Assumptions of Hamilton's rule Which elements of the following list are  assumptions of the Hamilton's rule?

Population structure (non-panmictic population)
Additivity

= Fitness of the heterozygote equals the mean of the fitnesses of both homozygotes

No epistasis or pleiotropy
Stable population size
Inifinite population size
Sexual reproduction
Selection on diploids or selection on haploids
Recombination (cross-over)
Mendelian segregation
Iteroparous population
smooth fitness landscape
mutation rate is high enough

Are there assumptions of Hamilton's rule that are not listed above?

Unfortunately, the answer depends completely on how stringent you are with "Hamilton's rule". If you just mean the equation $r \geq c/b$ then it is important to look at modern usages. In modern usage, all three of the terms $r$, $c$, and $b$ can be arbitrarily complicated. My favorite examples include when $r$ takes into account spatial structure saying that an agent near you is more "related" than a genetically identical agent far from you. Assumptions like that are a must, if you want to look at things that much of modern research is concerned with.

For this "most general" interpretation of Hamilton's rule, only one property is required and this property does not appear on your list: linearity. Note that this is not the same thing as the additivity you describe. Linearity means that your equations for small changes in proportions are linear in fitness: i.e. $\dot{p} = pf(E)$ where $E$ is some description of the environment, and $f$ is a linear function of the variables of interest (I used a continuous or large-population limit here, but similar things hold true for distributions over discrete populations).

Note, that in the above general and super-vague use of Hamilton's rule, the rule itself is not a biological observation but a simple fact of linear algebra. Of course, if you want to get linearity out as a consequence of some biological assumption, then the most common way to do this is by assuming weak selection.

If you put restrictions on what kind of features of the population, interaction, and environment structure $r$, $c$, and $b$ are allowed to incorporate then this will result in biological theories which will be mathematically true under only some of the assumptions you list. The subset of required assumptions will depend on what specific restrictions you place on $r$, $b$, and $c$.

There are no standard assumptions accepted on these parameters, so (unsurprisingly) I can't answer your question further without more specification on your part.


DNA mutations in CHO-KI mammalian cells The mammalian cell line CHO-K1 has 24,383 genes. After 70 doublings (from a starting number of cells, 1) a
total of ~4,000 mutations have occurred in the overall population of cells (i.e. not all in one cell), due to incorrect DNA breakage repairs (non-homologous end joining), with the mutations randomly distributed throughout the genome. Assuming that 2% of CHO genome consists of crucial genetic information (1.5% coding and 0.5% regulatory). What number of genes will be affected by these mutations?

My attempt:

I was thinking that the mutations should be spread randomly and so 24383*70/4000 genes may be affected but doesn't that assume the mutations are one per gene and the affected areas are actually important to protein expression?

I suspect this question is a lot easier than it makes itself out to be, though I may not be thinking straight. It doesn't matter how many cells you start with or how many doublings there are. Nor, for that matter, does it matter how many genes each cell has. There's a 2% chance that a random mutation will affect "crucial genetic information"; I must assume that that refers to genes. So $0.02*4000=80$ mutations would be expected to affect genes.


Is induction and derepression the same thing? Induction

This is a definition that our professor mentioned in class $-$the process of turning on the expression of gene in the response to a substance in the enviornment is called induction.

Derepression

From wikipedia $-$ in genetics and biochemistry the removal of repression, such as of an operon so that gene transcription occurs or is enhanced, with the net result frequently being elevation of the level of a specific enzyme. This effect is called derepression.

In lac operon when Allolactose molecule is present in the medium (in the bacterial cell) it binds to the monomer of repressor and reduces the binding affinity of repressor to the operator site and the RNA polymerase is free to synthesis a polycistronic mRNA. Thus the allolactose molecule turns on the expression of lac operon by removing repression.

So I conclude that in lac operon induction is same as derepression. But does it hold true for all operons or there are operons in which induction is achieved without repressing the repressor?

Induction is an effect of a stimulus on the cell. During an induction of gene expression a gene is expressed in response to a stimulus.

De-repression is a mechanism of gene regulation which may lead to expression of the corresponding gene. The gene can be expressed via direct activation as well. The action of CAP on lac operon would be an example of direct activation. There are several other examples too.


How to DIY preserve pet DNA today so that it can be used in 20 years I know that there are companies that offer a kit+storage of your pet DNA for around $2k.
My question is if there is any other option for doing this yourself with a thought in mind that in 20+ years the technology will get so advanced that even this DIY sample can be utilized.

Any ideas? Maybe drying a blood drop or mixing blood with alcohol/acetone?

Also, I read somewhere that it is better if the pet is still very young, because if you take old pet DNA the clone will exhibit mature signs even as a youngster. Is this true? If yes then what is the top age that is safe?

For the impatient, I'm going to say that probably if you only have a regular home freezer, its unlikely that you will be able to do this. If you have access to a -80C or liquid nitrogen storage its possible, but also less likely.

Cloning an animal typically starts with the transplantation of a nucleus into an egg cell whose nucleus has been removed.  So unless things change drastically in the next 20 years, just purifying DNA and keeping it in a tube of the fridge is not enough - you need to preserve epithelial (skin cells) or some other tissue in a state which can be revived to produce a live and intact cell when you want to do the cloning.

Its possible that we will have machines that can take DNA from a DNA prep and produce a living cell - this is what we hope to do with the mammoth and other extinct animals from fossil tissue some day.  But whether that will be the case in 20 years is just a guess, whether it is affordable is also just a guess.

So from what we know now, you will need to preserve a piece of tissue from the animal when it is alive.  I'm not an expert on how to do this, but you might be able to get the skin cells to sort of turn into a cell line and then freeze them for not too much money.

If you do this, regular freezers are not cold enough to prevent freezer burn.  This is what happens when you put a steak in to the freezer, wrapped in plastic even it will shrivel up and start to dry out as the water in the ice starts to sublime out of the package (the dry air in the freezer basically sucks the water out of the food).  If this happens to your animal tissue, its probably not going to revive.

Scientific labs use -80C freezers and liquid nitrogen storage because the water turns into a glass and all biochemical reactions are basically stopped. (besides drying out, the enzymes like DNAse are still nominally functioning in the cells at -20C and even simple bacterial cells don't live for more than a year at -20C, much less mammalian cells).  For preserving cell lines, liquid nitrogen is much more preferred.  I would say that properly produced cell lines can theoretically revive after indefinite liquid nitrogen storage.

So that's a quick answer.  Sorry to be a party pooper - things could change quite a bit in the next 20 years, but we just don't know how much.  popping a paw in a baggie or some DNA extract into the freezer might work, but its hard to say for sure.

As far as the choice of where the DNA comes from in the animal, its true that skin cell lines are often producing imperfect animals - the DNA may be modified in the skin in various ways that cause the animal to be smaller, weaker, or even deformed compared to the donor.  At this time all the protocols I see (and i could be wrong) are skin cells.  I would expect that there is a better tissue to preserve, but that might be just a guess at this point.  Its likely that in the next 20 years the choice of cell line from the donor will change quite a bit as well.


What properties (if any) do AT rich regions of DNA have? I was looking up the fluorescent stain DAPI and seeing that it

binds strongly to A-T rich regions in DNA.

That made me wonder what is special about AT-rich regions.

With regards to DAPI itself, one could tell that the molecule itself has a shape complementary to the shape of A-T rich DNA. So in this case it's "special" because DAPI happens to have the structure to form bonds to A-T rich DNA regions. (There can very well be another organic molecule that binds to C-G rich regions). A quick google search will show how it looks like

With regards to A-T in general, A-T share 2 hydrogen-bonds. However, this is not the reason why it's easier to break A-T rich regions. A-T rich regions destabilize the DNA double-helix. Refer to this http://nar.oxfordjournals.org/content/34/2/564.long. Transcription initiation occurs near T-A rich regions, e.g. TATA box in eukaryotes and Pribnow box in prokaryotes.


What determines the thickness of Cornea? In eye-operations such as Lasik and Femto, the thickness of cornea is key decision factor whether the operation is feasible. A normal thickness is between 500-600 µm. Cornea consists of a very special tissue having no blood supply and no vessels so it gets nutrients through diffusion of tear fluid and oxygen directly from air (hence in a way, it has its own respiration system not dependent on lungs).
Now I started to think the following questions:

I. What determines the thickness of cornea?

Helper questions

II. Is the thickness of cornea determined genetically so twins have the same cornea thickness?
III. Is the thickness determined by the environment and psychological things? Eg. how does diving affect cornea? Look it cannot get oxygen anymore through the air with the mask. What about drying? Does cornea gets too much nutrients all of a sudden from eye fluids?
IV. Does Homo Sapiens have more this kind of independent tissues? What about other animials? What determines the thickness of Cornea there?

The corneal thickness is genetically programmed. There are multiple genes that induce the final corneal thickness:

USP37, Chromosome 2;
GPR15, 3;
TIPARP, 3;
CWC27-ADAMTS6, 5;
RXRACOL5A1, 9;
LCN12-PTGDS, 9;
FGF9-SGCG, 13;

and at least 6 other genes.

source

other questions had to be asked as separate ones


Why does the thickness of the Loop of Henle have to be less than the convoluted proximal tube and the distal convoluted tube? We are currently being taught "Homeostasis through excretory system" in college. After seeing the structure of a nephron, it is not quite evident as to why should the Loop of Henle be the thinnest.
Only sense that I could make out of it is that- "Thin cross sectional area implies higher fluid velocity". Since, water and ions are majorly reabsorbed in the proximal convoluted tube, the loop of Henle is thin to increase the flow of fluid because there isn't much left to reabsorb and hence it won't require as much reabsorption time as the PCT. This decreases the filtration time and makes the process faster. I am not quite sure if this makes sense.
Can someone help?

there is a bit more to it actually,

The Henle -loop only occurs in birds and mammals, giving them the ability to make the urine hyperosmotic in comparison to their blood, other vertebrates can't do this.

how does the henle loop achieve this further concentration of urea(= more resorption of H2O)?:

-> by using the physical principle of countercurrent exchange
Beware: the explanation follows the opposite direction as the flow of the liquid!

