzymes without entering the nucleus? If the provirus was not formed yet, can the virus make viral enzymes?

(I know that it already has some, but supposing it doesn't)

I am afraid your question is really not clear. You are asking one thing in the title of your question, another in the question body and a third in your comments. If you are asking (as you did in your comment above) what would happen if a virus with no enzymes were to infect a cell, see below.

In the case of HIV (and other retroviruses) some of the most important enzymes contained in a normal viral particle are:

A reverse transcriptase (RT): this enzyme reverse-transcribes the viral RNA genome to cDNA,
An integrase: incorporates the cDNA produced by the RT into the host cell's DNA.
A ribonuclease : an enzyme that can degrade (cut up) RNA. In the case of HIV this is the same protein as the RT.
A protease: an enzyme that can degrade other proteins.

Viruses work by copying their genetic material (their DNA or RNA) into the host cell's genome and then hijacking the cell's replication machinery to make more copies of the virus. So, what would happen if these enzymes were absent?

Without an integrase, the virus would not be able to insert its reverse transcribed DNA into the cell's genome.
Without an RT, the virus would not be able to copy its RNA into DNA.
The ribonuclease activity is also needed for successful reverse transcription to double stranded DNA (see [1] for a review and explanation of why.)
The protease is necessary for the formation of new viral particles. Mutations in this enzyme result in aberrantly assembled virus particles with low infectivity [2].

What you really must remember is that viruses are extremely streamlined. Everything they contain is essential. In some ways, you could say that viruses are the most highly evolved species (assuming they are living species), they are the most highly specialized "life forms" we know of and they have managed to get rid of all non-essential functions. The flip side of this is that everything that is left is essential, the virus cannot function without it.

So, to answer your question, a virus without any enzymes is, essentially, not a virus. It would not work, would not successfully infect cells.

References:

Greg L. Beilhartz and Matthias Götte, HIV-1 Ribonuclease H: Structure, Catalytic Mechanism and Inhibitors, Viruses 2010, 2:900-926
Bukrinskaya A. HIV-1 matrix protein: a mysterious regulator of the viral life cycle. Virus Res. 2007 124(1-2):1-11.


How does smoking, an environmental factor, cause cancer, fundamentally a genetic disease? If cancer is fundamentally a genetic disease, how might an environmental factor such as smoking cause cancer?

Because cigarette smoke contains many carcinogens.  Carcinogens can cause cancer by directly affecting the genome.  Wikipedia has a list of those present in cigarette smoke, which includes classics such as lead, benzene, and formaldehyde, not to mention radioactive polonium.


Why does radiation sickness cause hair to fall out? As I understand it, radiation poisoning (acute radiation syndrome) is fatal because the radiation kills cells. However, why do victims experience hair loss at such an early stage in the process?

Radiation poisoning causes mutations in DNA that affect normal cell function, often causing them to die.  Cells normally have a number of repair mechanisms but if the damage is too great they won't be able to do so.  In particular, cells that are dividing quickly will not have time to repair their DNA before division and so die far quicker than other cells.  Chemotherapy is built on this concept.  By selectively introducing drugs or radiation that target fast-dividing cells, the cancer cells, which are very dividing rapidly and unchecked, are killed off before most normal cells.

However, there are some cells in the body that are very rapidly dividing.  Hair cells are one such type, hence hair will often fall out during chemotherapy or radiation sickness.  Another big cell type are those in the gut, which are constantly dividing.  That's why you often see people in movies who have been exposed to radiation vomiting.  The radiation targets those cells first, hence those are the first symptoms.


Temperature Tolerance In Relationship To Body Temperature A humans body temperature averages at around 98.6°F
A dog's body temperature averages at around 101.5°F

If the temperature outside is 45°F who would feel colder?

The dog's temperature is higher than the human. So you would assume since its temperature is higher it would feel warmer than the human.

However, the temperature difference between the body and the external temperature is the following:

Difference in humans internal and ambient temperate: 52.6°F
Difference in dog's internal and ambient temperate: 56.5°F

I'd like to know as I keep telling my mom that the dogs feel hot when she puts on doggy sweaters for them when its slightly cold for us humans.

