Why is selfishness the 'obvious' strategy? Thinking of behaviours an organism can adapt, at the very base an action can always be either selfish or altruistic (cooperative).

Usually, selfish behaviour is assumed to be the preferred choice and the question is how altruistic behaviour comes about.

But if reciprocal altruism can give both participants a higher benefit than their respective costs (which it usually does), why would selfish behaviour (in the sense of behaviour which reaps benefit at another entity's expense) be what we assume to happen? If evolution tends to optimise things, why does it not optimise this?

It basically comes down to a question of the unit of selection.

From the common viewpoint, in which natural selection is seen as acting on individual organisms, it's almost a tautology that the organisms favored by selection are those that maximize their own reproductive fitness.  Thus, the possibility that some organisms might engage in acts that help another organism at their own expense may seem like a paradox, or at least a puzzle in need of explanation.

One solution to this puzzle is offered by the gene-centered view of evolution, where selection is viewed as acting on genes, with organisms being merely convenient (and usually, but not always, cooperative) collections of genes that (usually) reproduce together.  From this viewpoint, it is not at all surprising that evolution might favor genes that cause an organism to help other organisms, provided that there's a statistical tendency for those other organisms to also be carrying the same gene.

Other mechanisms for the evolution of cooperation do also exist.  For example, organisms with sufficiently advanced cognitive capabilities may indeed engage in reciprocal altruism, where they help others only if those others have shown themselves willing to help them in exchange.  Such exchanges, being mutually beneficial, do indeed help both participating organisms, and are thus selected for even at the organism level.  However, to persist (in the absence of gene or group level selection effects), they generally need some form of enforcement and/or learning mechanism — if cheaters can keep receiving help without ever helping anyone else, they'll do better than the cooperators and eventually displace them.

Also, in some situations, an organism acting simply to help itself (e.g. by modifying its environment to be more suitable for itself) may also end up helping other organisms that just happen to be nearby.  In such a situation, selection indeed favors cooperative behavior in isolated organisms by default, with the evolution and persistence of "freeloaders" (who spend less effort on improving their surrounding, relying instead on others to do the work) being only possible as long as there are sufficiently many cooperators around.

Of course, none of these mechanisms are mutually exclusive.  Indeed, the presence of some gene-level selection effects tends to be unavoidable in any realistic situation involving cooperative interactions; it's hard to come up with a setting in which no two interacting organisms ever share genes, and obviously the fact that two organisms share a common genetic predisposition to cooperate makes them more likely to do so when they meet.

(However, one not-so-realistic theoretical limit case where that does happen is that of an infinitesimally rare cooperative mutant invading an infinitely large and well mixed population.  The popular use of this simplifying limit assumption in classical models of evolution may be one reasons why cooperative behavior is so often seen as something remarkable and hard to explain by evolutionary theorists.)


Do the right-handed people tend to use the right side teeth of their jaw to chew food more often than the left-handed people? And vice versa, do the left-handed people tend to use the left side teeth of their jaw to chew food more often than the right-handed people?Or the frequency of food chewing distribute fairly to both sides of the jaw?

Individuals have not only hand dominance but also a dominant foot, eye and ear. There has also been a belief that this sidedness applies to chewing as well. However, the short answer is that no one is sure, but that it may be related to handedness. I only looked at studies done after 2000.

One large study[1] found a questionable to weak correlation, not consistently maintained through different dentition (baby teeth, mixed, and permanent). A slightly smaller study showed a correlation; in 78% chewing side preference correlated with other tested lateralities (footedness, handedness, eyedness and earedness).[2] Another similar sized study found none.[3]

A small 2012 study found that there was a preference for right sidedness when chewing hard food (73.68%) and for soft food (57.89%) but failed to correlate this with hand/other-sidedness.[4] Another small study tested for sidedness, finding that 55% of subjects did not have any side preference, 30% preferred to chew on right and 15% preferred the left side, and this was reproducible in 90% of subjects only with almonds (a medium hardness food) as opposed to jerky or asparagus. Unfortunately they did not measure sidedness. Their findings were that chewing-side preference is not a fixed characteristic, and texture seemed to affect sidedness.[5] A review article determined that a person's dental condition to a large extent dictates how they chew.[6]

The studies were mostly designed very differently, making good comparisons difficult. I think it's safe to say it's possible but not known with certainty.

[1] Absence or weak correlation between chewing side preference and lateralities in primary, mixed and permanent dentition
[2] Chewing side preference as a type of hemispheric laterality
[3] Relationship between chewing side preference and handedness and lateral asymmetry of peripheral factors
[4] Chewing side preference in first and all mastication cycles for hard and soft morsels
[5] Chewing-side determination of three food textures
[6] Adaptation of mastication in response to the characteristics of the individual or the food


Is there theory that connects longevity, time-scale of environmental disturbance, and adaptation? I'm thinking here about environmental disturbance or like climate change-driven warming. It seems as if there are two macroevolutionary ways to deal with environmental change:

1) Have short generation times, and evolve fast. For instance, the mosquito Wyeomyia smithii is under selection by the warming climate in North America and it has shown an evolutionary repsonse. The response is "detectable over a time interval as short as 5 years" (Bradshaw and Holzapfel 2001).

2) Be hardy, and 'try' to wait out changes. No real-world example to cite, but imagine a long-lived tree growing in an area that has become to warm for its seeds to effectively produce seedlings.

It seems intuitively like strategy 1 is better in the case of ongoing climate warming. However, we could easily imagine a 5-year hot spell followed by a return to the normal as part of natural weather variation. Perhaps in this situation strategy 2 is better.

Essentially, having a longevity/generation time/hardiness that matches the time-scale of the disturbance would be important – if the disturbance is long (or unidirectional) compared to your lifespan, evolving fast seems best; if the disturbance is short compared to your life, it seems best to wait it out.

So the question is, is there theory that deals with this? I suspect that I just need to hit the population genetics books again or something; or perhaps there's a massive tome by Gould I should be reading?

 Bradshaw WE, Holzapfel CM. 2001. Genetic shift in photoperiodic response correlated with global warming. PNAS 98: 14509–14511.

If the disturbance is short compared to a species' lifespan, then it's would be difficult for any adaptations to that disturbance to become fixed. Say an individual with a novel mutation is born during the disturbance that would impart some benefit under such conditions; since the species lifespan is much longer than that disturbance, by the time the individual reproduces, the disturbance will no longer be in effect and thus that allele will no longer be beneficial. In fact, this is seen in the thrifty phenotype in humans. When the mother experiences a period of duress during her pregnancy (say, the Dutch Hunger Winter of 1944), the fetus will undergo epigenetic changes that signal, in effect, that food is scarce and resources should be used sparingly. When those children grow up, they find themselves no longer under harsh conditions and this thrifty phenotype becomes a disadvantage, causing diabetes, obesity and so on.

If the disturbance is on the order of the lifespan of the species or slightly larger and especially if it is cyclic, polyphenism would be advantageous. This might also impart some resistance against long-term change, at least up to a certain point. For example, the butterfly Bycyclus anynana shows marked differences when born in the cool, dry season versus the warm, wet season: different body mass, different resting metabolic rate, different wing patterns and so on. This is controlled by hormonal switches in response primarily to temperature.

It seems that the best strategy in the face of long-term change would be gradual evolution due to progressive selection on traits that impart resistance to the disruption, at the cost of being vulnerable to future reversions in the conditions.

But of course, none of this can be "planned for" by the species. In the face of a new change in environmental conditions, be it gradual or sudden, the species can only work from its current genetic background. So whether there is a specific theory that deals with this (aside from the examples given above) is not clear. I would think that what we will see with strong-but-gradual climate change is a progressive loss of biodiversity (due to the inability to adapt in time) followed by rapid expansion to fill newly opened niches. To that end, I guess Gould's "Wonderful Life" would be appropriate to read. Any book on Evo Devo would lend insight into understanding how species might be able to rapidly adapt to a slowly changing environment, albeit in an indirect/abstract manner (i.e. "food for thought"); I like Sean B. Carroll's "Endless Forms Most Beautiful".


Why is it beneficial for bacteria to conjugate? (Horisontal gene transfer) Why is it beneficial for bacteria to conjugate? I would think it's more beneficial to take a plasmid from another cell, than to give yours away or "share". Not homework, I'm just curious.

I am going to try answer it. Bacteria in general has different survival tactics. In general for bacteria the best way how to surviva is as much copies as it cans. So imagine situation, when bacteria is surround with others bacteria. Then the race will bega. All bacteria wants to survive with same tactic as i mentioned. Thats mean the best way how to archived this goal is make your replication fast.

So when you take plasmid with resitantion to antibiotics its advantige to have those, but when you actually is not exhibit to that antibiotic it slow down your chance to survive (because it slows down your replication, cell division)


Requirement of energy for metabolic processes Sorry if this is too elementary, but can someone explain why the following reaction can occur without a net influx of energy from some other process?

  $C_6H_{12}O_6 + 6O_2 \to 6 CO_2+6H_2O$

And why does this one need an influx of energy?

  $6CO_2+6H_2O\to C_6H_{12}O_6+6O_2$

The first reaction is catabolism. It does require some energy input in the beginning ("energy investment" of glycolysis) but ultimately leads to net energy release through "energy payoff" of glycolysis, citric acid cycle, and finally electron transport chain and oxidative phosphorylation.

The final result is oxidation of glucose, and reduction of oxygen.. At various points, electrons transfer to NAD+ and FAD. Then, the reduced forms of these 2 electron carriers (NADH & FADH2) go to the electron transport chain, where electrons transfer to oxygen at the end (reduction of oxygen). Meanwhile, protons were pumped into the intermembrane space to create the proton gradient that drives ATP synthesis.

The second reaction is anabolism. The Calvin Cycle requires energy from ATP and NADPH to create the necessary bonds to build up sugars.

In terms of bioenergetics, degradation of a molecule is exergonic. This is favorable if you think about the second law of thermodynamics: there is more entropy when there are multiple, separate sub-units, while there is more order when one molecule made up of those sub-units. Synthesis of a molecule is endergonic (requiring energy). It IS favorable in the sense that we get sugar to eat and burn in the future.