A potential is build up in the bigger upgoing part Pars recta by active Na+& Cl- resoption , the water cant go out because the membrane is impermeable here.

this leads to build up of osmotic pressure (positive osm. potential of 1200 mOsmol/kg)

The Henle -loop  loops back up as a thin part(!) the Pars ascendens

the downgoing part right after the PCT (pars descendens) uses the potential of the corticomedullary osmosis gradient to let water (resorption) out using passive osmosis while taking urea in (no ATP needed).

CONCLUSION: So why is the left and bottom part of this henle loop thinner?!  to resrobe H2O using passive osmosis ! (also, if the lowest bottom part would be thick, it would not loop so nice, therefore hindering the coutercurrence effect)


Are there any non-pathogenic gram-positive bacteria in human gut? I wish to know if there are any non-pathogenic (not even opportunistic pathogen) gram-positive bacteria in the human gut? Is there any reference that shows there exists a non-pathogenic gram-positive bacterium in the human gut?

I searched the internet but was unable to find anything conclusive.

A recent Nature article, entitled A new genomic blueprint of the human gut microbiota, contains the following Figure:

[Fig. 3 Phylogeny of reference and uncultured human gut bacterial genomes]

I don’t know much about bacteria, but, according to their entries in Wikipedia, Actinobacteria, and most Firmicutes are gram-positive and, as these appear to be present in abundance in the human gut of healthy individuals, one assumes that they are not pathogenic to humans.


Can a phenotype only have one allele? A phenotype such as hair color
like blonde hair.
I am curious because mutations cause new alleles but does that mean that there always has to be a dominant or reccessive allele?

Can there be only one allele at a given locus?

An allele is a variant of a gene. If there is only one allele at a given gene, it means that there is no genetic variance at this specific locus (a locus is a position in the genome. It can typically correspond to a gene). It is not rare at all that the whole population is fixed for the same allele at a given locus.

Number of alleles

In courses, it is common to consider only the case of 2 alleles. In reality, there might be any number of strictly positive allele. At a given locus, you might have 1, 2, 3 or 11 alleles for examples. The reason why we typically teach about the 2 allele case is that 1 allele is not of much interest as there is not genetic variance at this specific locus and 3 or more alleles makes everything a little more complicated.

Dominance relationship

In courses, it is also common to consider diploid individuals, 2 alleles and the phenotypes of the three possible genotypes assuming $h_N = 1$ (see here to understand $h_N=1$). In reality, the relationship between two alleles may be vastly more complicated. There is a gradient from complete recessivity to complete dominance (passing through perfect additivity). It is also possible that the heterozygote is more extreme than any of the two homozygotes.

Dominance relationship - Number of alleles

As the number of alleles varies, any pair of alleles have a specific relationship of dominance. While empirical studies suggest that if allele A is dominant over B and B is dominant over C, then A is likely dominant over C, it is not impossible that C could be dominant over A. And again here, I am considering only cases of complete dominance but any scenario is possible.

Dominance relationship - Ploidy

The ploidy also varies from one species to the other (and also from one moment in the life cycle to the other for sexually reproducing organisms). If you have  a polyploid, then the number of possible genotypes is higher than 3 (even for a 2 allele case) and therefore the concepts of recessivity and dominance don't necessarily apply that easily.

Dominance relationship - Epistasis

Finally, there might have interaction between loci making that the relationship of dominance at one locus may depend upon the genetic background (that is the other variants present at other loci). Of course, it may as well depends upon the environment but let's not talk about that for the moment.


Data Bias in protein-protein interactions data Databases like STRING have so many predicted as well as experimental interactions data for many organisms.However there is a bias in the data which they have?.

a)The first is gene co-occurrence  which is more like a circular argument.
b)And the second one is that all interactions that are predicted computationally are tested for experimental interactions.This leads to a bias in the interaction data available for organisms in STRING.

How do we overcome this data bias while using STRING interaction data for analysis purpose?

a)Avoiding evidence channels of gene co-occurrence is one way.Is there any other way other than this?
b)How to statistically say that the bias is not governing the data or any way to test statistical significance of the data bias?

I'm one of the STRING maintainers, so I hope I can clear things up a bit.

Gene co-occurrence: genomic context methods are very useful for bacterial genomes, but not so much for eukaryotes. However, they are actually the most unbiased data we have, since there's no human influence (beyond selecting species for sequencing).

Benchmarking: Interactions predicted from text-mining etc. are benchmarked against the KEGG database. However, this doesn't necessarily lead to biases, as this benchmarking is basically a calibration step.

Actual biases: For eukaryotes, most interaction data comes from the experimental, database and text-mining channel. All of these are biased in various ways: e.g. there are study biases (disease genes will get more attention) and technical biases (some proteins are hard to work with)

As we don't know the actual set of protein-protein interactions, we can probably not test for biases in the data.


How do people who have lost both of their legs produce red blood cells? As far as I know, just leg bones produce red blood cells. So, how people who lost their both legs produce red blood cells?

Red blood cells are produced in the red marrow which...

  "is found mainly in the flat bones, such as the pelvis, sternum,
  cranium, ribs, vertebrae and scapulae, and in the cancellous
  ("spongy") material at the epiphyseal ends of long bones such as the
  femur and humerus." - Wikipedia

So you are partly right; the femur is associated with red blood cell production, or Erythropoiesis to give it it's technical name, but there are other bones within the human body that also do this job. The process of erythropoiesis is stimulated when the kidneys detect low levels of oxygen in the blood stream and stimulate production of the hormone erythropoietin. Further, the role of the tibia and femur in erythropoiesis also decreases with age whereas...

  "the vertebrae, sternum, pelvis and ribs, and cranial bones continue
  to produce red blood cells throughout life." - again from the wiki page

So I'd suggest it is unlikely that loss of the legs would have a major impact on the production of red blood cells in adults. I imagine that with the loss of legs comes some reduction in functionality of erythropoiesis but also a lower requirement of red blood cell production (less blood capacity = less blood cells needed = less blood cells need to be produced). I can't find any studies which explore the ability or needs of amputees and non-amputees with regards to red blood cell production.


Is "Fight or Flight" distance genetic If you took a newborn animal and completely isolated it from its species, would it be capable of assuming a fight or flight distance preset by its species, due to their being no basis for what could harm the animal?

It probably is somewhat genetic.  A good example is pigeons.  When you approach them, they turn their back to you so that if you get close enough they can escape / fly away.  I'd be surprised if this is only a learned behavior, but I also note that pigeons who have been fed let you approach to a closer distance than other birds, so in this example a distance is not completely hard wired.

Such behaviors are more likely a combination of learned and genetic, especially as the animal becomes more complex (has a larger brain).  This is a major concern of 'ethology'.

I think few inherited behaviors are completely inflexible.


Consensus codon optimization by organism Does a public database exist that contains this information? I'm trying to make a simple gene annotation program that will let me input a DNA sequence and then optimize it based on one of these tables using the E. coli preferences, for example.

Try the Codon Usage Database at Kazusa. You can search by organism. The database contains 35,799 organisms and compiled from 3,027,973 complete protein coding genes (CDS's), but last updated in 2007.


Epistasis Across Chromosomes and Individuals 'Homozygous for Interactions' Apologies for any failures in nomenclature. I'm a mathematician who is making a foray into genetics for a masters thesis. Specifically, I'm generating artificial diploid genetic sequence data and phenotype data based on known epistatic interactions.
Primary Question
I am familiar with the concept that having multiple copies of a single allele (e.g. one from each parent) can actually increase expression and thereby change the quantitative phenotype (at least in some cases?). Can this also happen with epistatic effects? For example, consider the case that locus 1 ($L_1$) and locus 2 ($L_2$) exhibit some positive interaction ($\beta$) on the trait ($Y$).
$$E[Y]=\mu+\beta(L_1L_2)$$
If both chromosomes contain the allele in question at both loci, then does this individual exhibit more of a trait increase than if he only had one chromosome with the epistatic alleles?
Secondary question
Can alleles interact epistatically even when they are present on different chromosomes? e.g. assume allele A at locus 1 interacts with allele B at locus 2. Individual has A at locus 1 and b at locus 2 on chromosome 1. He also has a at locus 1 and B at locus 2 on chromosome 2. Do A and B from the different chromosomes interact? My intuition is yes but I want verification.
Many thanks!!!

Question 1: The phenomena you describe in which it matters whether you have one or two copies of an allele (e.g., the AA phenotype being different than the Aa phenotype) are known as dominance effects. Dominance effects can interact with epistatic effects (in which the phenotypic effect of one locus depends on the genotype at the another locus).

One good example is the interaction between the Agouti locus and the Mc1R locus in the oldfield mouse (Peromyscus polionotus) in determining coat color. Dark-color homozygotes for the Agouti locus have dark coats irrespective of the allele at the Mc1R locus, whereas color in Agouti heterozygotes or light color homozygotes depends on genotype at the Mc1R locus. The figure below, from Steiner et al (2007), illustrates:

Question 2: Epistatically interacting loci need not be on the same chromosome. The loci discussed above provide a perfectly good example. Mc1R is on chromosome 1, where as Agouti is on chromosome 7, yet they interact epistatically.


Is there any bank of animations for Embryology? I am trying to find animations which can anonymous or generalised for Embryology.
However, I have not find any single good source.

Is there any bank of animations for generalised embryos?

I don't know of any database, but a short search brought up a few candidates. Depending on what you would like to see, they should be a good start:

Human Embryology Animations
Simbryo (Flash based)
UNSW Embryology
Embryological Development of the human
Embryodynamics


Is there a free alternative to Gelcompar for comparing banding patterns across multiple gels? In order to run my microbial community samples from my experiments through DGGE, I was required to use multiple gels.