Things other than the temperature that could affect whether or not the coat is necessary: Is it raining? a wet dog will get cold quicker. How long/thick is the fur? thin coats of fur will be less efficient at keeping the dog warm than thick. Is it windy? Wind blows warm air out of the fur. How big is the dog? Size & body fat will affect the rate of heat loss. How active is the dog? A dog doing lots of fetching will keep warmer than a dog ambling along the pavement.

Clues as to whether the coats are necessary: Is the dog shivering? if yes, give it a coat. Is the dog panting? yes, take the coat off before you bake the thing!

this probably does not fully answer the question "If the temperature outside is 45°F who would feel colder?" but as requested by the OP I have posted my comments as an answer. I would expect a dog without a "doggy sweater" to be better able to cope with the cold than a human not wearing a "people sweater" or any clothes, just like the dog, if you want to make it a fair test!


Is this a carpenter ant? I stumbled upon a few hundred of these swarming around two different places in my living room today. They kind of look like a carpenter ant to me, but I'm not sure.

Also, I'd love to know how you identified the ant.

// EDIT, per a helpful suggestion, I'm in Los Angeles, CA, US. We just had rain come through within the last 4-5 days and it has since dried up.

No, this is not a carpenter ant...it's possibly a Pavement Ant (Tetramorium
caespitum) - only it's a male & hence winged....for identification...follow these guidelines-

  Pavement ant workers are small, l/8-inch to 3/16-inch
  long, and blackish brown with light-colored legs and two spines at the
  end of the thorax. A distinguishing character, visible with a hand
  lens or microscope, is the series of fine parallel groves on the head
  and thorax


How many mutated genes from a complementation test? With 1, 3, and 5 being defective together, that means they are on the same gene. 3 and 5 are defective together too, meaning they are on the same gene as 1. Why does this slide say that there are 3 mutated genes? I must be missing something, I don't think I understand something.

There are 5 mutations being tested in these complementation test.

The first gene, carries mutation number 2.  In other words, mutation number 2 complements mutations, 1, 3, 4, and 5, and fails to complement itself.

The second gene, carries mutation number 4. In other words, mutation number 4 complements mutations 1, 2, 3, and 5, and fails to complement itself.

The third of the three genes, carries mutation 1, in one strain, mutation 3, in a second strain, and mutation 5, in a third strain.  In other words, mutations 1, 3, and 5 all fail to complement each other, yet all three complement mutations 2 and 4.

There are 5 different strains in this experiment, and there are five different mutations (one in each strain), but the five mutations only affect three different genes.


What is the difference between xDNA and yDNA? Wikipedia states that:

  xDNA contains expanded bases, in which a benzene ring has been added, which may pair with canon bases, resulting in four possible base-pairs (8 bases:xA-T,xT-A,xC-G,xG-C, 16 bases if the unused arrangements are used). Another form of benzene added bases is yDNA, in which the base is widened by the benzene.

In this context, does widened and expanded refer to the same thing? If so, what would be the exact different between yDNA and xDNA.

NOTE: I am not referring to the X and Y chromosomes.

yDNA came first:

  Lee & Kool (2005) A New Four-Base Genetic Helix, yDNA, Composed of Widened Benzopyrimidine−Purine Pairs. J Am Chem. Soc. 127: 3332-3338

As seen in this Figure from the paper it is a DNA consisting of T and C substituted with yT and yC, widened analogues.

xDNA came next (also from the Kool lab.):

  Lynch et al. (2006) Toward a Designed, Functioning Genetic System with Expanded-Size Base Pairs: Solution Structure of the Eight-Base xDNA Double Helix. J Am Chem. Soc. 128: 14704-14711

As seen in this Figure from the paper, xDNA consists of an 8 base system A,C,G,T,xA,xC,xG,xT.

This field is reviewed in:

  The XNA world: progress towards replication and evolution of synthetic genetic polymers
  Pinheiro & Holliger (2012) The XNA world: progress towards replication and evolution of synthetic genetic polymers. Current Opinion in Chemical Biology 16:245-252


Do Class A biosolids count as organic fertiliser? Does Human Waste, which has been treated at least twice to remove pathogens & remove stink, still count as organic despite it passing the EPA's class A standard?

If so, does this mean that none-GMO crops grown in this fertiliser are still organic?

Thank you to those that take the time to answer.