In summary:

Breaking down a molecule = catabolism = release energy from chemical bonds
Building up a molecule = anabolism = absorb energy to FORM chemical bonds (think of the resources needed to construct a new building)

Note my answer leaves out specific details about the processes, but I hope this is basic enough to answer your question!

Source: Lehninger Principles of Biology, David Nelson & Michael Cox


How does a ribosome move along mRNA? I've been reading around Wikipedia recently trying to learn more about various biomechanisms. I’m intrigued by ribosomes — with how small they are, they’re basically chemical machines from what I can tell. I’ve got the general idea of what they do, which is nicely illustrated in the super common GIF below:

My question is how this happens, on a molecular/chemical scale. Even in the GIF, the way the mRNA is being so mechanically fed through the ribosome at the exact-right times seems so deliberate, and I can’t imagine a chemical process that does this so well. It seems like we know the exact protein by protein structure of a few types of ribosome; as such, I naively assume we can work out exactly why and how it does each thing it does. I’m sure it's not a simple question — if it's not really answerable in a stack exchange question, then I guess my question becomes where should I read to learn this.

Disclaimer

It is not clear to me that requests for references are on-topic here. In general I would think not, as they are subjective and not about biology per se. I therefore solicit neither votes for, or acceptance of, this answer. I would have used the comment area to provide references, but there isn’t really enough space, so I decided to flesh it out into what follows.

Overall perspective of elongation in protein synthesis

The main concern of the question is the movement of mRNA during translation, so I shall focus on elongation (rather than initiation). Most of our detailed knowledge of the ribosome is based on static ‘views’ of the ribosome at different stages, although there is a paper (reviewed in Nature by Ehrenberg) in which the dynamics have been deduced from millions of time-resolved electron microscopy images. I doubt whether that is what the animation in the Wikipedia article is based, however.

After an introduction to the subject from Wikipedia, I strongly recommend graduating to a good text book. Text books have the advantage over Wikipedia that they are comprehensive, integrated, professionally illustrated and sent out by publishers for review. Berg et al. is probably as detailed as you will find in a general text, the 2002 edition is available online (as are others such as Alberts et al. and Lodish et al.) through NCBI Bookshelf.

Figure 29.24 of Berg et al. provides a static general view of elongation:

You need the associated text to understand this properly, but the step at which the mRNA is thought to move with respect to the ribosome is the penultimate one in the diagram: translocation.

Unfortunately you can’t just read through books on NCBI Bookshelf — you have to search for particular topics. But Chapter 29 of Berg et al. is what you need, and the links to the relevant sections are:

29 Introduction
29.3
29.4
29.5

How exactly does the mRNA move?

The details of the individual steps in protein synthesis are being deduced from examination of high-resolution structures of complexes at different stages. For the student who as able to go beyond the accounts in general textbooks, a review such as that published in 2009 by Schmeing and Ramakrishnan is perhaps the next port of call. But, chemical virgins beware, this is structural biology, and there is no simple answer that you can scribble on a table napkin!


immune response towards sperm cells Question 1: Why does the immune system not act on sperm cells as sperm cells are developed after puberty?

Question 2: Does immune response occur when a person's own cells are injected inside their bodies?

Body does not act against sperms because the testes are isolated immunologically by the blood testis barrier.

In mumps due to this barrier becoming ineffective due to inflammation, orchiditis (inflammation of testis) may occur and this may render the person infertile in some cases.

Such antigens which are not exposed to body's immune system are called cryptic antigens.

One more example of cryptic antigen is the antigens of the cornea.

For more information see here.

For more you can search for blood testis barrier.

For the second question, immune reaction will occur if the injected cell contains cryptic antigens. If there are no cryptic antigens then there will be no reaction.

For cryptic antigens see here.


Resistance to Antiseptics I know that bacteria can become resistant to antibiotics.
Why do antiseptics like alcohols, PVP-I, still work on the strains of bacteria we have today? Shouldn't some bacteria have evolved to be resistant to them? I only hear about antibiotic resistance, so my assumption was that antiseptic resistance isn't a thing that happens.
What fundamentally differentiates antibiotics and antiseptics so that antiseptics are not resistance-prone?

For some classes of antiseptics the effect is more simple chemistry or even physics than biochemical toxicity. Ethanol will just denature proteins and dissolve the membrane, and the used concentration of ethanol is so high that no amount of efflux pumps is going to save the bacterium. Some other compounds work in a similar brute force way: QACs will break the membranes, hydrogen peroxide will just oxidize everything. For iodine (like in PVP-1) the mechanism is not really known, but probably it also just reacts with all kinds of things in/on the bacterial cell and kill them.

Antiseptic resistance could happen for some other antiseptics (or low concentrations of the compounds mentioned above). For some antibiotics, resistance is caused by the expression of efflux pumps that just pump out enough antibiotics so the cell survives. Bacteria could do the same for these antiseptics. The reason why it's not that much of an issue is that the application is rather different. Antibiotics are for inside use, antiseptics for topical use, you cannot just flood your whole body with 70% ethanol to kill all bacteria, but for a wound / something dirty this is just fine. This makes it much easier to avoid creating resistance.


Repair wrong DNA pair after ending replication? If there are wrong DNA pair, for example A=G, is there mechanism that could repair such things - after the replication was finished?

Or it happens only during replication?

DNA mismatches and indels can be repaired after replication through an aptly named mechanism called DNA mismatch repair.

I'll briefly describe the mechanism in Escherichia coli, but it's similar in other organisms. A protein called MutS scans DNA for lesions caused by mismatched nucleotides incorporated during replication that escaped DNA polymerase proofreading. These are detected by the kink they produce in the DNA backbone. MutS recruits MutL and MutH; the former activates the latter, which is an endonuclease. MutH cuts the DNA backbone near the lesion in the newly synthesized strand (the one containing the misincorporated nucleotide). This strand can be identified because it has not yet been methylated, while the parent strand contains the original methylation. After cleavage, UvrD helicase unwinds the strand and an exonuclease digests it. The gap around the former lesion can then be filled by DNA polymerase III and DNA ligase.

[ image adapted from ]

Here's an interesting review in a Nature publication that discusses it in more depth, as well as the mechanism in humans:
Guo-Min L. 2008. Mechanisms and functions of DNA mismatch repair. Cell Res 18:85-98


Optical density machine name What is the name of the machine used to measure optical density? We used it in a lab but I can't remember what they called it.

Optical Density is synonymous with absorbance which is based on the principle of absorption of light. The machine that is used to measure absorbance is called a spectrophotometer. Spectrometer does not indicate that light absorbance is being measured. A spectrometer can measure any spectrum; for e.g. Mass Spectrometer measures the spectrum of molecular mass (to be precice mass per charge).

Cell density can be also measured by the level of light scattering; turbidimeters or nephelometers are used for these kind of measurements.

PS: You should pay more attention in your class :P


What is the best way to clean immersion oil from the microscope lens? My job is to photograph mushroom spores at x100 using immersion oil.

What is the best practice for cleaning the oil from the lens?

Right now I am just wiping it with a cotton swab.

In my experience, any microscope worth using has a minder. I would strongly suggest finding that minder, their opinions about cleaning practice should be respected. Objective lenses can be very pricey so they should be handled with care.

Detergent or water are inappropriate for an oil immersion lens. Detergent is likely to damage anti-reflective coatings on the lens. Water doesn't mix with oil.

My standard procedure with oil objective lenses is to wipe oil off with a good quality lens tissue (Kodak). Do not use facial tissues or a lab tissues, such as kimwipes. They are too abrasive and may sractch the lens. If someone has allowed oil to dry on the lens, I take care to know what solvents are correct for the lens and oil that are being used.


What is meant by single molecule sequencing? When sequencing papers refer to single molecule sequencing, what is their definition of a "molecule". Are they saying base by base? The entire DNA chain in a chromosome can also be though of as a "molecule". In that case, that's a much larger read. What's the default interpretation?

For instance, is the Illumina sequencing "single molecule" as they fluoresce one base at a time?

Thanks!

For the classic Sanger sequencing you need quite large amounts of DNA to be able to run the sequence reaction. This is a problem when you want to sequence whole genome since the DNA needs to be amplified then, which for some sequences can cause problems, introduce errors or cause bias.

Single molecule sequencing is a huge step forward here, since only one molecule of DNA is used for sequencing. There are different sequencing technologies based on this principle.
The system of pacific biosciences uses a polymerase bound to a small well which binds a singlestranded DNA and begins to make the opposite strand, when nucleotides are present.
See the image below or this video, which explains the technique quite nicely.

Illumina binds singlestranded DNA molecules to the surface of the reaction chamber and starts amplifying them there. The use of fluorescently labelled nucleotide allows to monitor the reaction. This looks like the following (left side of the figure from the review mentioned below):

An illustration from Illumina which is more detailed, can be found here.
Although it is a bit older (and the technology develops fast), this review is a nice introduction: "Sequencing technologies - the next generation."


What is the point of having evolved two nostrils? How would having two nostrils be advantageous to your sense of smell or your ability to breath? I already hypothesized that either one of the nostrils could act as a back up for when another gets congested, but even then you can still breath through your mouth and at least for me I almost always have either both nostrils congested or neither at all.

There are two aspects to your question.

First, organisms have some kind of symmetry. The field of evolutionary developmental biology has some theories on why our anatomy is the way that it is.  So, we have two eyes, two halves of our nose and two nostrils, one "tube" that becomes the path from our mouth to anus, etc. Our nostrils are just part of that symmetry. It may be evolutionary advantageous to keep two nostrils so that an animal can tell what direction a smell is coming from.

Second, we see that evolution has provided a path to having just one nostril.  Blowholes in toothed whales are just one nostril.  The other nostril does not have an opening to the outside of the whale.  It would be interesting to explore the split between baleen (two nostrils) and toothed whales (one nostril).  This evolutionary divergence may have been caused by differences in communication styles or the different blowholes may have caused a difference in communications http://www.whoi.edu/science/B/people/kamaral/marinemammalacoustics.html .