Thus it is necessary to compare banding patterns across more than one gel.  This means that I need some way of assessing whether the 4th band on gel #1 is the same OTU as the 4th band on gel #2.

The industry standard for this procedure seems to be the Gelcompar software.  Unfortunately this software is greater than $10,000 and is proprietary (thus, not open science friendly).

Does there exist a free (ideally as in speech and beer) alternative to Gelcompar?

Try this one

Pavel, A. B. & Vasile, C. I. PyElph - a software tool for gel images analysis and phylogenetics. BMC Bioinformatics 13, 9+ (2012).

You can download here
http://sourceforge.net/projects/pyelph/


Are there any flowers that look like snakes? In Rio 2, they showed a flower that almost looks like a snake head (with two fangs and a long tongue).

Are there any such flowers in real life too?

There are quite a few examples of plants which look like snakes. I'll tell about them one at a time.

Darlingtonia californica: or Cobra Lily, is a type of pitcher plant which looks much like a snake. It is native to Northern California and Oregon, growing in bogs and seeps with cold running water. See this image:

Arisaema triphyllum: commonly called Jack-in-the-Pulpit, it is a type of corm which resembles cobra. It is native to eastern North America, occurring in moist woodlands and thickets from Nova Scotia west to Minnesota, and south to southern Florida and Texas. See this:

A similar and closely related plant, Arisaema griffithii, called Griffith's Cobra Lily, resembles even more. See this:

Pogonia ophioglossoides: also called Snakemouth Orchid, whose flowers resemble the face of a snake, pretty much like your image. It is a species of orchid occurring from central Canada to the east-central and eastern United States. See this:

Isotria medeoloides: named Little Five Leaves, its flower also resembles a snake's face. It is a threatened species of terrestrial orchid found in temperate eastern North America. See this:


Why do some viruses cease being a problem even though no vaccine or cure is found? No vaccine or cure has been found for SARS-CoV or MERS-CoV yet the world is not too concerned about them. How can it be? Did all people who had those viruses die or do viruses just randomly decide to stop being infectious at some point?

Infections spread in a population when the number of new infections caused by an infected person is greater than or equal to 1.

If each infected person spreads the virus to less than 1 person, eventually no one will be infected, without a need for any sort of cure. Of course, the longer a deadly infectious disease spreads in a population, the more people will die during this process. Ideally you want to get the number of transmissions as close to zero as possible as quickly as possible.

SARS and MERS are each a bit different, but share some similar characteristics. Compared to COVID-19 caused by SARS-CoV-2, both are more severe in a larger fraction of the people infected (note: all three viruses are closely related betacoronaviruses). This made it easier for public health officials to identify and isolate infected individuals.

The MERS virus is really not gone at all: it lives on in animal reservoirs, like camels (so it is primarily only a concern in places where those reservoirs live). Cases continue to occur sporadically. However, MERS is usually not that transmissible between people, having a natural transmission rate that is already less than 1: that means that most people who get it get it directly from an animal, and don't continue to spread it to others besides occasional infection of individuals with close-contact, like a family member. There have been exceptions where isolated incidents involved substantial human-to-human transmission. Some of these incidents were associated with "super-spreaders": particular individuals who got infected and spread the virus to way more people than the average. See https://wwwnc.cdc.gov/eid/article/26/2/19-0697_article for more.

SARS caused by the original SARS-CoV virus indeed seems to be gone, with no cases reported since 2004. The elimination of SARS from the human population occurred via controlling the human-to-human spread through isolation and contact tracing. See https://apps.who.int/iris/handle/10665/70863 for a report on the epidemic and how cases and spread in different locations were handled.

Viruses don't have any agency: they can't decide to do anything. However, humans can, and our best response to outbreaks of novel diseases is to trace the spread and try to limit transmission as much as possible.


What is the reason behind that sometimes when I see new thing I feel that I have already seen them? I have googled it and I found that it is, because of good memory, but how it can be due to good memory as it didn't happen before. It happened to me many times, that I feel that the scene which is happening now, has already happened to me in my past. But it was a new scene in my life, so why does I feel like this? How is it possible that a same scene happens twice?. What is the reason behind it, that we feel something twice in our lives.

What you are talking about is a déjà vu, the feeling of familiarity even though the situation is not familiar at all. It is, in fact, a very common phenomenon. A high percentage of people report having had déjà vus. It is nevertheless hard to put a number to it, because the experiences and déjà vu definitions might be different. I have found numbers between 60 and 90% of the population.

The claim that this is a sign of a good memory is related to the view, that a déjà vu is not a false memory, because you actually realize that the situation should be unfamiliar to you (also mentioned here).

But how do déjà vus happen? There are several theories...

It seems clear that déjà vus are associated with activity in the temporal lobe (on the side of the brain). That's where memory is processed, especially episodic memory (things that happen - in contrast to learning a skill). People with epilepsy often report déjà vus right before a seizure that starts in the temporal lobe.

One theory, put forward in this paper, says that the memory and feeling of familiarity are processed in different areas and there is a false activation of the familiarity area during a déjà vu. The brain is not always working proberly, e.g. false sensations can happen, like hallucinations. So, the false activation of that familiarity center could give us the sense of familiarity in an unfamiliar situation.

Similar to this is the idea, that there might be a mismatch between perception and memory formation. When something we are experiencing right now is "leaking" into our memory due to false activation, we think that this has happened in the past. There is a problem with this explanation: despite having a strong feeling of familiarity during a déjà vu, people fail to give any context to when this previous event happened or which other events have preceded it. So, it doesn't seem to be perceived as a memory.

Another explanation could be a false combination of the experience with something that is loosely connected to it (like planning the trip, watching a movie with a similar scene, etc.). Our brain always tries to connect experiences. It might falsely identify something you've seen in pictures or read in a book as a real experience.

As you see, we still struggle to explain the phenomenon. It is caused by some error in the way our brain perceives a situation, writes or retrieves memory or processes familiarity. This error might be a wrong activation or wrong timing or the like.


Is this sentence about RER correct on Wikipedia? While studying about Endoplasmic Reticulum on Wikipedia, I came across this sentence

  A ribosome only binds to the RER once a specific protein-nucleic acid complex forms in the cytosol. This special complex forms when a free ribosome begins translating the mRNA of a protein destined for the secretory pathway.

To my knowledge, most proteins are synthesized and modified post-translation in association with RER. Then why is protein destined for secretory pathway mentioned?

As stated in a comment, your understanding of protein translation in eukaryotes is not accurate. In order to provide a concrete reference that isn't wikipedia, I'll quote here from Biochemistry (2nd ed) by Voet and Voet (1995 / John Wiley & Sons) pg. 307:

  Cytologists have long noted two classes of eukaryotic ribosomes, those free in the cytosol, and those bound to the ER so as to form the rough endoplasmic reticulum (RER ...) Both classes of ribosomes are nonetheless structurally identical; they differ only in the nature of the polypeptide they are synthesizing. Free ribosomes synthesize mostly soluble and mitochondrial proteins, wheras membrane-bound ribosomes manufacture transmembrane proteins and proteins destined for secretion, operation within the ER, or incorporation into lysosomes ... These latter proteins initially appear in the RER

Pretty succinct and thorough description.

The wikipedia text you quoted is a bit shallow (on its own) and somewhat incomplete, but essentially correct. The RER isn't solely associated with synthesis of proteins destined for secretion, but this is one of the classes of proteins synthesized in association with the RER. It would be more accurate to say that proteins destined for transmembrane insertion, secretion, or certain other kind of 'special handling' are synthesized in association with the RER rather than free in the cytosol.

The details of how, for example, these different classes are targeted to the RER are fascinating but somewhat beyond the scope of the question. Well explained in the referenced text, though, if you're interested.


On evolution statistics This basic evolution theory question has been haunting me since childhood and I'm kind of embarrassed that I can't explain it yet:

Consider a butterfly. It's wings have evolved to look like the eyes of an owl, so to prevent it's predators who are themselves preys of the owl to attack it.

From what I've learned (and feel free to indulge me in the very basics if I get this wrong), natural selection suggests that the butterflies that didn't have the owl's eyes in their wings would be eaten, leaving the ones with the eyes to survive, right?

But that implies that this useful trait appeared in the butterfly's wings by chance. Now, I know trillions of butterflies have been born before this, but trying to figure out the possibility of this to happen by chance doesn't look like it's plausible. Let's go through the things that have to work right before this trait is passed over:

For a butterfly to be born in a different wing colour, it should be a genetic mutation which doesn't happen this often, for what I know.
The wings are composed of micro-scales. For every scale to compose an image so similar that confuses even us, the margin of error is very slim. It could be anything. It could be a picture of Tom Selleck for all we know. The scales must be in the correct spectrum of colour by a small margin of error. So that is already a very unlikely thing to happen.
Then, this butterfly cannot be eaten out of bad luck (mind you, the wings don't guarantee it will not be eaten, just enlarge her chances).
It has to mate, which also is not a guarantee to happen, since nature deals with competition. If this butterfly we are considering is a male, the female must find the wings hot, instead of being afraid of those creepy eyes.
The genes of this mutations must also be dominant, so when it mates and generates offspring, at least part of the new butterflies inherit this trait.

And this is a simple example. There are animals that evolved so smartly I can't even start to think of the possibilities.

My question is, more precisely, how likely is it for a species to evolve into complex solutions?

In your 5 points you basically cover several concepts of evolutionary biology.

1) The number of mutations depend on mutation rate. The mutation rate varies along genome sequences, species and individuals. According to the recent DECODE study (Kong et al., 2012) a human mother transmit on average 15 mutations to her offspring and a human father transmit on average $25 + 2(g-20)$ mutations to his offsprings, where $g$ is the age of the father and where the formula stands only for father older than 20 years old.

2) Mutations happen by chance and are not directed toward creating some specific feature. But it is much more likely to create a round of color on the wings of a butterfly than creating the picture of Tom Sellek. The reason has to do with the developmental and biochemical pathways linking the given mutation to its phenotypic effect. Looking at a given mutation, you can understand how it yield to the modification of some phenotypic trait by looking at the biochemical and devlopmental pathways.