Definition of "organic" in Science

In science (esp. in chemistry), organic matter loosely refers to matter that eventually make up living beings are are remains of living beings. Typically organic matter consists of long chains of carbon surrounded by hydrogen atoms and a few oxygens and nitrogens (and eventually other things such as sulfur and phosophorus).

Can we eat something that is not organic?

Unlike plants, we (all animals and fungi) are heterotrophs (feed on organic matter only). As a consequence, there is no such thing one could call food that would not be organic.

The (mis)use of the term "organic" in popular culture

In the popular culture organic is a term that tries to refer to certain type of food that are grown under certain conditions and treated a certain way. However, there is really no good definition of organic in the popular culture and there exists no objective definition that would satisfy someone that wishes to categorize food into what they like to call "organic food" and "not organic food". Similarly there is no good objective definition of GMO either.

Some organization may make up definitions of "GMO" or "organic food" but those definitions rely on a long list of products rather than to an actual definition.

I just want to attract the attention of the naive reader that I am not saying that the term organic as used in the popular culture is healthy/not healthy or good/bad. Arguments concerning whether it is ethical to buy organic food goes both ways and it is not the job of a science website to discuss questions of ethics.

Are GMO safe to eat?

You are not asking this question here. But in case you wonder you might want to have a look at the Skeptics.SE post: Is Genetically Modified food safe to consume?


What is the meaning of expansion of T cells? In immunology, what does it mean by the term 'expansion' of T cells ex-vivo and activate it (generally with reference to cancer immunotherapy)?

In immunotherapy, the T cells need to hit a therapeutic dose. The dose is normally determined pre-clinically or in a phase I or I/II trial. A good example is the YESCARTA label dose information:

  YESCARTA comprises a suspension of 2 × 10^6 CAR-positive viable T
  cells per kg of body weight, with a maximum of 2 × 10^8 CAR-positive
  viable T cells in approximately 68 mL (3).

YESCARTA commercial label

Lets run through a hypothetical situation based loosely on information obtained in this publication.

So say you have a cancer patient that weighs 70kg on the day they obtain a leukapheresis for their starting material. The manufacturing facility is going to say okay, we need to produced 2E6 viable CAR+ cells/kg for a 70kg patient in 68mL per the label indication. So your final product needs to have 140 million viable CAR+ cells.

The patient leukapheresis can go wildly different on a patient-specific basis due to factors such as current treatment or disease. Your separation method can result in loss. Cells die in their initial culture period pre-transduction, and they can die post-transduction. So case study in point from the paper I linked:

Their patient 029-03 ended up with 0.494E+09 cells in their leukapheresis. Transduction efficiencies aren't published for a lot of these, but lentiviruses are typically employed and efficiencies can range from 1-90% depending on numerous factors. The manufacturer needs a target efficiency of ~28% to hit 140E+06 total cells if they manage to isolate every single CD3+ cell, but if they're 85% viable for example, they still wont hit the target dose. So you need to expand the cells aka make them divide so you hit the target therapeutic dose.

You typically culture your cells in IL-2, a potent T cell stimulator, but activation can improve transduction and stimulate cell division aka expansion. You can use something like CD3/CD28 beads, for example. These provide the so-called signals 1 and 2 that stimulate T cells in a similar way antigen challenge would.

Let me know if anything is unclear.


Can you knockout specific receptors in an adult? Sorry I don't have a good understanding of this topic, but I'm guessing that "receptor knockout" is related to/a part of "gene knockout"?

And If I understand correctly, gene knockout is currently not yet possible to do in an adult (maybe possible in a small area/specific organ, but not systemically) ?

So does that mean a systemic receptor knockout is not possible and maybe possible in small specific areas?

Short answer: yes, it is possible.

But there are some requirements for your delivery system. "Gene knockout" ("gene KO") means such DNA modification that is permanent (get inherited by cell's progeny) and deleterious to gene function (e.g. protein no longer get produced).

So your system must deliver DNA "mutation agent" to all cells (of organism or small specific area). This can be done by using viruses and, for example, CRISPR/Cas9 system for genome editing. Idea  is that virus will get in the cell, start expressing component for genome editing, multiply and infect neighboring cells. Modification in virus can make it non-lethal and less harmful, so you don't kill tissue in process. Virus delivery can be site-specific (e.g. direct injection into the area), it also might be cell-type specific if virus is tailor accordingly.