How can enzymes be immobilised on glass? I’m studying a hypothetical model for urease activity, which involves fluorescence measurement, hence the need for an optical window to which the enzyme urease is immobilised.
From my previous knowledge, immobilisation of enzymes on a solid surface is done through the covalent bonding of the enzyme (outside its active site) with a functional group on the solid surface capable of covalent bonding.
My question is, isn’t glass supposed to be inert? How can enzymes be covalently immobilised on glass? And if they can’t be, are there other materials that could be used instead of glass for an optical window?

Glass can be functionalized by organosilanization so that biomolecules can be covalently attached via some cross-linker. As an example, one might aminosilanize the glass and then cross-link their enzyme of interest with glutaraldehyde.

For what it’s worth, urease activity can be measured in solution.


Correct enzyme nomenclature I notice many wikipedia articles, courses, pathway sites use a different abbreviation for the same enzyme. Eg: Wikipedia lists the abbreviation of phosphoglycerate mutase as PGM, whilst wikipaths lists it as PGAM in the glycolysis pathway. Then there's enzymes like glyceraldehyde 3 phosphate abbreviated either as GAPDH or G3PDH. This has led to many confusions, particularly when the enzyme abbreviation is completely different to the gene abbreviation, eg: protein kinase A (PKA).

For the official names of genes, I'm using genenames.org. I thought it might be common practice to abbreviate an enzyme with its gene abbreviation, but I see this is problematic due to many enzymes being encoded by multiple subunits and genes from different locations.

Is there a site, or a way, to unambiguously know the correct, and most widely recognized, official name/abbreviation for an enzyme, like there is for genes?

No, not that I have ever seen. Classically, the Enzyme Commission (E.C.) identifiers are the only way to be certain that two (or more) abbreviations or acronyms are all referring to the same enzyme activity. Sometimes, when the situation becomes very complicated interested parties will co-author a proposed new naming convention within their subfield. Some journals may require specific abbreviations, but otherwise authors are free to use whatever nomenclature they like.


How fast will cells lyse under hypotonic conditions? Routinely, lysis of cells with hypotonic solutions is carried out along with some physical (douncing) or enzymatic (lysozyme) method to break open the cells. If one were not to do any of these and just resuspend cells in water, how long would it take to lyse the cells? I was discussing with a lab mate who claimed it would take hours while in my understanding, salt equilibrium should not take very long (maybe on the order of minutes?) and hence, lysis should be done within 20-30 minutes.

In the case of red blood cells, hemolysis in pure water occurs at just over 1 minute, 30 seconds, according to this paper. (Osmotic Properties of the Erythrocyte, M.H. Jacobs and Arthur K. Parpart, The Biological Bulletin, 1932)


Linked genes outcomes in offspring This question is from a genetics session in my university:

The test cross between a plant with smooth and yellow seeds and a plant with wrinkled and green seeds gives the following results: 140 plants with smooth and green seeds, and 142 plants with wrinkled and yellow seeds.
These results are consistent with which case of the following?

Linked genes
Epistatic genes
Genes with intermediate dominance
Genes with complete dominance and independent assortment

In my answer key the correct choice is linked genes.

What I know is that in the case of linked genes, the outcomes are: either all parental (complete linkage) or the majority of offspring have parental traits and we have few recombinants(partial linkage).

But here it seems like all offspring are recombinants?! How can this be? Is there a mistake in the question, in the answer, or in my information?

Any help is appreciated. Thank you.

There is nothing wrong with the question and it can be explained with not much more than mendelian genetics + linkage.

What do you think are the genotypes of parents?

First hint: If there is more than one phenotype (for the trait) of the offspring at least one of parents must be heterozygote. So the idea of pure lineages goes out of the window here.

Ok, there is at least one heterozygote for each color and smoothness of seeds. What is the genotype of the other parent?

Hint 2: Test cross is a term for cross between recessive homozygote and individual of unknown genome (with dominant phenotype). The test cross reveals genotype of the parent with unknown genome.

Hint 3: 1:1 ratio of phenotypes is typical of cross between a heterozygote and recessive homozygote.

Ok so we have heterozygote and recessive homozygote for both traits. Which traits are dominant and which are recessive?

Hint 4: This question seems to be inspired by original Mendel work. Feel free to read it here to find out which traits are recessive and which are dominant. It is quite a good read, clear in its presentation of evidence and conclusions and I recommend it to everyone.

However, this knowledge is not necessary to answer the question. How are dominant genes organized in parents? Principally we have two options:

(AaBb x aabb) or (Aabb x aaBb)

If we consider organization on chromosomes it expands to basically 3 options:

Option 1:

chr ---A---B---
chr ---a---b---
         X
chr ---a---b---
chr ---a---b---

Option 2:

chr ---A---b---
chr ---a---B---
         X
chr ---a---b---
chr ---a---b---

Option 3:

chr ---A---b---
chr ---a---b---
         X
chr ---a---B---
chr ---a---b---

I leave it to you to figure out which of the tree options leads to result offspring described in the question.


How do PLINK files and HapMap Phased files differ? I know that PLINK and HapMap files show the same information, but can you give a thorough explanation of how exactly they differ.

According to http://pngu.mgh.harvard.edu/~purcell/plink/data.shtml#ped:

  The PED file is a white-space (space or tab) delimited file: the first six columns are mandatory:

 Family ID
 Individual ID
 Paternal ID
 Maternal ID
 Sex (1=male; 2=female; other=unknown)
 Phenotype

  [...]

  Genotypes (column 7 onwards) should also be white-space delimited; they can be any character (e.g. 1,2,3,4 or A,C,G,T or anything else) except 0 which is, by default, the missing genotype character. All markers should be biallelic. All SNPs (whether haploid or not) must have two alleles specified. Either Both alleles should be missing (i.e. 0) or neither. No header row should be given. For example, here are two individuals typed for 3 SNPs (one row = one person):

 FAM001  1  0 0  1  2  A A  G G  A C
 FAM001  2  0 0  1  2  A A  A G  0 0
 ...

And here is what I find in the begining of a HapMap .ped file I got a few years ago (hapmap3_r2_b36_fwd.YRI.qc.poly.ped):

 Y001    NA18488 0       0       2       -9      C C     T T     ...
 Y014    NA18519 0       0       1       -9      C C     T T     ...
 ...

So far, it seems to me than this is plain .ped format: the number of "header" columns is the same, and seems to conform to the specifications given in the above-mentioned web page.

Now let's have a look at the .map files.

  By default, each line of the MAP file describes a single marker and must contain exactly 4 columns:

 chromosome (1-22, X, Y or 0 if unplaced)
 rs# or snp identifier
 Genetic distance (morgans)
 Base-pair position (bp units)

  [...]

  Note: Most analyses do not require a genetic map to be specified in any case; specifying a genetic (cM) map is most crucial for a set of analyses that look for shared segments between individuals. For basic association testing, the genetic distance column can be set at 0.

  [...]

  The autosomes should be coded 1 through 22. The following other codes can be used to specify other chromosome types:

 X    X chromosome                    -> 23
 Y    Y chromosome                    -> 24
 XY   Pseudo-autosomal region of X    -> 25
 MT   Mitochondrial                   -> 26

  The numbers on the right represent PLINK's internal numeric coding of these chromosomes: these will appear in all output rather than the original chromosome codes.

Here we have something that may be different.
The end of the .map file corresponding to the HapMap .ped file looks like this:

 26      rs28357376      0       15825
 26      rs2853510       0       15925
 26      rs2854125       0       16149

The HapMap .map file uses "plink's internal numeric coding" for the chromosome instead of the letter code (MT).

Otherwise, it looks a pretty standard .map file, with no genetic distance indicated.


Do tall people have more cells? Within a single species, how does the relative number of cells in the body relate to the relative size of the organism?

Let's say we take two humans, one of them is 6 feet tall and the other one is 5 feet tall.  They have similar BMI, age, physical condition, genetic background (aside from height) and are the same sex.

Does the tall one have more cells? Or does he have bigger cells?

PS: Ideally, answers should be backed up by appropriate sources.

PPS: While I'm grateful to everyone for the very nice answers I got, I should point out that I'm waiting for an answer which includes references to accept it.

This is really the most fundamental concept of Cell Biology, so good question. If you look at the size of a any cell from a whale and compare it to the size of any of cells from a mouse, they are in fact quite similar, despite the extreme difference in the overall size of the organisms they are from. There is a reason why cells are small, and it has to do with the fact that they survive based on their ability to absorb enough nutrients from their environment. As a cell gets larger it needs more to survive (because it has a bigger mass). A bigger cell has also has a larger surface area around it (so it can absorb more nutrients).

HOWEVER, there gets to be a point where the mass of the cell is too large for the surface area to compensate for. Mathematically this is shown by what is called the "surface-area-to-volume ratio". Basically, it states that as a a sphere gets larger, the volume increases at a higher RATE than the surface area. So there is a reason cells get only so big, the 60's horror movie The Blob was not scientifically accurate, a single-cell that large (the blob) would not have enough surface area to absorb enough nutrients to sustain itself. Taller (or bigger) people have more cells (not bigger ones) than others.

Effects of osmotic pressure can alter cell size slightly.

When you are talking about taller individuals, you are (I think) really meaning larger people, people with a higher mass. And yes, they have more cells.

Another topic of Cell Biology you may want to explore is apoptosis. Let's say you have two individuals both 180 lbs. one of them is 5' tall and the other 7'. Both these individuals have the same number of cells, but the taller one has a higher percentage of them in the superior and inferior regions of the body. It is the process of apoptosis that sculps an organisms shape.


Would a hole in a heart make it unsuitable for transplantation? Would a hole in a heart instantly make it unsuitable for transplantation? Or could it be possible for a heart with a congenital defect to still be suitable for use is someone else's body?

I am assuming you are referring to a patent foramen ovale.

A Google Scholar search for donor heart "patent foramen ovale" returns many results about transplanted hearts with PFO, which suggests to me that this is not a contraindication for donation, though that may be up to the transplant team or hospital. In most cases, PFO is not symptomatic; it could also be potentially repaired at the time of transplant if it was deemed significant.


How does the genetic material differ between dizygotic twins and ordinary siblings? I am going to give a rough presentation on twin studies.
The terms heritability and concordance are included already, but I struggle with understanding the difference of the genetic material of dizygotic twins and ordinary siblings.