3,4) The third point that you raise is called "genetic drift". Shortly speaking the concept of genetic drift may be called the good luck/bad luck effects. Stating differently genetic drift is the random sampling of alleles (gene variant) from a population. If some alleles are favored over some others at a given locus, then sampling is not 100% random but is not either 100% deterministic. The only case where genetic drift is absent is in infinite population (which is obviously an unrealistic case). Genetic drift is inversely propotional to population size and you'll understand it better by reading this post.

5) When the mutation is at very low frequency, the mutation needs to be dominant in order to be expressed, this is true. But an allele may increase in frequency due to genetic drift up to the point that some individuals are homozygous for this allele and therefore express the trait. Dominance and recessivity are just extreme case of a continuum and most often alleles have intermediate level of dominance. Pleiotropy is also something to consider. Note also thaat the frequency of the three possible genotypes $AA$, $AB$ and $BB$ are given by Hardy-Weinberg law (under some assumptions) $x^2$, $2x(1-x)$ and $(1-x)^2$ respectively, where $x$ is the frequency of the allele $A$.

Hope that helps!


Calculation of the bacterial growth rate from a spectrophotomer growth curve Typically the microbial growth in liquid cultures is monitored by turbidity. Data is obtained with a spectrophotometer to measure optical density at 600nm. The slope of the bacterial kinetic curve in exponential phase is the growth rate.

But I have seen two ways of calculate the growth rate:

Growth rate = Maximum slope value of the Kinetic curve
$Log_{10}$ transformation of the growth data and then calculate the slope.

I think the second one is right if you want to calculate the generation time:

generation time = $\frac{ln(2)}{Growth rate}$.

What is the correct way to calculate the growth rate and then generation time?

This is a common experiment for microbiology courses and you can find instructions on the internet , here is an example from University of Wisconsin: http://inst.bact.wisc.edu/inst/index.php?module=Book&func=displayarticle&art_id=114

But the general method is measure optical density at regular intervals and plot them on a semilog graph, which has the normal linear scale on the X axis for time, but a base 10 log scale on the Y axis for optical density. You can set this up in microsoft excel or libreoffice calc by right clicking the y axis and going to format axis, there should be a logarithmic scale option somewhere depending on the version.

After you have the data plotted, the exponential growth phase should appear as a line with positive slope. The logarithmic scale on the Y axis will automatically transform the exponential curve into a straight line. To determine growth rate in terms of generation per hour, you need to get the optical density at time 0, which is the beginning of the exponential phase, and time t, which is just some other time on the exponential phase. Use this equation to determine growth rate: $k =\frac{log(X_t) - log(X_0)}{0.301t}$

Once you know the growth rate, you can determine the generation time with $t_{gen} = \frac{1}{k}$, which gives time for 1 generation in hours. To convert to minutes, just multiply by 60.

As a side note, remember to blank your spectrophotometer with sterile media. Also, if the optical density goes over 2 it won't be as accurate, so dilute the aliquots to make the optical density go below 2. Remember to record the dilution factor so you can multiply the density by the dilution and get back to the "original" optical density for plotting.


What is going on in these cells? Here are some pictures of human iPS cells in culture. After several passages, some cells look really weird, can you help me understand what is going on? What am I looking at? What are those blastocyst-like structures? (bluish picture) and what about that cell full of vacuole-like thing?

P.S. do not pay attention to the scale bar, it's incorrect.

Extra info:

I did not induce them, I got them already dedifferentiated so I can't be specific on that part of the protocol. However, I am growing them in Essential 8 Flex Medium (with supplements as specified from the kit protocol), I add rock inhibitor 4h before passaging them. Passages are done by dissociating colonies using EDTA only (no enzymes). Most of the expanded cultures look normal, some showed the formation of embryonic bodies (the last picture added) but the blastocysts are very different and not really expected.

they might be embryoid bodies:

https://en.m.wikipedia.org/wiki/Embryoid_body


Is it essential to add cholesterol to agar or liquid culture for C. elegans? In preparing agar plates with NGM, and also liquid cultures for growing c elegans, how essential is the addition of cholesterol and heavy metals? I have prepared both. I can't notice any obvious difference and I hate having to add all these supplements.

I'm using yeast extract and peptone as the primary components of the base.

Isn't this just supposed to be a moist semi-soft substrate for them to crawl around, their nutrients come from the bacteria they eat.

C. elegans needs cholesterol, but can't make it. Since bacteria don't make cholesterol either, the food bacteria aren't a source. As explained in the linked paper,  lack of cholesterol affects normal development.


Do dead cells always contain no nucleus? If I examine a dead cell, can I be sure that it has not a nucleus?

And what about the other organelles?

If you're looking at cause of death by standard apoptosis, to initiate the process, cytochrome c will be released from the mitochondria, bind with apaf-1, and undergo a structural change resulting in what looks like a biochemical ninja star (figure 4). This will activate caspase-9 which will activate other executor caspases, eventually creating an avalanche of protein-degrading enzymes that will leave the structure and organelles of the cell looking like paper mache. Regarding the nucleus, the complexes of enzymes meant to maintain dna integrity and structure will be degraded, the DNA's network influence on the cell will become largely inert, and the dna will be condensed and broken apart by nucleases. The membrane of the nucleus is full of proteins and ribosomes, and these will be degraded too. If you are looking to simply identify an inert nucleus by its skeleton, you may not have much success either - here are a few good images from a nice study showing the progressive destruction of a nuclear structure.


Does human behaviour that is caused by inheritance depend on the environment and lifestyle in general? Different breeds of common domesticated animals such as horses and dogs clearly show different behaviour, instincts, social relationships and similar, due to their biological inheritance. Still they can easily mate with other breeds of the same species. This also applies to wild animals, for example the wolfs living in the rainforest on the Canadian west coast prey on fish (and are maybe expected, with time, to go through a similar transformation as the predecessor to dolphins, that where actually wolf like animals, did when they resettled to the oceans) while inland wolfs prey on moose and elk etc, which requires completely different hunting technique, tactics, pack size and so on.

Are there any similar examples for humans? I reckon that living in the jungle or in the desert or on Greenland should reward different behaviours/traits that influence behaviour. Also going from a hunter-gatherer society to an agricultural society should reward different behaviours, social skills and similar aspect of human life.

Are humans like other animals in this respect (any examples?) or are we unique (?) in the animal kingdom when it comes to the influence of genetics on our behaviour?

One reason I ask is that I got second hand (without sources) information claiming that the natives of Mexico has the highest prevalence, of any population measured, of genes that are known to be connected with/causing ADHD. Mexico was also one the last places on the planet where humankind settled.

The argument went something like this: "during prehistoric time individuals with ADHD tendencies tended to be more adventurous than their peers and therefore traveled further". If this is true, people in Mexico's behaviour should be slightly different from people in current Kenya and Tanzania (by many scientists claimed to the birthplace of humankind), at least if you measure ADHD related traits.

I feel that 99% of the time that someone asks "are human unique concerning ?", the answer is nope. There's nothing exceptional about humans in this respect.

Rephrasing your question

Your question can be rephrased

  Is heritability sometimes different from 0 or 1 for humans too?

If you do not understand well why this is a good rephrasing of your question, then you should definitely have a look at this post.

Is heritability sometimes different from 0 or 1 for humans too?

Yes, humans are not exceptional in this regard. In humans, other animals, plants, fungi, bacteria, archeabacteria and for any other living things, any behaviour (and any phenotypic trait in fact) can have a heritability that differs from both 0 and 1, or in other words, there can be for any trait both genetic and environmental variance underlying phenotypic variance in the population.

In fact, very few traits that have a non-zero genetic variance has no environmental variance. Have a look at the post List of heritability estimates in humans? for a list of traits on which we measured heritability.

ADHD

The difficulty with a trait like ADHD is that the methodology to measure it vary a lot from one country to another or even from one practitioner to another. But yes, for ADHD too, there is both genetic and environmental variance underlying the observe phenotypic variance (Thapar et al., 2000).


Origin of different brainwaves I'm creating a project in which I can measure brainwaves (more or less like EEG). Since I'm not a medical student im having a problem finding the origin or most prominent regions for measurements of alpha and beta waves. I have researched on the internet but can't find a definite solution. So can  someone please tell me the exact origin or the most prominent region (active region) of our brain where  the alpha and beta waves can be measured reliably??( Like ocipital region or frontal temporal etc)

Alpha and beta brainwaves are just two of several arbitrary, named frequency ranges for a brain-wide phenomenon. See Types of Brain waves. These so-called brainwaves are big electrical events that sweep across the entire brain.

My recommendation for electrode placement is based on my engineering experience. Pick any location on the scalp. You could start with the temples. Take your measurements. Then move the electrodes to a different location and repeat the measurement. Continue this experimentation until you discover by observation which location yields the best results. When you have finished with the experiment, you can post your experimental results on SE Biology and answer your own question.

I suspect that electrode type and method of contact (dry versus conductive gel) will be more significant than actual placement on the head.


Why do endotherms need more food than ectotherms? I have a rough idea: endotherms need more food to keep their temperature stable whilst ectotherms use less of their food in respiration.

but that's just me parroting the textbook I don't really understand it.

Could someone help out? Thank you.

Endotherms also called warm blooded animals have the ability to regulate their body temperature by themselves.

If the endotherms are in a cold place their body increases the metabolism and generates more heat. This will compensate for the cold outside.
In a hot region the body metabolism is tuned down (this is not as efficient as the adaptation to cold region - as the metabolism can't be turned down below a certain limit - this will result in death) a little and heat generation is somewhat reduced. The second and more efficient mechanism is the heat dissipation by sweating and through skin (directly).

Ectotherms on the other hand, do not have efficient temperature regulation systems.

In warm regions when the temperature is high, the ectotherms seek shade and low-temperature areas to prevent over-heating
In cool regions they seek sunlight and expose themselves to the sunlight for warmth. For the same reason, they can also search out and stay near fire pits, campfires etc...