Also, remember that CRISPR/Cas9 and other similar techniques have efficiency well below 100% and also that you often have two copies of the same gene. This means that total KO probability goes as square of single copy KO probability. If for one event probability is 50%, for both it will be 25%; 10% becomes 1%.

So, all principle component for such experiment already exist.


Can the innate immune system defeat a pathogen by itself? Fast enough that we don't develop antibodies, etc.? Would we have any way of knowing if our innate immune system destroyed a pathogen without involving the adaptive?

Could a symptomless person who tests positive for COVID-19 with the RNA test, e.g., later test 'negative' for exposure on the antibody test?

Generally antibodies are formed, but it is possible that innate immune system has cleared out the pathogen. But antibodies will be formed even after that, as adaptive immune system has received  the stimulating signals from helper T cells, which are matured during the innate immune responses triggered by an infection.
This signal triggers B cells to produce antibodies. Antibody production is activated because of signals from innate immune system.

So, even if infection is cleared by innate immune system, still antibodies will be synthesized.

Reference:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3399021/

https://medicalxpress.com/news/2020-05-dont-antibodies-immunity.html


How does the brain regulate its temperature? I recently ran into a bio-physical paradox while trying to solve an engineering problem, using nature's way as a guide; namely the brain.

I'm working on designing a totally new system of liquid/gas cooling for a project. In Normal systems, the coolant is first cooled at a point, then sent along to the target areas; however, the coolant gets too hot along the way and cannot meet my target at one of the end components. Additional external cooling fins along the path still do not compensate.

I took biology classes in college and recall some mechanisms of the brain and pictures too (usually depicting the brain as all white internally). So, I theorized that maybe the coolant (blood) was not in direct contact with the brain in a substantial volume; however that was debunked: Why is the brain white?

From what I gather from the major answer, the brain's way of achieving homeostasis might present the answer to my problems. There is a lot of blood in the brain. This blood comes from the carotid arteries, which means it comes from the main circulation, and is hence at body temperature {considering homeostasis of all the body organs i.e. the lungs in this case}. By connotation, the brain should be the hottest organ in the body!

Considering the volume of blood in the brain, how does it regulate its temperature?

From what I can make up from your question is that you assume the blood in the brain is a bad thing in terms of temperature control. It is not. On the contrary, blood circulation is crucial in maintaining brain temperature.

Under conditions where the brain is heating up, which seems the focus of your question, there are mechanisms in place to extract this heat and dissipate it. Ambient temperature is often lower than body temperature, and even in hot climates, transpiration and water evaporation may cool the skin nonetheless.

Indeed, during hyperthermia, venous blood flow from the skin of the face and scalp fed to the dura mater (the brain's membranes) is enhanced and cools the brain (Brinnel et al., 1989). Moreover, blood from the nasal and paranasal mucous membranes flowing to the dura mater cools the brain due to the evaporative cooling of sweat or mucus. The dura mater may also transmit temperature changes to the cerebrospinal fluid compartment (Zenker & Kubik, 1996).

References
- Brinnel et al., Arch Dermatol Res (1989); 281(1): 66-72
-  Zenker & Kubik, Anatomy Embryol (1996); 193(1): 1-13


What is the definition of a mutation? There are two alleles that determine the sensitivity of a person to Coumadin (a medicine for blood thinners used to treat a stroke etc). Sometimes you encounter the terminology that one has a mutation on both alleles (father's and mother's side). But why is that called a mutation and not just a variation? Does a mutation mean that it changed during lifetime, or is the difference between mutation and variation arbitrarily defined? Or is there really a kind of standard taken where deviations are considered to be mutations?

Good question!

The term mutation can be used with two different meanings. Each definition can further be split into two different more detailed definitions. The reason for this slight mess is mainly historical. In short, a mutation can refer to

An event

narrow sense
broad sense

An allele

definition based on ancestral/derived states
definition based on frequency

Before going into the details of these definitions, it is important to first define a few other terms.

A few other definitions

The terms I want to define here are Locus, polymorphic locus, allele, nucleotide and phenotype.

In short (simplified version), a phenotype is the way an individual look. The variations of phenotypes of the individuals in a population depends upon the variation of genotypes and the variation of environments that they encounter. This concept is very much related to the concept of heritability. You may want to read more about it here.