While ordinary siblings evolved from different sperm and egg cells, I only know that dizygotic twins form when two different sperm cells fertilize egg cells of the same cycle. However, I'm not sure if these cells are identical products of the same meiosis process.

I appreciate your help and time.

Differences in genetic material between dizygotic twins and siblings are likely to be very similar.

  Dizygotic twins, or so-called fraternal twins, on the other hand, are no more genetically similar than any other set of siblings. - Utah.edu

Since all oocytes are all synthesized during fetal development, dizygotic twins are no more likely to come from a single mitotic division than siblings are.

Also note that in human females, only one egg comes from the a full mitotic division:


Normal position of Electrical axis only in the III lead? I found this sentence in my notes which is not exact enough:

  Electrical axes

  Excitatory processes have definite direction and magnitude and could therefore be represented as vectors. At any moment there are two
  points in the heart with the biggest potential difference, which is
  called electrical axis, characterized by the angel α.
  Under normal conditions -> 30°< angel α < 90°
  Electrical axis gives information about the position of the heart, where the normal position ([arrow to south-east]) represents the
  biggest amplitude in the III lead

What is the exact electrical axis and of what they are talking about?

Let's consider the definition of the electrical axis.
The text does not specify which type of electrical axis and of what.
For instance, Guyton discusses Mean Electrical Axis of the Ventricular QRS only.
However, Guyton says that the mean electrical axis of the normal ventricle is 59 degrees.
In many pathological conditions of the heart, this direction changes markedly, sometimes even to opposite poles of the heart.

So the original author must have considered the Mean Electrical Axis of Ventricular QRS.

I would change the paragraph to

  Mean Electrical axes of the Ventricular QRS

  Excitatory processes have definite direction and magnitude and could
  therefore be represented as vectors. At any moment there are two
  points in the heart with the biggest potential difference, which is
  called electrical axis, characterized by the angel α.
  Under normal
  conditions -> 30°< angel α < 90°
  The Mean Electrical axis of normal ventricles is 59 degrees, which gives information
  about the position of the heart, and it represents the biggest amplitude in the lead III.


Does bright environment strain eyes more than dim? I'm trying to figure out how to modify my working conditions so that I can program longer without harming my eyes. Because doing so experimentally hasn't given conclusive results so far, I decided to ask for studies in this area.

Does looking at a bright screen in a well lit room strain eyes more than looking at dark screen in a dark room for prolonged periods of time? Or is there a middle ground somewhere in-between that is most harmless? Or is it a combination of contrasting screen/background?

I'm not asking for medical advice here. I already went to several doctors and they gave me different, sometimes contradicting answers, so I'm just looking for research.

I think the principle is "everything in moderation". Environment should be not very bright and not very dimmed. Also, the contrast should be moderate too, i.e. having bright screen in dark room is not good. Also, he type of work should not be very constant, i.e. you should sometimes change looking at the screen to looking in the window and similar.

Remember, that the light is required for stimulating the brain activity.


What if there are no bacteria such as Streptococcus mutans If someone removed all bacteria such Streptococcus mutans in her mouth by starving long time, or by some chemical method, would she never have such bacteria?

In my thought, because S.mutans only spread out through human teeth, and if there are some in the air, white blood cell might kill all from the air completely because they are very little.

Is this foolish hypothesis of mine possible?

Thanks for your answer in advance.

As shigeta touched on, there's no practical way to avoid cross-contamination from other humans. Assuming by magic you delete all your mouth bacteria, there are so many paths to re-inoculation you couldn't avoid it without living in extreme isolation.

A non-exhaustive list of all the ways you could get re-inoculated:

kissing
licking
aerosolized saliva from coughing/sneezing
eating food exposed to same
Touching something contaminated then brushing your teeth
Essentially putting anything another human has touched in your mouth

Other humans get saliva on things they touch and things they breathe on. You can't breathe or eat those things without cooking them. No fresh vegetables.

Your white blood cells or your immune system in general won't help, because S. mutans is already adapted to live in your saliva and there's not (to my knowledge) any adaptive immune system components active in your saliva.


Currency metabolites vs. current metabolites: What's the right term? I have seen the two terms currency metabolite and current metabolite used interchangeably. Is there a consensus on which is the right term?

Currency refers to anything that is used in any circumstances, as a medium of exchange [1]. That's why ATP and NAD are considered as currency metabolites [2]. So currency metabolite can be used for any metabolite that has multiple uses in different reactions/pathways.

Current refers to something that is prevalent at the present time [3]. So current metabolite is used to refer a metabolite that is already available for a specific reaction/pathway and doesn't need to undergo supplementary transformations to fit for that specific reaction.

The same metabolite can be simultaneously a currency metabolite and a current metabolite for a specific situation.

References:

Wikipedia contributors, "Currency," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Currency&oldid=611672968 (accessed July 12, 2014).
Gerlee P, Lizana L, Sneppen K. Pathway identification by network pruning in the metabolic network of Escherichia coli. Bioinformatics. 2009 Dec 15;25(24):3282-8. doi: 10.1093/bioinformatics/btp575. PubMed PMID: 19808881.
The Free Dictionary by Farlex. http://www.thefreedictionary.com/current


What's the relationship between oxygen consumption and ambient oxygen concentration for a lobster? I was looking at a research paper by Thomas (1954) and came across a graph with ambient oxygen concentration plotted against oxygen consumption rate of a European lobster kept in water.

As we can see, this is a linear relationship, but I'm unable to figure out the reason behind this direct linear relationship.

I would be glad if anyone out there can suggest a possible reason, because just rote learning the graph is not something which should be done.

Increasing the ambient oxygen concentration increases diffusion of oxygen across the gills, thereby increasing the oxygen uptake by the lobster.
This can be proven by the fick's law of diffusion-

r=[-DA(P2-P1)/L]

L=thickness of diffusion membrane

D=diffusion coefficient

A=cross sectional area of diffusion membrane

P2-P1=pressure difference


Want to know about a creature which bite me I am Sachin from MP India. Few minutes back I have gotten bite by a creature. What is its name? Is it harmful if I got bitten by it? Feeling little pain there.

That is an insect, in the order Zygentoma. These are harmless, and do not bite. If you were bitten by something, it was not this?


Is there any evidence that sexual selection may lead to extinction of species? Darwin suggested that sexual selection, especially by female choice, may counter natural selection. Theoretical models, such as a Fisherian runaway process, suggest that evolution of preference and preferred phenotypes may drive each other in ever increasing speed.

Because one male may fertilize many females, one could imagine that natural selection against preferred but energetically costly phenotypes may be weak, and the whole process may not slow down fast enough (i.e., be sufficiently self-limiting). If male mortality is high and their number is low, the random fluctuations may easily cause the extinction of population.

Is there any fossil or experimental evidence that this may really happen?

TL;DR:

There is a dearth of actual experimental evidence. However:

there is at least one study that confirmed the process ([STUDY #7] - Myxococcus xanthus; by Fiegna and Velicer, 2003).
Another study experimentally confirmed higher extinction risk as well ([STUDY #8] - Paul F. Doherty's study of dimorphic bird species an [STUDY #9] - Denson K. McLain).

Theoretical studies produce somewhat unsettled results - some models support the evolutionary suicide and some models do not - the major difference seems to be variability of environmental pressures.
Also, if you include human predation based solely on sexually selected trait, examples definitely exist, e.g. Arabian Oryx

First of all, this may be cheating but one example is the extinction because a predator species specifically selects the species because of selected-for feature.

The most obvious case is when the predator species is human. As a random example, Arabian Oryx was nearly hunted to extinction specifically because of their horns.

Please note that this is NOT a simple question - for example, the often-cited in unscientific literature example of Irish Elk that supposedly went extinct due to its antler size may not be a good crystal-clear example. For a very thorough analysis, see: "Sexy to die for? Sexual selection and risk of extinction" by Hanna Kokko and Robert Brooks, Ann. Zool. Fennici 40: 207-219. [STUDY #1]

They specifically find that evolutionary "suicide" is unlikely in deterministic environments, at least if the costs of the feature are borne by the individual organism itself.

Another study resulting in a negative result was "Sexual selection and the risk of extinction in mammals", Edward H. Morrow and Claudia Fricke; The Royal Society Proceedings: Biological Sciences, Published online 4 November 2004, pp 2395-2401 [STUDY #2]

  The aim of this study was therefore to examine whether the level of
  sexual selection (measured as residual testes mass and sexual size dimorphism) was related to the risk of extinction that mammals are currently experiencing. We found no evidence for a relationship between these factors, although our analyses may have been confounded by the possible dominating effect of contemporary anthropogenic factors.

However, if one takes into consideration changes in the environment, the extinction becomes theoretically possible. From "Runaway Evolution to Self-Extinction Under Asymmetrical Competition" - Hiroyuki Matsuda and Peter A. Abrams; Evolution Vol. 48, No. 6 (Dec., 1994), pp. 1764-1772: [STUDY #3]

  We show that purely intraspecific competition can cause evolution of extreme competitive abilities that ultimately result in extinction, without any influence from other species. The only change in the model required for this outcome is the assumption of a nonnormal distribution of resources of different sizes measured on a logarithmic scale. This suggests that taxon cycles, if they exist, may be driven by within- rather than between-species competition. Self-extinction does not occur when the advantage conferred by a large value of the competitive trait (e.g., size) is relatively small, or when the carrying capacity decreases at a comparatively rapid rate with increases in trait value. The evidence regarding these assumptions is discussed. The results suggest a need for more data on resource distributions and size-advantage in order to understand the evolution of competitive traits such as body size.

As far as supporting evidence, some studies are listed in "Can adaptation lead to extinction?" by Daniel J. Rankin and Andre´s Lo´pez-Sepulcre, OICOS 111:3 (2005). [STUDY #4]

They cite 3:

  The first example is a study on the Japanese medaka
  fish Oryzias latipes (Muir and Howard 1999 - [STUDY #5]). Transgenic males which had been modified to include a salmon growth-hormone gene are larger than their wild-type counterparts, although their offspring have a lower fecundity (Muir and Howard 1999). Females
  prefer to mate with larger males, giving the larger
  transgenic males a fitness advantage over wild-type
  males. However, offspring produced with transgenic
  males have a lower fecundity, and hence average female
  fecundity will decrease. As long as females preferentially
  mate with larger males, the population density will
  decline. Models of this system have predicted that, if
  the transgenic fish were released into a wild-type
  population, the transgene would spread due to its mating
  advantage over wild-type males, and the population
  would become go extinct (Muir and Howard 1999).
  A recent extension of the model has shown that
  alternative mating tactics by wild-type males could
  reduce the rate of transgene spread, but that this is still
  not sufficient to prevent population extinction (Howard
  et al. 2004). Although evolutionary suicide was predicted
  from extrapolation, rather than observed in nature, this
  constitutes the first study making such a prediction from
  empirical data.