So when we calculate the energy demands, the ectotherms need more energy as they regulate their own metabolisms to match the need.

The increase in need for energy in hot condition maybe due to:

The extra-processes that are regulated like sweating, increased peripheral vasodilation - thereby increasing circulatory rate (increased work for heart)
This thermo-regulation inturn affects other processes and systems like electrolyte and water balance, excretory system, endocrine system, thrist, etc...

During the cold season increased metabolism itself is the main cause for increased need for energy.


Why is stimulation of nerve tissue with a negative pulse called "cathodic" stimulation? By definition, the cathode is defined as the terminal through which current exits a polarized device. But in the context of neuromodulation, such as spinal cord stimulation, deep brain stimulation, the "cathodic" pulse refers to a negative current pulse that elicits action potentials. A negative current is by definition a current flow that enters the electrode.

Can anyone explain where this terminology comes from and help me resolve this apparent contradiction? It's driven me mad for the past years.

The answer to your (excellent) question is a matter of definition, which has its roots in the 18th century.

A cathode is the electrode where conventional positive current leaves a current source. Conventional current is positive, due to historic reasons. Around 1750, Benjamin Franklin described the flow of current between wool and wax after electrostatically charging the former. He defined the flow of current as being positive, flowing from the surplus side (which he defined as positive) to the current sink (defined as negative). This unfortunate choice is sometimes referred to as the Franklinian approach to electricity, and is still widely used today to describe electronic circuits and referred to as the conventional flow notation (Fig. 1) (Efron, 1960).

Fig. 1. Franklinian approach: the conventional flow of current still in use today for electronic circuits. Source: All about circuits.

The electrical current was only later found to consist of negatively charged particles, namely electrons. The work of Luigi Galvani on electrical stimulation in frog muscles around 1780 and the invention of the electric battery by Alessandro Volta in 1800 eventually led to the discovery of the electron in 1897, attributed to J.J. Thomson and his work on cathode rays shown in Fig. 2. As the figure shows, the true flow of electrical current is the reverse, namely an electron current flowing from from negative to positive. In the meantime, however, the convention of positive current flowing from the positive pole (cathode) to the negative (anode) was already established. Note that this holds for a discharging device. In a charging device, such as the battery, the cathode is negative, and the anode is regarded as positive.

Fig. 2. Cathode ray showing electron flow. Source: TutorVista

Hence, in a stimulating (discharging) device, the cathode is in truth negative, because it is the source of negative current (electrons). Cathodic stimulation therefore means electrical stimulation with a negative current. A cathodic pulse is therefore injection of a negative current pulse.

Reference
- Efron. Chapman & Hall London, Rider Publisher New York (1960)


In the induced fit model for enzyme action, does the enzyme active site change slightly after products form? The reason why I am asking is because I am looking at a past paper and they highlight that it does. I have attached it below. Could you explain why this is the case.

I am just looking for a quick overview of why this is the case.

I understand now that they are highlighting how during the transition state the enzyme was induced to change shape, but once products formed and left active site, there was further changing of shape of the enzyme active site so it could return back to its original shape - therefore it could be reused again, as in line with the role of an enzyme/ catalyst.


How can rapid growth cancer get nutrients in vivo? When I was little, before I get into biological studying, I read a news talking about cancer would be totally cured after decades. I still remember that researchers had a theory to claim if they could limit the blood vessel generation near to tumor, then the rapidly growing cancer cell couldn't get enough nutrients and would kill them. However, this theory seems not to work well. Cancer cells or tumor still have another way to get enough nutrients to live, or at least, maintain themselves to survive and endanger the host. So, my question is how can rapid growth cancer get nutrients without blood vessels in vivo?

Long back in 1971 Falkman and others put forward new therapeutic implications of targeting blood vessels supplying nutrients to tumors.   Treatment you are mentioning is called 'Anti-angiogenic therapy '. However current challenges in this therapy are resistance to antiangiogenic agents and non specificity. Plus there was huge 'normalization effect' which was actually helping other blood vessels around tumor. To answer your question, Cancer cell makes their own blood vessels instead relying on host machinery. There are many other factors also why this kind of treatment is not successful yet.


Is coral photosynthesis dependant on the wavelength or frequency of light? When buying a light fixture for a marine fish tank, it is often sold with some technical data reguarding the spectral output of the light, with a peak in the blue region of visible light, somewhere around 430 to 460nm in air.

As light enters the water with a refractive index of approximately 1.33, the peak wavelength will reduce, but the frequency of light will remain constant. So, for example, a monochromatic light with wavelength 460nm in air would have a wavelength in water of about 345nm, but the frequency is the same. Physics so far, so here comes the biology question....chlorophyll a and b have peak responses between 400-500nm light, so is it the wavelength of light in water that is important to photosynthesis, or is it actually the frequency(therefore the photon energy) that is what counts?

If we were to discover a purely theoretical new plant that grew equally well in air or water, and discovered that photosynthesis only occurred at 650nm wavelength light in air, and not at all to any other wavelength. Then we place this plant in water indoors in the dark and shine a monochromatic 650nm light source at if from air, into the water,  would photosynthesis still take place because the photon energy is the same in water or air (e = hf). Or would we need to shine a monochromatic light source of approx 865nm in air, which would reduce to 650nm in water (865/1.33)? I suspect the answer is that photsynthesis is dependent on the photon energy not wavelength, but I am far from sure about this!

Short answer: Coral doesn't need the light, it's the zooxanthellae that is symbiotic with some corals that relies on light to grow; it adapts to the frequency spectrum available at the depth the particular coral grows, full spectrum at shallow depths and at over ~30m the zooxanthellae relies on blue light because other frequencies are absorbed by water.
Some species of coral, such as Lophelia pertusa, grow in water so deep that there is too little light for them to rely on zooxanthellae, instead their polyps gather food directly with their tentacles, feeding heterotrophically.
There are even instances of coral feeding on jellyfish, see: "Opportunistic feeding by the fungiid coral Fungia scruposa on the moon jellyfish Aurelia aurita" (May 21 2009), by A. Alamaru, O. Bronstein, G. Dishon and Y. Loya
Longer answer:
The physics portion of your question is best answered on our Physics.SE site's question: "Why doesn't the frequency of light change during refraction?"
Light's wavelength and frequency are related to each other based on a mathematical formula, it's the intensity that is affected by passing through a medium; different materials will attenuate some frequencies more than others. Water doesn't transpose light's frequency or wavelength as much as it absorbs (filters) the frequencies of light affecting which color can penetrate deeper.

"What is a light wave?
Light is a disturbance of electric and magnetic fields that travels in the form of a wave. Imagine throwing a pebble into a still pond and watching the circular ripples moving outward. Like those ripples, each light wave has a series of high points known as crests, where the electric field is highest, and a series of low points known as troughs, where the electric field is lowest. The wavelength is the distance between two wave crests, which is the same as the distance between two troughs. The number of wave crests that pass through a given point in one second is called the frequency, measured in units of cycles per second called Hertz. The speed of the light wave equals the frequency times the wavelength.".

See this other Physics.SE question: "Does light color change when refracting?":

"The color will not change. What you're not taking into account is the speed of light in the medium. It's not the same $c$ en vacuo. The frequency stays the same. What changes is that speed of light in the refracting medium and as a result wavelength.".

Here is what sunlight (natural light) looks like underwater:

Despite that fact in shallow water enough full spectrum light penetrates sufficiently, and the zooxanthellae adapts to the spectrum available, no longer requiring blue light for growth.
See: "The spectral quality of light is a key driver of photosynthesis and photoadaptation in Stylophora pistillata colonies from different depths in the Red Sea" by T. Mass, D. I. Kline, M. Roopin, C. J. Veal, S. Cohen, D. Iluz, O. Levy in the Journal of Experimental Biology 2010 213: 4084-4091; doi: 10.1242/jeb.039891

"Depth zonation on coral reefs is largely driven by the amount of downwelling, photosynthetically active radiation (PAR) that is absorbed by the symbiotic algae (zooxanthellae) of corals. The minimum light requirements of zooxanthellae are related to both the total intensity of downwelling PAR and the spectral quality of the light. Here we used Stylophora pistillata colonies collected from shallow (3 m) and deep (40 m) water; colonies were placed in a respirometer under both ambient PAR irradiance and a filter that only transmits blue light. We found that the colonies exhibited a clear difference in their photosynthetic rates when illuminated under PAR and filtered blue light, with higher photosynthetic performance when deep colonies were exposed to blue light compared with full-spectrum PAR for the same light intensity and duration. By contrast, colonies from shallow water showed the opposite trend, with higher photosynthetic performances under full-spectrum PAR than under filtered blue light. These findings are supported by the absorption spectra of corals, with deeper colonies absorbing higher energy wavelengths than the shallow colonies, with different spectral signatures.".

"Fig. 4. Percent surface irradiance received of different wavelengths at 3 m (grey) and 40 m (black) depth in the waters adjacent to the Interuniversity Institute for Marine Sciences, Eilat, Israel, on 3 April 2008.".

So if you deep dive for your own coral you should be aware that it will thrive under blue light. If you obtain shallow water coral, or buy from the local aquarium supply store, white light is suitable.
Also from: "The spectral quality of light is a key driver of photosynthesis and photoadaptation in Stylophora pistillata colonies from different depths in the Red Sea", (full info above):

"Studies in the Caribbean have found that other corals that are found along a broad depth gradient switch from hosting clade A or B zooxanthellae in shallow water to clade C in deeper water, possibly owing to the ability of the different clades to adapt to different light levels (Rowan and Knowlton, 1995; Baker et al., 1997).".


What determined the evolution of different faces in humans? The most distinctive characteristic of a human is it's face - it is unique among each individual (with the exception of identical twins). It is uncertain to me if whether we best identify other humans by their face due to special brain parts developed for this (there are people with disease that cannot recognize faces) or for actual very distinctive physical face forms; maybe it is a combination of this.