The DNA sequence is made of four nucleotides. It is the sequence of these nucleotides that affect the phenotype of an individual

A locus is refers to the position of a DNA sequence of arbitrary length. At a given locus different types of sequence can exist, such a coding or non-coding sequence, a gene or just an intron, only a few codons, etc..

An allele is one variant of a sequence (often a gene) at a given locus. If, in the population, more than one allele exists at a given locus, than the locus is said to be polymorphic. Most polymorphic loci have only two alleles. In such case we can talk about bi-allelic loci.

Mutation as an event

A mutation can refer to an event.

Narrow definition

A mutation may refer to the event of a spontaneous change in the nucleotide sequence of an individual such as typically an indel (insertion or deletion of one or few nucleotides) or a substitution (substitution of a nucleotide by another one). In other words, a mutation can refer to the event of changing allele (eventually making up a new one) at a given locus.

Broad definition

The broad definition is similar to the narrow one expect that it encompass more types of genetic changes. In the broad sense, a mutation may refer more globally to any genetic spontaneous change. For example a whole chromosome deletion or a full genome duplication are examples of mutations.

In my experience, most often when the term "mutation" is used, it is to refer to the broad definition of mutation.

Mutation as an allele

A mutation can refer to an allele. Note however that very often we prefer using the terms "mutant allele", "mutant state" or just "mutant" as synonym to refer to this allele. Pretty much the only circumstance in which we would use the term mutation here is in sentences of the kind "Individual A carries the mutation.".

Definition based one ancestral/derived states

A mutation can refer to the allele that is derived from a more ancestral allele. Consider for example, a given locus was NOT polymorphic in the past. A mutation (in the sense of "event") occurs and the locus is now polymorphic. The allele that has been created by the mutation (in the sense of "event") is sometimes called "mutation".

Definition based on frequency

A mutation can refer to the allele that is at the lowest frequency in the population. For example, consider a bi-allelic locus with two alleles A and B. If the frequency of the allele B is lower than $\frac{1}{2}$ (that is lower than the frequency of the allele A), then the allele B can be referred to as the mutation. The reason for calling "mutation" the allele that is at low frequency is that most mutations are deleterious and as a consequence the mutant allele is often at low frequency. As a consequence, using the Definition based on frequency and Definition based one ancestral/derived states is often not important.

To address your question specifically

It is a little hard to directly address your question as it seems to have several misunderstanding on the concept of mutation. In the same time however, it feels like you are turning around the realization that there are several definitions in use.

  Sometimes you encounter the terminology that one has a mutation on both alleles (father's and mother's side). But why is that called a mutation and not just a variation?

The term mutation (whichever definition you pick) is intrinsically related to the concept of variation in the population but not so much to variation within a single individual (homozygote vs heterozygote).

If an individual "has a mutation on both allele", refers to the term mutation as an allele (in the narrow sense probably) and not as an event. More specifically it refers to one allele at a polymorphic locus (probably a locus of only one nucleotide) within the allele considered at the larger polymorphic locus considered.

  Does a mutation mean that it changed during lifetime

A mutation (in the sense of event) is a change that if often view at the moment of reproduction but the mutation may have occurred anytime in the lineage of the germ cells. Note, one may consider also mutation that occurred (during the lifetime of the individual) but in the soma cells. Such mutation will NOT be transmitted to the offspring.

  Or is there really a kind of standard taken where deviations are considered to be mutations?

Well...yes! A deviation is a deviation to a reference. In other words, we can replace "deviation" by "one allele of a polymorphic locus" in your question. And yes, a mutation (in the sense of a given allele) can refers to one allele of a polymorphic locus.


High Current (Speed) Transfer Buffer Recipe Does anyone know an effective buffer mix to use for high current Western transfers?  We are successfully using the vendor's premixed buffer to transfer a wide range of protein sizes to PVDF membranes at 1A/25V for 10 min.  We get great results with the vendor's expensive buffer.

I haven't been able to find a non-proprietary recipe that works.  The best ones we have hold the 25V, but then have a decrease in conductivity (increase in resistance) where they will start at 1A, but drop to 0.4A by the end of the 10 min.  The vendor's buffer seems to hold the high current and results in better transfers.