  In cod, Gadus morhua, the commercial fishing of large
  individuals has resulted in selection towards earlier
  maturation and smaller body sizes (Conover and Munch
  2002 [STUDY #6]). Under exploitation, high mortality decreases the
  benefits of delayed maturation. As a result of this,
  smaller adults, which mature faster, have a higher fitness
  relative to their larger, slow maturing counterparts
  (Olsen et al. 2004). Despite being more successful
  relative to slow maturing individuals, the fast-maturing
  adults produce fewer offspring, on average. This adaptation,
  driven by the selective pressure imposed by
  harvesting, seems to have pre-empted a fishery collapse
  off the Atlantic coast of Canada (Olsen et al. 2004). As
  the cod evolved to be fast-maturing, population size was
  gradually reduced until it became inviable and vulnerable
  to stochastic processes.

  The only strictly experimental evidence for evolutionary
  suicide comes from microbiology. In the social
  bacterium Myxococcus xanthus individuals can develop
  cooperatively into complex fruiting structures (Fiegna
  and Velicer 2003 - [STUDY #7]). Individuals in the fruiting body are
  then released as spores to form new colonies. Artificially
  selected cheater strains produce a higher number of
  spores than wild types. These cheaters were found to
  invade wild-type strains, eventually causing extinction of
  the entire population (Fiegna and Velicer 2003). The
  cheaters invade the wild-type population because they
  have a higher relative fitness, but as they spread through
  the population, they decrease the overall density, thus
  driving themselves and the population in which they
  reside, to extinction.

Another experimental study was "Sexual selection affects local extinction and turnover
in bird communities" - Paul F. Doherty, Jr., Gabriele Sorci, et al; 5858–5862 PNAS  May 13, 2003 vol. 100 no. 10 [STUDY #8]

  Populations under strong sexual selection experience
  a number of costs ranging from increased predation and
  parasitism to enhanced sensitivity to environmental and demographic
  stochasticity. These findings have led to the prediction that
  local extinction rates should be higher for speciespopulations
  with intense sexual selection. We tested this prediction by analyzing
  the dynamics of natural bird communities at a continental
  scale over a period of 21 years (1975–1996), using relevant statistical
  tools. In agreement with the theoretical prediction, we found
  that sexual selection increased risks of local extinction (dichromatic
  birds had on average a 23% higher local extinction rate than
  monochromatic species). However, despite higher local extinction
  probabilities, the number of dichromatic species did not decrease
  over the period considered in this study. This pattern was caused
  by higher local turnover rates of dichromatic species, resulting in
  relatively stable communities for both groups of species. Our
  results suggest that these communities function as metacommunities,
  with frequent local extinctions followed by colonization.

This result is similar to another bird-centered study: Sexual Selection and the Risk of Extinction of Introduced Birds on Oceanic Islands": Denson K. McLain, Michael P. Moulton and Todd P. Redfearn. OICOS Vol. 74, No. 1 (Oct., 1995), pp. 27-34 [STUDY #9]

  We test the hypothesis that response to sexual selection increases the risk of extinction by examining the fate of plumage-monomorphic versus plumage-dimorphic bird species introduced to the tropical islands of Oahu and Tahiti. We assume that plumage dimorphism is a response to sexual selection and we assume that the males of plumage-dimorphic species experience stronger sexual selection pressures than males of monomorphic species. On Oahu, the extinction rate for dimorphic species, 59%, is significantly greater than for monomorphic species, 23%. On Tahiti, only 7% of the introduced dimorphic species have persisted compared to 22% for the introduced monomorphic species.

  ...

  Plumage is significantly associated with increased risk of extinction for passerids but insignificantly associated for fringillids. Thus, the hypothesis that response to sexual selection increases the risk of extinction is supported for passerids and for the data set as a whole. The probability of extinction was correlated with the number of species already introduced. Thus, species that have responded to sexual selection may be poorer interspecific competitors when their communities contain many other species.


Does crossover happen between chromosomes from grandparents? Rephrasing question: does crossover happen after sperm and egg meet each other, but before formed fetus starts to grow?

As I understand sperm and egg of human are haploid cells. That means this cells undergone meiosis and chromosomes crossover before meet each other. If so then crossover happened between a pair of chromosomes which came from parents of the parent of the fetus, not between chromosomes of mother and father of the fetus.

Am I wrong?

Your question and your rephrased question aren't asking the same thing, so you may want to edit your question.

Crossover occurs during meiosis, which is a type of cell division that occurs in the generation of gametes, during which of course only the chromosomes from one of the eventual parents would be present. Meiosis doesn't occur in the fetus, except eventually in the germ line cells.


How do we know Neanderthals DNA? According to this article, a small amount of Neanderthal DNA was introduced into the modern human gene pool. How do biologists even know what the Neanderthals' DNA look like?

The article doesn't mention how the science recognize what the Neanderthals' DNA actually is at the first place. So how do we know what the Neanderthals' DNA is if I'm guessing we never tested Neanderthals body cell samples?

If you say "From their bones/skull" but how do you know they are actually Neanderthals and not modern humans with some rare gene mutation or something else?

Neandertal DNA has been completely sequenced multiple times now, using DNA from bone and tooth samples found in cool or cold environments.  The first Neanderthal genome sequence was described in 2010:

A Draft Sequence of the Neandertal Genome

Since then, as well as higher-quality sequence, more genomes have been completed; at least 6 individuals have been sequenced (perhaps more; I've lost track a little).  As well, complete genome sequences from several Denisovans -- a Homo species that were approximately contemporary with Neandertals, but a distinct species -- have been recovered.

The science of recovering ancient DNA has advanced very rapidly in the last decade, and while it isn't routine to sequence 50,000-year-old DNA it isn't as magical as it used to be.  The current record for sequencing ancient DNA is 700,000 years, which is earlier than the sapiens/neandertalis split.


Cause of hexadactylisim in Amish people Is it caused by inbreeding of many generations within an isolated population?

Short answer

Yes, you pretty much nailed it. Inbreeding of (and from) an isolated population.

Long answer

According to wikipedia > polydactyly, there are 39 known polmorphic sites underlying variance in polydactyly. It is therefore not a trait with a simple mode of inheritance.

There are two important (somehow related) concepts to understand to explain the relatively high frequency of polydactyly (and other genetic disease such as maple syrup urine disease) in Amish.

High inbreeding
Important population bottleneck

If you have no absolutely no background in biology, the following might be a little bit complicated. You might want to make sure you know some concepts (such as deleterious, recessive, dominant, homozygous, Hardy-Weinberg equilibrium, locus, allele and of course inbreeding and population bottleneck) by googling them.

Inbreeding

I will, here talk only about one mechanism by which inbreeding causes those diseases.

There is a positive correlation between how deleterious is a mutation and how recessive it is (the more deleterious, the less dominant, the more recessive). The post "Evolution of dominance of alleles" will probably help you to understand why this is true.

Inbreeding increases the frequency of homozygote loci and therefore, increase the probability of a locus which polymorphism explain variance for the disease to be homozygote deleterious. Using Hardy-Weinberg formula with Sewall Wright work, if at a given locus the allele A is deleterious and is present at frequency $p$, then the frequency of the homozygotes AA is $p^2$ without inbreeding (under Hardy-Weinberg assumptions). Taking inbreeding into account, this frequency becomes $p^2 + Fp(1-p)$ (where $F$ is the coefficient of inbreeding). In words, the higher is the inbreeding coefficient, the higher is the frequency of homozygotes (including homozygotes for the deleterious alleles).

In short, inbreeding matters because of dominance. There are other reasons why inbreeding matters though but that would be the subject of another post.

Bottleneck

In population biology, a bottleneck is is a sharp reduction in the size of a population. Imagine you have a population of size $N$ and you selection a fraction $\frac{N}{1000}$ of this population, you are going to lose a lot of alleles due to random sampling. Most of the times you are going to lose deleterious alleles (as they were already present at low frequency in the original population) but sometimes you are going to pick up a deleterious allele. The frequency of this deleterious allele was maybe 0.00001 in the original population and then suddenly its frequency jumps to 0.1. This is a big deal.

The Amish went though an important bottleneck, there was a time when the descendent of the modern-day Amish reproduced with everybody and at some point, they stopped doing so as they decided to create the amish community (I actually know little about the Amish history but I assume something similar happened). This community was formed by about 200 families only (according to this not-necessarily-trustable source, so very little genetic variance) in 1693 in Switzerland (according to wiki). They probably "won" by not having the alleles coding for clubfoot, sickle-cell and cystic fibrosis alleles (just to cite a few example) but they "lost" by drastically increasing the frequency of alleles coding for polydactyly (and some other diseases).


At what age does the mouse skull stop growing? Unless otherwise mandated, neuroscientific research on mice is done with ~7-week old animals. There is a sort-of mantra that at this age their skulls stop growing.

However, recently, I noticed a rather robust difference in how I have to place ~4-month old mice in a scanner versus 7-week old ones. I am pretty sure this is due to skull size, since I am fixing all my animals relative to the ear canal, and there should be no fat/hair accumulation in the inner ear. Also, if there would be, I am quite certain I would feel it.

This made me try to look up the source of the 7-week recommendation, but up until now I found nothing. Do you know whether it is correct that the mouse skull "stops growing" at 7 weeks of age, and if so, what studies support this observation?

This doesn't fully answer the question, but for those mouse skull sutures that do fuse, fusion is complete by about 45 days of age, according to Studies in cranial suture biology: IV. Temporal sequence of posterior frontal cranial suture fusion in the mouse.  That suggests that most cranial expansion is more or less complete by about 6 weeks of age.  I think there is still the potential for remodeling of the skull, especially bone thickness and so on, but since your interest is on the internal size of the cavity, this may help address it.