Anyway, the question is about evolution. Why would distinct faces (or ability to recognize distinct faces) be something useful that would be retained by evolution? How is this better at survival?

Given the prevalance of myopia in humans I would have thought that facial recognition was secondary to other indicators such as gait recognition which is also unique to individuals though can be copied to an extent. Voice and shape are also used to identify people.

Being able to recognise individuals would allow the formation of groups, allow for structures of trust, reciprocal altruism to develop as well as punishing transgressors. Repeat interactions with other people require some kind of identification, but I dunno if facial recognition is the only/primary one.


How far does your center of mass move from stance to stance? When the human body is perfectly centered, the center of mass is on the centerline around the belly button.  However, the human body is not always in this rigid posture.  We have many postures that we use.  How much does the center of mass shift, left to right, if we look at different stances.  I'm not so much interested in dynamic motions like walking, but rather static positions like:

At attention (obviously the center of mass will be very centered)
Weight shifted to one leg
A S-Curve, like from the traditional Greek statues

Obviously the center of mass will shift with respect to the ground, staying between the feet, but what I'm interested in is how it shifts with respect to the torso's centerline.

You can find the relevant math here:

http://hypertextbook.com/facts/2006/centerofmass.shtml

The key factors are the body mass distribution, height, standing center of mass, heartbeat, clothing, etc. You can approximate the center of mass for a given stance as:

  In order to determine the center of mass of a person, we used the formula for torque:

$\Sigma\tau = r \times F$

  The torques due to the weight on each end of the person were set equal to each other. The displayed weight on the scale was the force, and there are two different radii. The first radius is the distance to the center of mass from the person's feet, and the second radius is the length of the board minus the distance to the center of mass from the person's feet. The net torque of the system is zero and therefore the torques on the opposite sides of the boards must be equal:

$w_1\times x = w_2\times (l~-~x)$

  where w1 is equal to the weight at the person's feet, x is equal to the distance from the person's feet to his/her center of mass, w2is equal to the weight at the head, and l is equal to the length of the beams. The resulting formula, when solved for the distance to the center of mass from the person's feet (radius one) is:

$x = \underline {~~~w_2\times l~~~}$

$\hspace {11mm}w_1~+~w_2$

  After determining the location of each person's center of mass, the ratio of the center of mass to the height of each person was calculated using the formula:

$x/h$

  where x is the location of the person's center of mass and h is the person's height.


Beginner question about growing E. coli I have bought a hobbyist kit which involves growing E. coli. The steps said to grow the E. coli on an LB agar Petri dish overnight. No incubation devices were included in the kit.

I let the E. coli grow overnight at room temperature (65-75°F), but there's pretty minimal growth, if any. I found this question which seems to imply that it's hard to grow E. coli without having temperatures near 37°C, which is much warmer than I can reasonably make my house.

Is it possible for me to do this experiment without purchasing an incubator of some sort? If so, does the lack of growth indicate that I've made a mistake somewhere?

The higher the temperature the faster E. coli will grow, with a maximum growth rate around 37 Celsius.

If you grow E coli at lower temperature, the ecoli will grow slower.

At 37°C you will see colonies overnight (16hr).

At 30°C you will see colonies in about 1 and a half days.

At 25°C you will see colonies in about 3-4 days.

You can do experiments at room temperature, but you will be waiting for days for what you will normally see after a 37°C overnight incubation.

As for satellite colonies.. yes ampicilin does break down with time and water. You can solve that problem by increasing the amount of Amp you are using from 25ug/ml to 100ug/ml. Or use 75ug/ml Carbenicilin. Or change your selection markers and use a more stable antibiotic like Chloroamphenicol.


Can methylation from DNA get copied to RNA during transcription? Methylation on gene-body and 3'UTRs if copied to mRNA can potentially regulate post-transcription modifications or expression regulation. But I'm not sure if they are maintained after transcription or if they get all de-novo methylation.

I don't believe anything should change in the majority of DNA->RNA transcription. DNA methylation typically occurs on the non-watson crick side of Cytosine so it shouldn't affect the base-pairing.

However, there are a few hypothetical situations that would result in alterations of the transcribed RNA. The sponatneous deamination of the 4' amine would convert the base into uracil. If there is an additional 5' methyl, the 5-methyluracil would be recognized as Thymine.

(edit) I've talked with several genomics folks about this topic and it turns out that M5Cytosine is very resistant to deamination due to the presence of the Methyl group. As a result, the instance that I have just described is actually very rare.

5mCytosine to Thymine deamination

The other situation would be to errors in DNA proofreading. Does the 5mCytosine affect the fidelity of RNA polymerase? I honestly don't know but it would be worth examining.


Book recommendation on selective breeding? I am looking for a good book that gives a nice overview of the science and technics of selective breeding. I am particularly interested in the use of population genetics to support decision in this applied field. So do you have any suggestions?

Below are some examples of question that I would hope that book answers.

If the artificial selection is too strong, it is very likely that some beneficial alleles will disappear. How strong do we decide artificial selection to be?
How do we deal with various lifetime?
How do we deal with species that can have only few babies so that we are obliged to limit the strength of selection to keep a stable population size?
How do we make sure to not reduce the immunologic genetic diversity within the population to zero but only to reduce the diversity of genes that influence the trait of interest?
Is it better to wait to be able to measure the quantity of milk in the sisters of a bull in order to infer about the quality of the bull or is it wiser to directly allow the bull to reproduce to speed things up?
How are the estimations of heritability performed?
How do we measure the impact of various environment of the trait of interest?
Which cultural traits should we allow to spread and which should we stop?
How can we use a correlated trait to infer more simply or more rapidly of the amplitude of the trait of interest?
How much outbreeding should we allow?
When is mutation breeding preferable?

and more globally some questions of the kind:

What are the different solution to artificially inseminate?
Can we select on the spermatozoids?
What financial elements should be taken into before creating a breeding plan?
GWA's studies in selective breeding
What is the relative importance of selective breeding and GMO in current economy and in our current ability to improve strains for our purposes?

I will Suggest:

Selective Breeding in Aquaculture: An Introduction

Authors: Trygve Gjedrem, Matthew Baranski

ISBN: 978-90-481-2772-6 (Print) 978-90-481-2773-3 (Online)

http://image.slidesharecdn.com/selectivebreedinginaquaculture-anintroductionreviews-methodsandtechnologiesinfishbiologyandfisheries-140725230642-phpapp01/95/selective-breeding-in-aquaculture-an-introduction-reviews-methods-and-technologies-in-fish-biology-and-fisheries-10-1-638.jpg?cb=1406347865


What happens during kefir fermentation process? I’ve found many sources about the positive effects of kefir for the digestive system. However I haven’t found any information about the fermenting process.

What is the exact biology (chemistry?) behind the process of milk becoming kefir?

What do the kefir grains exactly consume from the milk? And what do they defecate?  What happens inside the microbes?

Well essentially the added Lactobacillus species ferment lactose and other sugars to lactic acid, thus lowering the pH of the product (they take up lactose use it as an energy source under anaerobic conditions and secrete lactic acid). This gives the kefir and other fermented milk products their sourness. Also the lower pH prevents many other bacteria from growing in the product so this is also serves as a natural preservation method. Further more the low pH can denature some of the protein in the milk/kefir resulting in a more solid form. Many of these Lactobacillus species or their relatives are natural part of our gut flora.


Bird identification from Nepal I just stumbeld across a picture and wonder which species it is?

I took the below picture of a bird, probably a raptor, in mid-January 2011, 7 pm, on the Annapurna Trek in Nepal. My altitude was around 2000 m.

Since I took the picture a long time ago I cannot recall any information about the size.

Your image does not depict a predator, instead it's a scavenger. It's definitely a vulture, and by the looks of it a Griffon Vulture, which are a common siting in India.

The picture you provide is a bit grainy, and the apparently low-set sun colors the image somewhat yellow, but it does appear similar to below image of a Griffon vulture.

Griffon vulture. source: Vulture conservation in India and Nepal


Gloves for Cell Culture? I always wear gloves when I'm doing cell culture. Moreover, I always spray my gloves with ethanol to disinfect, so that I don't contaminate everything.

However, I recently heard the argument that EtOH could impair the integrity of the glove, making it an unsuitible barrier between your hand and the culture. According to this argument, the best idea is to not wear gloves during cell culture, but instead thoroughly spray your hands with EtOH to ensure decontamination.

I don't believe it, but I'm wondering if anyone else has heard a similar argument and if there is any truth to the claim.

In my opinion wearing gloves during cell culture is a good idea. It works both ways as a protection: For your cells since you are not loosing small danders from your hand and for you since you are not getting media or chemicals used in cell culture on your skin when you are uncautious.

I usually prefer nitrile gloves over latex, since nitrile gloves are ways more stable and pose no risk for allergies (I am not allergic, but minimizing risks is always a good idea). The downside of nitrile is, that they are a bit more expensive (thats the point where you need to argue with some coordinators about what to buy).

I never had problems with desinfectants and gloves, but this is my personal experience and probably not more than an anecdote. I desinfect my gloves, since I touch different things with them, but I usually don't spray everything which comes around with alcohol since this is usually pointless. To be useful, it needs to reach all points of a surface and also needs to stay there for a while. What I make sure is that all the stuff, which goes into the hood is either very clean or packaged sterile anyway.

After my experiences some data, this PDF has quite a lot of information. The list below is taken from the PDF:

Nitrile gloves:

Acetone - fair
Ethanol - excellent
Isobutyl - alcohol excellent
Isopropyl - alcohol excellent
Methanol - fair

Latex gloves:

Acetone - good
Ethanol - excellent
Isobutyl - alcohol poor
Isopropyl - alcohol excellent
Methanol - fair


Is there a way for a 19th century scientist to prove that the octopus doesn't revive? Say a sophiscated scientist in the 19th century noted that applying soy sauce on a dead octopus leads to movement of the legs, as a result of the voltage differences resulting from the salt in the soy sauce. (For example, see this video)

Is there a way for that scientist to prove, using only the methodologies available at that time, that the decapitated octopus doesn't regain the functions that a octopus brain normally has, for even a few seconds, when the soy sauce is applied?