I don't know if it will be helpful to list all the variations I've tried in detail, but they have revolved around modifying a traditional Towbin buffer plus SDS, more glycine/Tris, or MgCl2.  These were all various suggestions from people around the department, but I haven't found much published evidence for a buffer under these conditions.

I realize 1A (and no I don't mean 1mA) is a lot of current, but the vendor's system works really well.  Any pointers on what I might try/add would be appreciated even if you don't have a worked out protocol.

Edit: Info from the MSDS indicates it has 3 reagents:

Listing of dangerous and non-hazardous components:
Proprietary Reagent K
10-20%
Proprietary Reagent EB II
5-10%
Proprietary Reagent S
1.0-2.5%
7732-18-5 water
50-100%
·
.....
Solvent content:
Organic solvents:
0.0 %
Water:
74.8 %
Solids content:
25.2 %

[I'm not sure if this MSDS info should be put here, just because I'm looking for someone who has already used a high current buffer they know the formulation for, not a guess to what I have.]

So after a lot of work in optimization, I thought I would post what worked best for me.  This buffer recipe was able to successfully transfer EGFR and insulin from the same lysate, and a clear band for both (large and small protein respectively). 10% SDS-PAGE gels were transferred at 1A for 10 min.

High Current Transfer Buffer

48 mM Tris
15 mM HEPPS
1.0 mM EDTA
1.3 mM NaHSO3
1.3 mM N,N-dimethylformamide
25 Mm gLY-GLY
20% Methanol (v/v)

I do hope this can help someone else, and want to site Garic et al as wonderful starting point.  Their publication was made after I asked the question, as @user4148 pointed out.


Is there a metric for “evolutionary agility”? By "evolutionary agility" I mean how fast an organism can adapt to changes in the environment. I’d imagine that a population with more offspring and a shorter time between generations would be more “evolutionary agile”.

Yes, there is a measurement laid out by Haldane (1949) called 'Darwins'. One Darwin is given an $e$ fold change in a trait over the period of 1 million years.
As to your second point, yes there are different variables which control the rate of adaptation within a population. The classic factor is genetic variation, as given by Fisher's (1958) fundamental theorem of natural selection, which states:

The rate of increase in fitness of any organism at any time is equal
to its genetic variance in fitness at that time

So broadly speaking, individuals with more additive genetic variation will adapt more rapidly.
Of course, there are many other factors such as generation time, effective population size and mutation rate will influence the response to selection. However, such as in the case of generation time, the relationship is not necessarily a simple one (Gandon and Mikalakis, 2002).
EDIT
After re-reading your question, I think I perhaps misunderstood it.
I suppose the term you are looking for is 'evolutionary potential', which is defined by Steeves et al (2017) as:

The capacity of a population to evolve in response to environmental
change.

There is a nice chapter in this book which gives a good overview of the topic. The chapter may perhaps be available for free on certain websites.
References

Haldane, John Burdon Sanderson. "Suggestions as to quantitative measurement of rates of evolution." Evolution (1949): 51-56.
Fisher, Ronald Aylmer. The genetical theory of natural selection. Рипол Классик, 1958.
Gandon, Sylvain, and Y. Michalakis. "Local adaptation, evolutionary potential and host–parasite coevolution: interactions between migration, mutation, population size and generation time." Journal of Evolutionary Biology 15.3 (2002): 451-462.
Steeves, Tammy E., Jeff A. Johnson, and Marie L. Hale. "Maximising evolutionary potential in functional proxies for extinct species: a conservation genetic perspective on de‐extinction." Functional Ecology 31.5 (2017): 1032-1040.


Hayflick limit and hair or nails 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.

Let's do some math.

Also, let's ignore your examples, and use a clearer one - instead of fingernails, let's look at the cells that line the intestine.  Intestinal epithelial cells are shed and replaced constantly and very rapidly, roughly every 5 days.  So that means about 50-70 cell generations per year.

Each time the cell replicates, it loses a little bit off the end of its telomeres.  How much does it lose?

We know that for lymphocytes, adults lose roughly 30 base pairs of telomeres per year.  Lymphocytes don't replicate as fast as the colonic mucosa, though.  The estimate for these rapidly-dividing cells is about 44 bp/year. We can say 50 for a round number.