Is there a circadian component to hunger? I'm wondering what produces the feeling of hunger in humans. Checking Wikipedia revealed that leptin and ghrelin are two hormones involved. I've also read that the digestive system produces its own melatonin.

Because melatonin is related to circadian rhythm and the biological clock,Is melatonin involved in feeling hungry? Is there a circadian pattern to the levels of leptin and ghrelin in humans?

Yes, absolutely. A major focus of understanding obesity, diabetes and other metabolic disorders are targeted to understanding the circadian (and other cyclical nature) systems in neurobiology and endocrinology. I can speak within the study of diabetes, there is an observed diabetic "dawn effect" in which there is an early morning (dawn) spike in blood glucose. The exact mechanism for this spike in blood glucose is not fully known, but the general circadian nature is intriguing and would suggest a dominant hormonal cause.

Some other review articles may be found here. An overall review of homeostatic balance as it relates to the central nervous system and apetite regulation. The second review more closely focuses on the biochemistry and endocrinology of central and peripheral regulation on food intake and physical activity.

Berthoud HR, Morrison C. The brain, appetite, and obesity. Annu Rev Psychol. 2008;59:55-92.
Lenard NR, Berthoud HR. Central and peripheral regulation of food intake and physical activity: pathways and genes. Obesity (Silver Spring). 2008 Dec;16 Suppl 3:S11-22.


Do animals get Post Traumatic Stress Disorder after escaping from a life threatening situation out in the wild? Can animals come down with PTSD in the wild by themselves? For example, would a gazelle that nearly pulls away from a cheetah at the last second and heard the cheetah's jaws clamping down at air right behind it's tail, show symptoms of stress and anxiety after the event?

And if not, why can we as humans succumb to these kinds of disorders, and not animals in the wild?

Peter Levine speaks to this in his book, "Waking the Tiger:  Healing Trauma".  Most animals in the wild which experience a trauma through natural species interactions will go through a sequence of recovery stages.

First, when the trauma or death is considered inevitable, the animal will "faint", losing sensory awareness and consciousness. If the trauma or death is averted, the animal will then partially waken out of that faint, and "shake off" the trauma.

This "shaking off" looks remarkably like an epileptic fit, but when the movements are analyzed, they are a muscle-twitch repeat of the sequence of movements that animal took from the time it realized its hazard to the time it fainted. It is this same muscle-twitch capacity which allows human athletes to practice their skills both mentally and physically, without moving from one spot.

Once the "shaking off" is complete, the animal is able to rise and continue its life activities without any longer-term impacts such as PTSD.

Neurologist Dr. Robert Scaer has an explanation for this lack of PTSD.  Lasting trauma is only taken on when the "victim" experiences repeated episodes of the same kind of helplessness and hopelessness.  We humans are very good at giving ourselves and other species repeated episodes of helplessness and hopelessness, and animals which interact with us often pay a price in PTSD.


Why should a tumor look like a crab? Origin of the word "cancer"

  The disease was first called cancer by Greek physician Hippocrates (460-370 BC). He is considered the “Father of Medicine”. Hippocrates used the terms carcinos and carcinoma to describe non-ulcer forming and ulcer-forming tumors. In Greek this means a crab. The description was names after the crab because the finger-like spreading projections from a cancer called to mind the shape of a crab. – source

So the cancer cells spread in a way that tumor looks like a crab. Why? Why doesn't it, for example, have a potato-like spread in which cancer cells form a sphere?

Such projections are more formally known as spiculations. Most commonly, we talk about spiculations with respect to the radiographic appearance of malignant breast and lung lesions. This paper* describes the correlation between the mammorgraphic appearance of spiculated breast lesions and their pathology (microscopic appearance), which is a reasonable start at addressing the "why" question you pose. The authors define spiculations as follows:

  A spiculated breast lesion is defined as a mass or an architectural distortion characterized by thin lines radiating from its margins.

Here is a picture taken from that paper which shows the mammographic appearance on the left and the microscopic appearance on the right, with the arrows pointing to the spiculations.

The linked paper gives many other examples of the microscopic and radiographic analysis of such tumors. It also explains that the two primary reasons for the spiculated shape are:

desmoplastic response
tumor infiltration (which occurs along anatomic ductal structures)

According to this report, the first explanation is more common. To understand the why behind the shape, we need to know the mechanism of this desmoplastic response. As described in the linked Wikipedia article, desmoplasia is not actually the tumor itself but dense fibrous tissue that is induced with malignant tumors invade healthy tissue. The mechanism of this is not entirely clear, but the Wikipedia article sets forth two theories:

The reactive stroma hypothesis postulates that tumor cells cause the proliferation of fibroblasts and subsequent secretion of collagen that acts as a scaffold. This scaffold apparently forms the outline of the "crablegs".
The tumor-induced stromal change hypothesis states that tumor cells themselves differentiate into fibroblasts and secrete the collagen that forms the spiculated scaffold.

*Franquet T, De Miguel C, Cozcolluela R, Donoso L. Radiographics. Spiculated lesions of the breast: mammographic-pathologic correlation. 1993 Jul;13(4):841-52.


Human Endogenous Retroviruses I am reading this paper, which shows that a Human Endogenous Retrovirus (HERV) K provirus is present at the orthologous position of gorilla and chimpanzee genomes but absent in the human genome.

If it's not present in the human genome, why is it still called a HERV? Should it not just be an endogenous retrovirus?

(I am not a biology student, so I might not have understood the idea of a provirus/retrovirus entirely.)

First of all, the HERV-K virus is present in the human genome, in fact it is one of the most common endogenous retroviruses there (see references 1 and 2).

In a viral infection, these proviruses get integrated into the human genome and can be found later there. This is a useful tool when you want to find out details about the split of closely related species like the great apes and humans. If you find such a provirus in all analyzed species, the integration must have happened latest at the last common ancestor. If it is only found in a part of them, it happened after the species divided. The figure (from reference 3) shows this shematically:

The authors of "your" article did this and found the integration of the retrovirus in a specific locus in the genome of gorilla, chimpanzee and human and found it only in the first two. From this they conclude that the apes are closer related to each other than to the human.

So in summary it means that the HERV-K is not present at one specific site of the human genome, not in general.

References:

HERV-K: the biologically most active human endogenous retrovirus
family.
HERV-K(HML-2), the Best Preserved Family of HERVs: Endogenization,
Expression, and Implications in Health and Disease
Differences in HERV-K LTR insertions in orthologous loci of humans
and great apes.


Can you please help me identify this insect? I have been trying to get rid of this bug and need help to identify it.
I found this in my bedroom first.

I don't think this is a bed bug as I saw it fly. It is black with some white spots on it.

Any suggestions on what it could be are greatly appreciated.
Thank you!

That is a bean weevil, family Chrysomelidae, subfamily Bruchinae. If you have dried beans at home, check for an infestation. Throw out the contaminated beans, and put your others in sealed plastic containers, or in the fridge. https://bugguide.net/node/view/13857


what is the effect of soda water on digestion? what is the effect of soda water on the process of digestion? As it has been seen that after drinking soda the process is increased...I just want to know that what is the chemistry behind this?

Soda, anything carbonated causes bloating, which stretches the stomach. Mechanoreceptors in stomach detect the stretching resulting in parasympathetic innervation to GI smooth muscle. This causes an increase in GI motility.


Is dinoprost PGF2-alpha or PGE2? In many places it says PGF2-alpha.
Now, I am thinking PGE2 is a substype of PGF2-alpha.
However, I am not sure.

Is dinoprost PGE2?

Prostaglandins A,B,C,D,E,F represent different non-inclusive classes of prostaglandins and all have different chemical structure. Hence (by classification), PgE cannot be subtype of PgF:

PgE have an oxo group at C9, while PgF have hydroxyl group at C9.

Back to Dinoprost, it is PgF2alpha and not PgE2 which is Dinoprostone.


Concerning Apoptosis What if cellular growth and repair is 'forced' to occur repeatedly in a region where it wouldn't normally happen , if the biological area was 'healthier'. Could this more aggressive cellular growth and repair cause any apoptosis mechanisms to shut down permanently?

One long standing hypothesis of cancer formation is that it originates in a 'wound that never heals'.  I was about to add that there is little hard evidence for wounding as a significant cause of cancers but Google found this fascinating report on Marjolin's Ulcers
 which I had never heard of.   Whether it was the wound or a comorbid virus or something else.....

You may also want to search the current thinking of how a chemically inert 'irritant' - an asbestos fibre - can cause mesothelioma.


Does sleeping fewer hours than needed cause common cold? Does sleeping fewer hours than needed cause the common cold? If so, how?

There have been some studies directly linking sleep deprivation to increased risk of catching a cold  ("Behaviorally Assessed Sleep and Susceptibility to the Common Cold Sleep". 2015;38:1353–9.).

Colds are caused by a family of viruses. There is pretty solid evidence that sleep deprivation has a significant weakening effect on your immune system. Given a weakened immune system, it would be more likely that you would catch a cold if you are exposed to one of the cold-causing viruses.


How does hydration affect digestion? My textbook( biochemistry by Satyanarayana, 4th edition pg.no:166) says:

  The polysaccharides get hydrated during heating which is essential for their efficient digestion.

(I think there is a typo , heating should be replaced with eating)

How does water add into polysaccharides? Am I right if I say it is by hydrogen bonding? It also says  that efficiency increases, is it so because the substance is now more diffused so that enzymes act on an effectively larger surface area(making colloidal solution)? Or if the added(hydrated) water plays some role in interaction between enzyme and polysaccharide?

That's not a typo. The author is talking about cooking polysaccharides (gelatinisation), which in fact increases the digestibility:

  Gelatinization refers to the irreversible loss of the crystalline regions in starch granules that occur upon heating in the presence of water. The temperature range during which the crystalline structure of the starch granule is lost is dependent on the water content, and on the type of starch. The gelatinization dramatically increases the availability of starch for digestion by amylolytic enzymes. (emphases mine)

Source: FAO: Effects of Food Processing on Dietary Carbohydrates.

You can read more about it in this Wikipedia page.