Yes. The scientist could cut a small piece of the octopus's tentacle and perform the experiment again. If the same result is observed, no other organs are involved.


Whole Genome Sequencing vs Whole Exome Sequencing I am working on a project where I want to discover causative genes for a certain disease I may have. I was wondering whether to get WGS or WES to perform this experiment:-

I am looking at SNP's and CNV's of my genes and I want to compare my data with that of normal and diseased individuals. For a gene I calculate the document distance for each group (normal and diseased) using this algorithm (https://math.stackexchange.com/questions/1080377/how-close-apart-are-two-message-document-distance-algorithm) as this will allow me to determine which genes I have that are abnormal or are "close" to being classified as abnormal and which genes are normal or "close" to being called normal per the algorithm and the data obtained from the two groups.

To perform this experiment I need to sequence my genome AND identify databases that would allow me to conduct my analysis. I wanted to know which is better for my experiment WGS or WES as publicly available data might also influence the decision.

Also, I believe alternative splicing adds a layer of complexity and wanted to know why WES is performed anyways.

Thanks in advance for your replies. Please do answer whatever you can. Thanks once again!

WES, almost certainly. First of all, the vast majority of phenotype-causing variants are found in exons. For most analyses that are looking into disease causing mutations, WGS is pointless. It only makes your analysis harder and doesn't actually add anything useful.
If you know you're interested in CNVs, that's different. CNV detection is hard in general but is particularly hard from WES data. Detecting CNVs in WGS data is much less error prone. However, you really should bear in mind that there are currently no 'good' methods to detect CNVs. This is a non-trivial problem and still in its infancy. While there are various methods that can detect CNVs, none of them find all (or even close to all). In fact, this is such a problem in the field that the currently accepted wisdom is that you should use multiple methods and combine the results. In fact, many recent CNV detectors do exactly that. And they still don't find all of them (especially not in WES data). Basically, CNV detection is not for the fainthearted and is certainly not for the non-expert.
The good news is that if you do have a disease causing mutation, it is very unlikely to be a CNV. It is far likelier that you're just looking for SNPs. Which brings us to the next issue. I'm afraid the algorithm you linked to, from what I can tell, won't help you at all. You're not trying to compare your gene to a list of healthy and unhealthy ones and figure out which group is most similar to what you have. First of all, because there are many differences (mutations) that don't actually have any effect whatsoever. These so-called synonymous mutations would still be counted by your algorithm but should be ignored. Second, because tiny differences can be enormously important. There are specific tools for what you want to do; don't try and apply broad, general mathematical approaches. You need algorithms that are specifically designed to deal with biological data and which take the underlying biology into consideration.
So, what you're looking for are programs called "Variant Callers". Two of the most popular ones are GATK and FreeBayes. These will read an input genome and compare it to a reference genome and give you a list of "variants", sites where the input differs from the reference. You then want to use resources like ClinVar or MutationTaster to check whether those variants are considered pathogenic. This is a bit of shameless self-promotion since I work for the company which created it, but VarSome, "The Human Genomic Variant Search Engine" is a new variant search engine that combines information from many different sources in a centralized and easy to search repository. I recommend it highly (and it is free).
However, before you get to finding your variants, you will need to align your genome to the reference. Basically, modern sequencing methods work by cutting the genome into many, many small pieces, copying each piece multiple times and then sequencing each piece. So the output of a sequencing run is a text file that looks like this:
@SN956:1934:H55WMBBXX:2:1101:0:15733 1:N:0:NTTACTCG
NCCCCAAGGAGACTTGCTGAGACCTTGAACAAGTGACACAATGTGAGCAGAACTTGTCTTGACAGAAAATGCTTTG
+
#AAAFJJJJJJJJJFFJJJJJJJJJJJJJJJJJJJJJJJJJJFJJJJJJJJJJJJJJJJJAJJJJFAJJJJJFJJ7
@SN956:1934:H55WMBBXX:2:1101:0:15743 1:N:0:NTTACTCG
NCTTCCTCACTAAAGTCCCATTTAGTGCTGATTGTGCTTTGGCTACTTCTCCTCTTGCCATTTTCCTGAACCCACG
+
#AAFFJJJJJJJJJJJJJJJJJJJJJJJJJFJJJJJJJJJJJJJJJJJJJJJJJJJFJJJJJJJJJJJJJJJJJJF

This is usually several gigabytes (something like ~2-3G for WES and >80G for WGS). Therefore, the alignment of these sequences needs a powerful machine and you don't even want to try to align WGS sequences on your laptop. It will take weeks and will probably fail. Another reason why you should prefer WES over WGS for this. In my work, I routinely align WGS data to the reference genome and that can easily take >100GB of RAM.
The bottom line and what this rambling answer is trying to get across is that:

WES is better than WGS when searching for disease causing mutations. It is far easier to analyze the data and 99% of the cases you want are in exons. It is also much, much cheaper.
This isn't simple. You seem to think you can sort of waltz in and do it yourself. You can, but it is very far from trivial. It is also not cheap.

So, if you do actually have the money to pay for a WGS analysis (this costs several thousand euros/dollars, in case you didn't know), which is very surprising if you're just a private individual, instead of spending it on WGS, get a WES and spend your money on getting an expert to analyze your data for you. Seriously, this is what I do for a living, you really don't seem to have grasped quite how complicated it is. And no, I am not suggesting you hire me :). There are, however, companies that offer this sort of service. Use them, don't reinvent the wheel.
References
Useful review articles for CNV detection:

Zhao et al. BMC Bioinformatics, 2013, 14(Suppl 11):S1 (DOI: 10.1186/1471-2105-14-S11-S1, link)
Tattini L, D’Aurizio R and Magi A
Front. Bioeng. Biotechnol, 2015. 3:92. (DOI: 10.3389/fbioe.2015.00092, link)


Why mutations in genes involved in general processes like DNA repair increase the risk of developing specific types of cancer? For example, mutation in MHS2, which encodes a protein involved in the repair of mismatches that occur during DNA replication, dramatically increases the risk of developing colon cancer.
(There are many other examples, like the RB gene which encodes a tumor supressor protein and is correlated to retinoblastoma, thus its name)

My question is: how a gene like MHS2 which participates in a general mechanism of DNA repair increases the risk of a specific type of cancer? Why doesn't it increase the risk of developing cancer in other tissues as well?

I can't fault @WYSIWYG for mentioning the cited Vogelstein article in providing an answer. You point to what seems like a great explanation for why certain cancers arise in some tissues but not others. However, for those who look closely this paper has some serious errors in its derivation of the model, and for good reason it has come under strong fire in the last couple of months.

See this for a really important rebuttal:
http://ameyer.me/science/2015/01/02/vogel.html

Unfortunately, the paper provides an elegantly specious explanation for, in part, the longstanding paradox of why cancers more readily arise in some tissues like the intestines and from seemingly identical mechanisms, but do not seem to arise in other tissues. My favorite example, though @El Cid you do list some good ones, are inactivating BRCA1 mutations which normally play a role in repairing double stranded DNA breaks. And yet even when mutated in the germline this only seems to increase cancer risk in the breast, and really only in one gender (females).

So the answer is still quite certainly that the field does not understand this paradox, and the cited Vogelstein paper was a total tragedy of a publication. There have been a number of officially submitted critiques of the paper and the Vogelstein lab has been trying to defend it as best they can. This is however a great example of how big name labs can seem to get anything published in Cell/Nature/Science.

Another thing to consider and @El Cid points to a good example, is the pRb mutations (in a very central tumor suppressor pathway for all cells) cause retinoblastoma and not for instance intestinal or blood cancers very readily, and the retina is not a rapidly dividing tissue. So the Vogelstein paper cannot explain this.


Why does influenza sometimes cause GI symptoms? I'm speaking strictly of influenza, not gastroenteritis which is sometimes mistakenly called "stomach flu." I just read this article on the mechanism through which rotavirus causes diarrhea and vomiting. Since the flu is a respiratory disease, through what mechanism does it sometimes cause diarrhea and vomiting? Does it also release proteins that activate the enteric nervous system in the gut? Is it caused by inflammation from cytokines being washed down the throat in mucus? Or is it the result of a secondary infection resulting from the decreased immune system?

Article: How influenza virus infection might lead to gastrointestinal symptoms Source study: Respiratory influenza virus infection induces intestinal immune injury via microbiota-mediated Th17 cell-dependent inflammation.

The idea is that Influenza virus infection originates in the respiratory tract. In response, the body produces these CCR9+CD4+ Th cells denoted Th17 in the lungs. Gut epithelial cells produce CCL25, a chemokine made to attract cells expressing CCR9 chemokine receptor. Th17 cells are a subset of T-helper cells that produce interleukin-17, more about that here. So what they found, is that the Th17 cells produced by influenza infection in the lungs migrate to the gut through this CCR9/CCL25 interaction, and they secrete cytokines that are meant to defend against infection. Of course, mucosal immunity at the gut epithelium is always active, because there are commensal bacteria there that out-compete pathogens among other roles.

Down in a section titled "Lung-derived CD4+ T cells destroy microbiota homeostasis and promote resident Th17 cell polarization" their conclusion is that IFN-gamma secreted by the lung-derived Th17 cells destroys the homeostasis of the gut microbiota, and cause other Th17 cells to become polarized in a way that they end up producing the specific set of cytokines causing the trouble in the first place. You also have to understand that the other cytokines the Th17 cells are secreting are causing tissue damage, leading to symptoms of intestinal disease concomitantly with what we've been discussing above.

I think that the process is just recently being illuminated so it may not be completely understood, either.

  How are the lung-derived Th17 cells getting to the gut?