That doesn't tell us much unless we know what we're starting and stopping with.  Humans start life with about 10,000 bp of telomeres.  At least in cultured cells, once telomeres reach 1000-2000 bp, cells become senescent and stop, or greatly reduce, their growth rate.

So we start at around 10,000, we can lose up to 9000, and we lose around 50 per year. That means that the intestinal epithelium, which have about the most rapidly-dividing cells in the body, are good for about 180 years of life, assuming that the loss remains constant.

(I don't know if loss does remain constant in these cells, but in lymphocytes, the loss of telomeres accelerates in elderly people, from about 30 to about 60 bp/year in people over 60. However, it's likely that reflects increased lymphocyte turnover in older people, not something intrinsic to the age per se.)

So bottom line, we're good for it.

More generally, keep in mind that the popular media have seized on telomeres as a simple answer for everything related to aging.  Obviously, that's not reality.  Telomeres certainly reflect aging; in some cases, perhaps many cases, they may be one influence on aging; but in most cases, telomere shortening is probably only a minor aging factor, and many other causes are more important.


why and how multi allele gets reported during variant calling in vcf? This might be a very basic question for many here. With the basic understanding of inheritance, eventhough there is a possibility of multiple genotypes due to multi alleles, the resulting genotype can only have two alleles(paternal and maternal) that way after variant calling, an allele at one position can be homozygous or heterozygous. So there can be max of two alleles, but why do we see multiple alleles at a given position in VCF. I am trying to understand the science behind this. Please help out. Thanks!

chr5    127640782   .   AG  A,AA    .   .   .   GT:AD:DP    1/2:0,28,409:437

In your example the 4th column contains the reference allel on the given position. It is not said, that your sample has this. The 5th column contains all alternative alleles found on the given position.

Which alleles are present in your sample is given in the last column by 1/2. This means you have one allel with the first value in the 5th column and one allele with the second value given in the 5th column. You see, that your sample has exactly alleles, but none of them is the reference. This would be indicated by a 0.


What is this fruit (round, 3 cm diameter, yellow outside, 1 black seed, found on Easter Island)? What is this fruit (round, 3 cm diameter, yellow outside, 1 black seed, found on Easter Island)?

Some fruits may have more than one seed:

I think you are looking at Syzygium jambos in the Myrtaceae.  The first link at Wikipedia has a number of pictures which are quite similar to your pictures.


Non-radioactive nucleotide labeling compatible with reverse transcriptase? Are there any methods for nucleotide labeling which are compatible with use for reverse-transcription, besides radiolabeling, and for which the regulatory framework in the EU / USA are permissive ? Regulatory obligations around radionucleides being too strict.

Biotin-labeled nucleotides can be incorporated into cDNA by reverse transcriptase.  Jena Bioscience, a provider of biotin-labeled nucleotides, has a table showing which nucleotide chemistries have been successfully used with reverse transcriptase, though you'll have to delve into the data sheets of specific products to get the references.

One reference provided on the product page for biotin-11-dCTP:

APOBEC3G Inhibits Elongation of HIV-1 Reverse Transcripts

This study looks at natural endogenous reverse transcription (nERT) in HIV.  From the methods:

  For this assay, a nERT reaction was performed essentially as above, with the exception of the dNTP addition: pelletted virions were resuspended in PBS, 2.5 mM MgCl2, 15 µg/ml melittin and 0.5mM biotin-11-dCTP (Jena Bioscience), and incubated at 37°C.


Can this theory on the evolution of human appearance be flawed? This is what a friend of mine said:

  When there's human offspring, it will look a rough 'medium' between
  the two parents, with it sharing features from the two. well if the
  offspring of one set of parents has sex with the offspring of another
  set, the outcome becomes a 'medium' of those two. So the range from
  what we shall call 'completely average looks' (a hypothetical state of
  the average of everyone in the world, which is acceptable as we're
  looking at a process of millions of years) becomes less and less the
  further into the future we go. Eventually, there is almost no range
  between people and 'completely average looks'.

In summary: take the hypothetical average of everyone in the world, and because the offspring of two people is a slight mixture of those two people, they are a tiny bit closer to the hypothetical average of everyone in the world, which means that eventually people will be getting closer and closer to this average, so will one day look the same.
So he's suggesting that slowly people will become more and more similar.