What evidence do we have to derive a rate of evolution? When analyzing how the human species evolved and will continue to evolve over time, what evidence and tools (theory/models) do we have available to derive the rate at which this happens? Is it even possible to set reasonable bounds on such a rate?

Also, how large is the available dataset? And how does the dataset match with theory? I would especially like to get an idea of how well statistical (Bayesian/likelihood) analysis matches with empirical data and more conceptual models.

This question is very broad. And because of its broadness, I am afraid you won't find a database that will give you what you're looking for.

Are you interested in some specific phenotypic traits?
Or in some specific genes?
What time scale are you interested in?
Do you want to know about the time that a given allele needed to reach fixation?
Do you want to compare the number of mutations that accumulated in a given DNA sequence between human and close relatives (apes, primates, mammals, ..)?
Do you want to compare the evolution of the mitochondrial DNA between human populations that have different mating systems?
Evolution in response to HIV?

If there is one specific gene or trait (including traits such as the mutation rate) that interest you, you might want to ask a more specific question on another post.

Concerning the methodology, I agree with shigeta that probably the main methodology you'd be interested in is molecular clock. The ratio of synonymous over non-synonymous mutations are also of interest to compare rates of evolution. Comparisons of mutations accumulation between different sequences. But you might also be interested in fossil records (depending on the trait and the time scale you're interested in). Or more interestingly in selective sweeps. Selective sweep is the reduction in polymorphism and heterozygosity of linked loci to the locus under selection. In humans examples exist in the microcephalin gene or in the lactase gene for example. You might also be interested into allele frequency cline over spatial distribution and things like that. Comparison of evolutionary rates between populations of different size might also give you some insights in how quick does evolution occurs in humans. There are probably tons of other methodologies one could use.

You talk about comparisons between empirical data and theoretical model. But again the question is too broad I think. There a tons of different models to be considered depending on what you are interested in.


At what rate do chromosomal rearrangements occur? How often do chromosomal rearrangements occur?

I am interested about these kind of chromosomal rearrangements that are passed on to the descendants, i.e. germ line chromosomal rearrangements. The value I am looking for is similar to the mutation rate but only take into account major mutations such as chromosomal rearrangements.

Supposing there might have some important variance in this rate among species, then I am interested in eukaryotes and particularly in plants. If needed, the answer can be split into the different types of chromosomal rearrangements (robertsonian translocation, other translocations, inversions, ...)

Obviously, there won't be a single number for this.
The phenomenon is fairly well understood in yeast. Unfortunately, most studies tend to focus on the rate of formation of specific well-understood rearrangements, and then use that as a baseline. I am having trouble finding a measurement of overall rearrangement rate, although the system is ideal for this.
There has been some work on characterizing rates of rearrangement (and its evolution) across evolutionary history, I don't know if that is directly relevant.
This paper has a decent breakdown of the incidences in humans across different kinds of translocations. For example:

Additional studies (5, 6) followed and the incidence of balanced translocations was ultimately determined to be 1 in 500 in the general population.

Studies using cleavage stage biopsy for reciprocal translocation PGD have reported proportions of unbalanced embryos as high as 82% (57).

There is good reason to expect that it varies significantly across species and across chromosomes. For example, the Drosophila Y is a hotspot.
And (first paper):

Rearrangements involving chromosomes 13 and 14 (der(13;14)(q10;q10)) account for 75% of Robertsonian translocations (12).

For an early paper looking at a large population, you can see here.
Note that most of these human numbers are indicative of population incidence rather than rate of occurrence. Others have attempted to study effects on the translocation rate directly.
The best citation that I found for directly measuring translocation rate is here. However, the data are apparently for somatic translocations and are rather unevenly sampled so I am unsure of how generalizable it is. I looked at WYSIWYG's papers and they might provide some specific examples but they don't seem to address translocation rate directly either.
Take-home, it's hard to directly measure rearrangement rate in humans due to inviability of many/most aneuploidies early after fertilization. Somatic is easier to estimate but may not be representative of rearrangements in the gametes.


Why are dietary recommendations for methionine consumption combined with cysteine? I want to understand the amino acids missing in certain vegetables. I looked up the US recommendations for amino acids
(source: wikipedia).
I don’t understand why they pair

Methionine + Cysteine: 25 mg/g protein
Phenylalanine + Tyrosine: 47 mg/g protein

I searched for a justification but I cannot find one. While I acknowledge the chemical and structural similarities between them, they are separate amino acids. If these pairs could simply be transformed from one to another, then why bother considering methionine and phenylalanine to be essential? If you could easily convert cysteine to methionine, then methionine could be manufactured by the body. Similarly, so could phenylalanine. But it is commonly assumed this does not occur. Thus, an answer based on the idea that they can be "easily transformed into one another", if true, needs to address these issues.
Here are references for methionine:

The intimate relation between amino acids and protein and nitrogen requirements is well recognized. Nutrition research has focused on the capacity of food to meet the need for nitrogen and indispensable amino acids (IAA) and led to the conclusion that the quality, not just the quantity, of protein is critical. This is especially relevant in regard to the sulfur amino acids (SAA) methionine and cysteine because of the increased understanding of their relation to chronic diseases (e.g., cardiovascular disease, dementia, cirrhosis), immunomodulation, DNA transcription, and RNA translation. Considerable effort has been expended to determine whether and to what extent cysteine can spare the requirement for the IAA methionine. In vivo studies in humans generally concur that the dietary requirement of the SAA ranges between 13 and 16 mg/kg/d, but how much can be met by cysteine relative to methionine remains controversial.
Using the indicator amino acid oxidation (IAAO) approach to further examine this issue, Di Buono et al. (9–11) confirmed the mean requirement for methionine as 12.6 mg/kg/d in the absence of exogenous cysteine but noted that a safe level of intake of total SAA for the population was substantially higher at 21 mg/kg/d.

Naomi K. Fukagawa; Sparing of Methionine Requirements: Evaluation of Human Data Takes Sulfur Amino Acids Beyond Protein, The Journal of Nutrition, Volume 136, Issue 6, 1 June 2006, Pages 1676S–1681S
...and phenylalanine:

Conclusion: On the basis of the 24-h IAAO and 24-h IAAB methods, a mean phenylalanine requirement of 38 mg/kg/d is proposed for healthy well-nourished Indian adults in the absence of tyrosine intake. This finding is similar to that in Western adults.

Anura V Kurpad, Meredith M Regan, Tony DS Raj, Vidya N Rao, Justin Gnanou, Vernon R Young; The daily phenylalanine requirement of healthy Indian adults, The American Journal of Clinical Nutrition, Volume 83, Issue 6, 1 June 2006, Pages 1331–1336
Questions:

Why would amino acid requirements be grouped together?
If methionine is considered an essential amino acid, wouldn't grouping it with cysteine allow a food high in cysteine to appear as though it is satisfying your methionine requirement?
Suppose I consume 12.6 mg/kg/d of methionine, would this affect my ability to consume cysteine?
If the recommended level of methionine and cysteine is 19 mg/kg/d and this article proposes 12.6 mg/kg/d, then is it logical to consume approximately 6.4mg/kg/d of cysteine?
If true, would the same logic apply to phenylalanine and tyrosine?

In humans, cysteine can be synthesized from methionine and tyrosine from phenylalanine (note that the reverse pathways do not occur). Because their synthesis requires essential amino acids and the biosynthetic capacity of the organism does not always meet its need, they have been labelled conditionally essential. Under normal circumstances, an adult human can live with no dietary source of cysteine so long as dietary methionine is adequately supplied since the dietary deficiency can be compensated for by biosynthesis. Because of this, though, less dietary methionine is required when the diet is also supplemented with cysteine since less methionine is required to synthesize cysteine. This effect is known as cysteine sparing and a similar effect is observed with tyrosine/phenylalanine.
The data you cite are the reference values for PDCAAS, which is an indicative tool to evaluate the essential amino acid composition of protein sources. This system was introduced in 1991 by the WHO, and in this report they give the following rationale for their combined scoring of methionine and cysteine as sulfur amino acids:

The total of methionine and cystine [is] used for scoring purposes... Cystine is not an essential amino acid but can be synthesized from methionine. Cystine in a diet can thus "spare" methionine, and the total of the two has been found more satisfactory for scoring purposes than methionine alone.

They also recognize and somewhat address the weakness in this methodology that inspired your question:

While it is known that cystine can spare part of the requirement for methionine, FAO/WHO/UNU 1985 does not give any indication of the proportion of total sulphur amino acids which can be met by cystine. For the rat, chick and pig, the proportion is about 50%. Most animal proteins are low in cystine; in contrast, many vegetable proteins, especially the legumes, contain substantially more cystine than methionine. Thus, for animal protein diets or mixed diets containing animal protein, cystine is unlikely to contribute more than 50% of the total sulphur amino acids and scores calculated using cystine plus methionine will be appropriate. However, in certain all vegetable combinations, e.g. wheat and legumes, part of the cystine value may not be realized. Because of insufficient data on human requirements, however, the total of the two sulphur amino acids should, for the present, remain the recommended approach for computing amino acid scores.
...
A further complication arises from our lack of knowledge of the proportion of the total sulphur amino acid requirement which can be met by cystine. Without that knowledge, expression of protein values in terms of the sum total of methionine and cystine has both theoretical and practical limitations.


How can I find some pieces of the genome of a microorganism? I have figured out how to download the fasta of the genomes of microorganisms, for example the botulism bacteria and the spirulina algae. However, I want to find a fasta file for some significant extraction of those genomes - say, some important gene, some mutation, some protein that occurs in a microorganisms genome. What should I look for, and how can I find it in genbank?

You can use already available tools to extract information from available database. For finding specific genes, use this. For protein, use this. There are lot more tools. Just explore NCBI, EMBL or DDBJ sites. All information is self explanatory.
If you want specialized information for specific organism, you can use specialized database ( like Flybase for flies, SGD for common yeast, EnsemblBacteria for bacteria and archaea or HGMD for human mutations. Best way is to search in Google. You will get everything you want :D


Is it possible there were multiple origins of life? And, if so, why did the one which became the common ancestor between all organisms prevail? I have learned that all currently-living organisms come from a common ancestor, which I theoretically understand. However, my professor in a class mentioned that there is a chance that there were multiple origins of life, but that all the creatures living today all came from the same one and the others died. How can we be sure that before the other origins of life died, they didn't somewhat evolve, and the species from that origin didn't just evolve in convergence with those of this one since through natural selection both would need similar characteristics to survive on Earth?