Generally, leukocytes in the lymphatics enter the blood through the left subclavian vein. Once there, they traffic to vascular endothelium expressing chemokine attractant molecules and utilize a number of adhesion molecules in concert to extravasate into the tissue expressing the attractant. This could mean multiple tissues given the right circumstances. The important thing to remember when i mentioned mucosal immunity is lots of effector cells are already there due to the presence of microbiota at all times, unlike the systemic response where effectors must be generated.

Here's a figure about extravasation, and another about mucosal immunity, and if you look here you can see that the Th17 lineage is under investigation due to it's inflammatory characteristics in autoimmune disease.


120-year-old gene regulation problem independently solved by a computer. How? My Background:

I'm a mathematics graduate student with a physics background.  I have a very little biology knowledge and a little knowledge of machine learning and statistics.

Topic:

I recently found out about the following computational biology breakthrough: A computer managed to independently develop an explanatory theory for a 120 year old problem in biology. It is detailed in the popular media here and here and in great detail in this paper.

Questions:

I lack domain expertise but I'm very curious as to how this was possible and why it happened now. For example:

Were these methods novel (from a machine learning perspective), or does the novelty lie in using old tools/techniques and adapting them to a
workable problem?
Mathematically speaking, what kind of models were produced by the computer? Are these standard in this field of genetics/biology? Is this area particularly mathematically tractable?
What about this particular biological problem made it amenable to this machine learning approach?
What other kinds of low hanging fruit (in biology or science in general) could we expect to see tackled with these techniques?

The paper by Lobo and Levin is an attempt to learn a model that represents the inner workings of a biological system by fitting parameters to data. This is a common topic in "systems biology", a model-based approach to studying biology that is popular in some fields.

Even for small systems, this is a phenomenally hard problem. Unlike most machine learning problems, achieving good accuracy (on independent test sets) is not enough; the model structure itself must be correct, meaning that it should reflect the actual mechanisms operating in the cell or organism. It's like trying to identify the actual structure of an integrated circuit by only observing inputs and outputs --- not only identifying the logical rule that the system exhibits, but the actual wiring diagram that implements that rule. It is of course quite possible that alternative models exist that perfectly captures the behavior, and yet is completely different "on the inside". In other words, the system may not be identifiable from the data --- two different models may produce exactly the same behavior. So there's no way to know beforehand if these problems are even theoretically solvable (let alone practically feasible).

Lobo and Lewin claim to have accomplished this task for a small system of gene products. As far as I can tell, the central piece of evidence is that the model they come up with does capture some mechanisms previously known to exist. Whether this is just plain luck, overfitting, or a special case where (parts of) the system is actually identifiable from data is hard to tell. But it's notable that Lobo and Levin fall back on demonstrating predictive accuracy in the end, which is not enough to support their thesis. The critical test is to take a new prediction from their model and actually test it experimentally, to prove their (strong!) claim that their method can actually infer new mechanisms. Doing so is expensive and time-consuming, and much more difficult to get right than tweaking models to fit mechanisms you already knew beforehand --- which is exactly why I want to see that evidence. If the authors really believe that their method is a breaktrough, those experiments should have been done.

Finally, these type of algorithms are applied to models containing only a handful of components, and typically to systems that have been studied for decades and are very well-characterized to begin with. In most of biology, the problems are orders of magnitude more complex, and often we don't even know what the components are. So I thik there are a limited number of cases where this approach is feasible.


Are there completely self-sufficient autotrophs? Are there completely self-sufficient autotrophs which can survive and reproduce indefinitely by consuming exclusively non-organic matter (plus energy from sunlight or thermal vents etc.)? I'm asking specifically.

It really depends on what you mean by "organic matter".  No cell is going to be able to grow and reproduce without an appropriate source of CHON atoms (plus lesser amounts of the other necessary elements).

So, if by organic matter you mean CHON+, then no, everything needs organic matter to grow and reproduce.

If by organic matter, however, you mean natural organic materials like soil or groundwater, then yes, there are lots of things that can live on chemical mixtures that can be produced by purely synthetic means.  A simple example is M9 media, which is a commonly used bacterial culture medium.


Evidence of species transitions I had a debate with a person who believes in some kind of creativism, let's call it that way.

And in the middle of the "debate", an interesting question popped up.

What are evidences of "transition between species". Is there a fossil record that shows us the "transition".  I googled it and it was pretty obscure subject.

I would like to answer that question and really it "hits" my beliefs.

People who think in creationism or think about species rigidly might have a bit problem with that, so let me describe an example:

When are humans "adult"?
Legally, at 18 (or your national equivalent). However, everyone understand that people are becoming adult gradually. Sometimes, they "age" very quickly after some harsh experience (16 years old student who parties all days because parents pay for it vs 16 years someone whom father died and he has work to help feed his small sisters as family did depend on father's wage).

Now imagine that you don't have all this information, but very incomplete "images" or "screenshots" of this kind of development. There would be quite a mess from it. You have image of one kid at 13 who is still young, another kid at 19 who is partying, single image of this 16 year old adult who has to feed his family and image of 48 year old gentleman.

If you go with this mindset that most of species that ever lived you can't get and you are just guessing something from a few snapshots that are themselves incomplete as well (e.g. we often don't have whole skeleton but just single bone from a lot of species), your idea on what to expect will change. This is a first step. Then you need to realize that most of fossils that shows some transition do not form lineage, but instead branches that are related. Finally, when you understand this (and modify your expectations and "what to look at", you can take any relatively complete and well-studied set of fossils like human ones. On human lineage (with great apes), we can see gradual increase of brain and in the case of human, gradual decrease in size of jaw. Development of hip bone is nice as well as it shows gradual process of adaptation to upright walking.

Another line of examples, but again, you need to redefine your expectations, is to point on dogs. If we had dogs in our fossil records, there would be large amount of species, instead of one "dog" species.

Or you can just point out at plants and say that "species" does not really mean anything.


Double stranded RNA Single stranded DNA I have seen in textbooks referring to ds RNA and ssDNA.
How a RNA can be double stranded and likewise how a DNA can single stranded  and if they do exist why are there names not interchanged?

The main differences between RNA (ribonucleic acid) and DNA (deoxyribonucleic acid) is that DNA contains a hydrogen atom where RNA has a hyroxyl (-OH) group and RNA's uracil is substituted for DNA's thymine.  The below image shows several deoxyribose molecules bound together, and off to the side, a ribose molecule. It is the OH group on the bottom right of the ribose molecule that is exchanged for a hydrogen in deoxyribose.

The structures of RNA and DNA are almost identical, so there is no reason why you can't have double stranded RNA. Similarly DNA can be single stranded. In fact, for DNA replication and transcription, the DNA strands must be separated. dsRNA and ssDNA are most commonly found in viruses. Check out these lecture slides for more about them: http://www.columbia.edu/itc/hs/medical/pathophys/id/2009/viruses2Color.pdf


What gives diarrhoea caused by Cholera its milky colour? The diarrhoea caused by the Cholera bacteria is a milky colour, also known as 'rice-water' like. Why is this? I have a fairly good understanding of how Cholera acts on the body.

The color of our feces is caused by the breakdown products of the hemoglobin, namely Bilirubin and Stercobilin, which depending on the concentration, cause a yellow to brown color. See here for details.

Since the amount of liquid lost by the cholera diarrhea with up to 250ml/kg bodyweight is really high, there is only very little to nothing of these breakdown products available in the feces. This causes an absence of color.


What does endochorous dispersers means? In an article (Guerrero and Tye, 2009) it talks about endochorous dispersers.

Guerrero, A. M., and A. Tye. 2009. Darwin's Finches as Seed Predators and Dispersers. The Wilson Journal of Ornithology 121:752–764.

  The highest proportions of feces containing viable seeds were of Small
  Ground Finch (G. fuliginosa) and the ‘‘insectivorous’’ species
  Woodpecker Finch (Camarhynchus pallidus) and Warbler Finch (Certhidea
  olivacea). These two may be more important endochorous dispersers than
  other species that eat more fruit but are better seed predators.
  Intact seeds were found in 23% of fecal samples; 50% of the samples
  with intact seeds had viable seeds.

I've looked on google and found nothing...

Do you know what that means?

It seems it relates to mast-fruiting plant species.

I found the definition here, which is a cool package in R:

  animal - all vertebrate dispersed seeds, without distinction between
  attached(epichorous) and ingested (endochorous) dispersal of seeds


XXY (Klinefelter's) & Trisomy 21 & X-inactivation I read that X-inactivation doesn't tend to happen in males, but then when someone is XXY, they are a male because of the Y. However these individuals tend to live. So does that mean that X-inactivation happens in males or else these individuals would die?

X-inactivation does occur in XXY individuals.

In phenotypically normal XX females, one X chromosome is inactivated.  Which one of the two X chromosomes is inactivated in any given cell is random. Therefore, about one half of the cells should have the maternal X active and the other half should have the paternal X active.

XXY individuals show a wide range of clinical symptoms and intellectual ability.  Iitsuka et al. (2000) suggested that this variation may be explained by a bias in X-inactivation.   They found that about 31% (5 of 16) individuals (either XXY or XXYY) shows a very strong bias of X inactivation, which they defined as at least 80% of the cells inactivating one particular X chromosome. Two individuals has biased inactivation of the paternal X and the other three had biased inactivation of one of the maternal X chromosomes. The sample size is rather small (not surprising) but X inactivation is occuring.  Samango-Sprouse (2001) argues that incomplete inactivation of one X chromosome may also explain some of the more severe clinical mental disorders.

For Trisomy 21 (Down's Syndrome), the individual as three copies of chromosome 21, so X inactivation is not an issue. However, scientists are studying whether Xist can shut down the third copy of chromosome 21.  The Xist gene is transcribed to produce a large molecule of RNA. That RNA is what usually causes X inactivation.  Jiang et al. (2013) were able to show that Xist can coat one of the chromosome 21 copies, performing essentially the same inactivation function that it does for the X chromosome. So far, though, this work has been entirely in the lab (in vitro).