My argument is that, although this baby may be that tiny bit closer to the overall average, they're new look has effectively altered the average, meaning that they aren't actually getting closer to the average.

I'd like an opinion and flaw from some experts, such as yourselves, so please...

Quantitative genetics is one reason why this doesn't happen. For example height is affected by many genetic loci, not just 1 gene, and we can for the sake of the following illustration call them Locus A through Locus J - 10 Loci.

Now this is purely illustrative and hypothetical - in actuality there are some differences between this example and the real world, but nevertheless I shall plough on. Imagine everyone carries a basic set of genes which makes them 150cm tall. Loci A-J each have two alleles, either T or t, with one inherited from each parent. Each T allele adds 2.5cm to the basic height per copy (each parent has two copies, one goes to the offspring) and t has no effect. The parents are both heterozygous at each loci, that is they have one T and one t at each pair of loci. Therefore both parents are 175cm tall.

When these parents mate the offspring inherit one copy of each parent at random. As such the most likely single outcome is that the offspring will inherit 10 T's and 10 t's - roughly five of each from each parent. However, purely by chance they could receive 10 T alleles from each parent, giving them a height of 150+(20*2.5) = 200cm. Likewise, a sibling could also inherit only t alleles thus giving them a height of 150+(0*2.5)= 150cm. Thus variation can actually increase from one generation to the next.

There are other reasons why we do not regress to the mean as well, but I am writing a quick answer over breakfast, but I will be in the office soon where I can get some more thorough explanations from text books. E.g. (Dis)assortative mating, Mutation, Recombination, Environmental variance, Selection. However, with the increase in global movement it has become easier for dominant alleles to spread which is why the number of blue eyed people in the US is decreasing.

Here is an interesting article which backs up what I said about quantitative genetics, called "Will humans eventually all look like brazilians?" Also for good quantitative genetics texts take this as a basic intro and this for further reading.


What's the evolutionary reason behind decussation? A bunch of stuff in the human nervous system decussates. Optical information inputs from the eyes cross over in the optical chiasm. Multiple sensory and motor pathways cross-over before ascending the spinal chord or within the brain stem.

What's the current hypotheses being explored for justifying this anatomical phenomena?

I don't think it is a clever thing to group all types of decussation and look for a general explanations. I would tend to think that different decussation have different explanations. It is like asking what are the hypothesis to explain evolution of body size. There is no general answer to that but only a list of case specific impact of different factors on body size (see this post). Consider the two case-studies 1) "why does left brain controls the right part of the body" and 2) "Torsion in gastropoda" as examples of how different explanation applies to different decussation.
why does left brain controls the right part of the body?
See @shigeta's answer to this post. It is very interesting.
Torsion in Gastropoda
Torsion in Gastropoda is an interesting case. In this lineage individuals undergo some torsion during their development. This wikipedia articles say:

Snails are distinguished by an anatomical process known as torsion, where the visceral mass of the animal rotates 180° to one side during development, such that the anus is situated more or less above the head. This process is unrelated to the coiling of the shell, which is a separate phenomenon. Torsion is present in all gastropods, but the opisthobranch gastropods are secondarily detorted to various degrees.[13][14]
Torsion occurs in two mechanistic stages. The first is muscular and the second is mutagenetic. The effects of torsion are primarily physiological - the organism develops an asymmetrical nature with the majority of growth occurring on the left side. This leads to the loss of right-paired appendages (e.g., ctenidia (comb-like respiratory apparatus), gonads, nephridia, etc.). Furthermore, the anus becomes redirected to the same space as the head. This is speculated to have some evolutionary function, as prior to torsion, when retracting into the shell, first the posterior end would get pulled in, and then the anterior. Now, the front can be retracted more easily, perhaps suggesting a defensive purpose.
However, this "rotation hypothesis" is being challenged by the "asymmetry hypothesis" in which the gastropod mantle cavity originated from one side only of a bilateral set of mantle cavities.[15]
Gastropods typically have a well-defined head with two or four sensory tentacles with eyes, and a ventral foot, which gives them their name (Greek gaster, stomach, and poda, feet). The foremost division of the foot is called the propodium. Its function is to push away sediment as the snail crawls. The larval shell of a gastropod is called a protoconch.

You can find more information there