It is interesting that all forms of life use the same genetic code. The nucleotides composing DNA and RNA are universal. Eric Lander, geneticist from Harvard/MIT cites this as evidence for evolution from a single ancestor. I think your instructor may be saying that it's possible alternative adaptations for initiation of life may have occured and perhaps not worked out. They become just another of nature's experiments that ended in extinction. I seem to recall reading somewhere all but 2% of species have ended in extinction.


What are the environmental conditions for SARS-CoV-2 to survive? What do we know about the environmental limits for nCoV to survive outside the body? For example, in:

In open air
On surfaces
In water

What are the limits for temperature, humidity and air pressure, where the virus, can or cannot survive?

Because "any" Coronavirus is so dangerous, much research have been done on viruses with similar properties. They are called "surrogates". Because nCoV is new, we don't have any studies, so we need to estimate it's behavior from previously studied similar viruses.

Here:

RH   = Relative Humidity.
Tr   = Room Temperature
TGEV = Transmissible Gastroenteritis (surrogate)
MHV  = Mouse Hepatitis (surrogate)

Viral survival for the TGEV/MHV surrogate:

on stainless steel:      4°C @ 20% RH:  28 days
in water/sewage (TGEV):  25°C: 22 days
in water/sewage (MHV):   25°C: 17 days
contaminated water is a potential vehicle for exposure if aerosols are generated

For airborne Human Coronavirus 229E (HCV/229E):

Optimal survival:  6°C @ 50% RH:
Poor* survival:     20°C @ "High" relative humidity (RH)
(* "poor" in terms of 20°C but varying RH.)

For SARS CoV-P9:

Serum: 96 h = 4 days
Sputum & Feces: 96 h = 4 days
Urine: 72 h = 3 days

For SARS-CoV (GVU6109):

in diarrheal stool (at low pH): 4 days
in respiratory/air droplets:  >7  days @ 20°C (Tr)
in respiratory/air droplets:  >20 days @ 4°C

  "The main route of transmission of SARS CoV infection is presumed to be respiratory droplets. However the virus is also detectable in other body fluids and excreta. The stability of the virus at different temperatures and relative humidity on smooth surfaces were studied. The dried virus on smooth surfaces retained its viability for over 5 days at temperatures of 22–25°C and relative humidity of 40–50%, that is, typical air-conditioned environments. However, virus viability was rapidly lost (>3 log10) at higher temperatures and higher relative humidity (e.g., 38°C, and relative humidity of >95%)."

  "We and others have reported that infectivity of SARS CoV (SARS coronavirus) was lost after heating at 56°C for 15 minutes but that it was stable for at least 2 days following drying on plastic."

UPDATE: 2020-03-13

From [7]:

  "We found that viable virus could be detected in aerosols up to 3 hours
  post aerosolization, up to 4 hours on copper, up to 24 hours on
  cardboard and up to 2-3 days on plastic and stainless steel. HCoV-19 and
  SARS-CoV-1 exhibited similar half-lives in aerosols, with median
  estimates around 2.7 hours. Both viruses show relatively long viability
  on stainless steel and polypropylene compared to copper or cardboard:
  the median half-life estimate for HCoV-19 is around 13 hours on steel
  and around 16 hours on polypropylene. Our results indicate that aerosol
  and fomite transmission of HCoV-19 is plausible, as the virus can remain
  viable in aerosols for multiple hours and on surfaces up to days."

For SARS-CoV-2:
Experiments were performed @ 40% RH and 21-23°C.

Copper (Cu):      4 hours
Stainless (Fe):   48 hours (2 days)
Cardboard:        24 hours
Plastic:          72 hours (3 days)
SARS-CoV-2 is most stable on plastic and stainless steel.

References:

[1] 20xx https://aem.asm.org/content/76/9/2712.short
[2] 1985 https://www.microbiologyresearch.org/content/journal/jgv/10.1099/0022-1317-66-12-2743
[3] 2005 https://academic.oup.com/cid/article/41/7/e67/310340
[4] 2009 https://www.sciencedirect.com/science/article/abs/pii/S0043135409000785
[5] 2010 https://www.hindawi.com/journals/av/2011/734690/
[6] 2003 https://www.ncbi.nlm.nih.gov/pubmed/14631830
[7] 2020 Aerosol and surface stability of HCoV-19 (SARS-CoV-2) compared to SARS-CoV-1


Skeletal muscle has got many many peripheral nuclei. What does "peripheral" mean here? Cardiac muscle has got a central nucleus similar to smooth muscle, but skeletal muscle you may recall has got many many peripheral nuclei.

What does "peripheral" mean here?

'Peripheral' in this context refers to the position of the nuclei within the skeletal muscle cell.  They are in the periphery (outer part) of the cell body rather than central as in most cell types.  More specifically, they are "subsarcolemmal", i.e. just under the sarcolemma, the cell membrane of the muscle fiber cell (source):

(Image from Wikipedia)

The many nuclei of a skeletal muscle cell are spaced out along the length of the cell (source 1, source 2).


Muller's ratchet and viruses Do viruses suffer from Muller's ratchet?  Can it significantly influence the current coronavirus pandemic?

As with most things in the natural world, there isn't really a single straightforward answer to this question! It depends largely on the ecological contect and the population dynamics.

Basically, in organisms with high mutations rates (such as RNA viruses), Muller's Ratchet suggests that the mean fitness in a population will always decrease. In small populations, mutation-free individuals are rare, and they will be lost through genetic drift. In 1990, Chao showed that deleterious mutations are generated at a sufficiently high rate to advance Muller's ratchet in an RNA virus.

However, in general, Muller's ratchet can be argued to be ineffective in viral populations because populations are never 'small', and drift is usually very weak (or selection is strong, in other words). Chao also notes that the effective population size in nature, 8x10^9 is often irrelevant to whether or not Muller's Ratchet is active, because Viruses often pass through the bottleneck of a single individual. Additionally, frequently recombining viruses such as HIV can also be subject to Muller's Ratchet Yuste et al (1999). The results of Chao have been generalised to many other viruses.

However, these studies are lab-based and don't pertain to your question about what might happen to SARS-CoV-2 'in the wild'. RNA viruses show the highest mutations rates in nature (Sanjuan et al 2010). This can lead to Muller's Ratchet in small populations where selection is weak and drift is prominent, but can lead to high levels of adaptation in large populations. It is not just the census population size which is important, but the effective population size, which can be thought of as a proxy for the amount of genetic diversity within a population. If a population rapidly expands from a single origin, as is expected to have happened with the SARS-CoV-2 outbreak, then the census population size would be larger than the expected diversity. Novella (1995/1996) showed that there is an interplay with the size of the bottleneck and the fitness of the surviving clones; when a more fit viruses passes through the bottleneck, they are more likely to avoid Muller's Ratchet. So in the case of SARS-CoV-2, whether or not the virus would be subject to Muller's Ratchet would depend on both the variation and fitness of mutation of the viruses who jumped from the intermediate animal to humans.

At the risk of overcomplicating things, population/deme structure also plays a role. If the virus evolves in different demes within a structure population, viruses within a deme can evolve population specific mutations. If there is then gene-flow between the demes, there can exist selection between the different mutations, driving up the average fitness across demes (Mirales et al 2009) and avoiding the Ratchet.


What is the purpose of measuring both VS (volatile solid) and TS (total solid)? In the biogas process you often measure Volatile solid and Total solids. Can any one explain these concepts more accurately and why it is interesting to look at these properties.

The biogas process I refer to is a process of fermenting waste food materials and slaugther house waste in to bio fuels, consisting largely of methane. The fermentation is conducted in anaerobic milieu in large plants.

Total solids and Volatile solid are measurements on the sludge the currently fermented waste,(the gooey stuff that is in the bio-reactor).

Total solids (TS): The part of the sludge that remain after drying at 105$^{\circ}$C for 20 hours:

$$ TS(\%) = \frac{\textrm{weight dried at } 105^{\circ}C}{\textrm{wet weight} }\times 100 $$

Volatile solids (VS): The part of the sludge that is combusted at 550$^{\circ}$C after 2 hours:

$$ VS(\% \textrm{ of TS}) = \frac{\textrm{dried weight at }105^{\circ}C -
 \textrm{dried weight at }550^{\circ}C}{\textrm{dried weight at }105^{\circ}C}\times100$$


How are proteins containing other elements encoded? If I understand correctly, proteins are formed by associating each three-letter DNA sequence  to a certain amino acid. Yet there seem to be proteins which contain elements such as copper, which isn't present in any of the amino acids. How are these encoded?

Let's use an example, a case in point: the best known and plentiful one would be hemoglobin. It is a protein formed through the association of alpha- and beta-globin peptides into dimers or tetramers. The shape is largely a result of the sequence (peptide folding is reproducible, especially with the help of chaperones which may aid the correct folding process) and they fulfill their function by making use of an iron atom which they capture allow for their oxygen-carrying capacity. The iron is not encoded (since it's not an amino acid) but the sequence certainly determines the ability for globins to come together and sequester iron. If you wish, you could mutate the sequence to produce globins which would have reduced (or a complete inability) to use iron at their cores! The organism would be anemic, and depending on the extent of the effect, would be impaired or die.
Quoting the beta-globin gene page:

More than 10 mutations in the HBB gene have been found to cause
methemoglobinemia, beta-globin type, which is a condition that alters
the hemoglobin within red blood cells. These mutations often affect
the region of the protein that binds to heme [iron].

Lastly, a quick note on exactly how iron fits into the picture... inorganic iron can't simply be sequestered by the hemoglobin protein. The iron atom must first be covalently bound to form an organic compound called a heme group (see picture 1 below) which then acts as a 'prosthetic group' for the hemoglobin protein. When both enzymatic protein and prosthetic group come together, we jointly call them a holoenzyme, the complete unit which performs the oxygen capturing, carrying and releasing function inside red blood cells (see picture 2 below).