What are some difficulties animals had to overcome to reproduce on land? This is for AP Biology, but the assigned textbook chapter doesn't contain any information about the question.

  What are some difficulties animals had to overcome to reproduce on land?

Some disadvantages I brainstormed are

the formation of bones—need for vertical structure and support against gravity (?)
development of lungs

Are there any more?

Thanks,

The disadvantages you mention have not much to do with reproduction, but with locomotion and oxygen absorption.

Difficulties to reproduce on land are the fact that aquatic egg-producing creatures typically lay soft eggs with porous shells to promote exchange of water and waste products with the surrounding water. Water is essential for growth as a typical creature consists for some 70% of water. Soft-shelled porous eggs when laid on on land dry out very quickly and are prone to predation.

The main adaptation to reproduce on land instead of water has been the development of the amnion. The amnion is basically a membrane filled with water (the amniotic sac) in which the embryo is immersed during development. Hence, you could argue that the transition to land in terms of embryonic development has never taken place, as the embryos develop in a protected aqueous environment contained within the amnion! The early amniotes laid eggs on land where the embryos develop, while the later ones such as humans carry their embryos/fetuses around. But early as well as late amniotes are characterized by a developing embryo immersed in a watery environment contained in the amnion. Other structures that aided the transition to land were eggs with hard shells, and the allantois. A hard outer shell in amniotes that lay their eggs on land  helps to protect them against drying out, the harsh terrestrial environment and predators. The allantois helps to exchange and store waste products produced by the embryo, a structure not needed when eggs are immersed in water and waste products can diffuse freely through a weak and porous shell.


Do egg laying animals experience a pregnancy? Does a female animal that lays eggs experience a pregnancy-like period of time, where she will feel and behave differently as if she were fertilized and her body is prepared to lay a fertile egg, not a sterile egg (like the chicken eggs we eat)?

For example,

does the egg takes more time to be formed?
is it different in size?
maybe the animal will feel hormonal changes that cause it to increase body heat to help her sit on the egg, etc.?

In oviparous animals the egg retention phase in the uterus is brief. After fertilization eggshell mineralization is triggered but it seems the initial triggers of the pathway is not understood. The uterine fluid is rich in calcium and bicarbonates and calcium carbonate, in the form of calcite, precipitates around the egg. Shell mineralization is quite a rapid process and there are some specific proteins involved in this pathway. Have a look at these:

http://www.ncbi.nlm.nih.gov/pubmed/22201802

http://hera.ugr.es/doi/15773115

In ovo-viviparous animals the egg is retained in the uterus for a longer time and embryo is quite developed when the egg is laid (happens in boas). You can call it a sort of "pregnancy".

However progesterone pathway exists in birds and is involved in oocyte maturation

Oxytocin pathways also exist in birds, acting through oxytocin homolog Mesotocin, and perhaps they cause development of maternal care as they do in mammals.

This article talks about effects of oxytocin on birds but not exactly about its role in maternal care.

However i believe that the shell size and mineralization time shouldn't differ much between unfertilized and fertilized eggs in oviparous animals.


Blomberg's K and branch length Do different values of the smoothing parameter lambda for estimating the divergence times (in situ Sanderson 2002) will affect trait conservatism (e.g., Blomberg's K)?

I don't know if lambda for estimating divergence times works in the same way as it does for scaling internal tree nodes, but I'm going to assume it does given the context of your question.

My gut reaction was: of course it must because K is the ratio of observed to expected variance and tip variance is moderated in part by branch lengths. So if you change the node positions, the expected tip variance should also change.

A quick simulation shows that this appears to be true.

library("ape")
library("picante")
library("geiger")

set.seed(5)

tree <- rtree(30)
y <- rTraitCont(tree)

lambdas <- seq(1.0, 0.05, by = -0.05)
M <- data.frame(lambda = lambdas, k = numeric(length(lambdas)))

for (lambda in lambdas){
  tree_trans <- rescale(x = tree,
                        model = "lambda", lambda = lambda)
  M$k[M$lambda == lambda] <- phylosignal(y, tree_trans)$K
}

plot(k ~ lambda, data = M)

Generate a tree with 30 tips and generate random data along the branches. Then rescale the tree for a series of lambda values and calculate k for each lambda scaling.


How are the very first telomeres added? Here is an image of telomerase adding telomerase.

As we can see, the telomerase sort of binds to a bit of the existing "3' flanking end of [the] telomere" - it's almost half and half.

My question is, where did that existing telomere come from? And the telomere before that?

Essentially, the telomeres must have begun from some point on the chromosome/DNA, but how were those telomeres added if the telomerase has a preset RNA sequence that it uses to bind to specific nucleotide bases? Does our human DNA coincidentally end with TTAGGG as well or something?

Telomeres are maintained by telomerase (in certain cell types, not all of them) at every replication. So, the answer to your questions "where did that existing telomere come from? And the telomere before that?" is: "because there was already a telomere to extend at the end of this chromosome".

Your questions boil down to "how did telomeres appear in the first place?" (because once telomeres and a maintenance mechanism have been established, they will simply remain unless some major genomic catastrophe happens), and this is a difficult question. As Whitney pointed out in the comments of your question, some hypotheses about the origin of telomeres are discussed in this article.
Interestingly, Drosophila doesn't have telomerase, and maintains telomeres by a transposition mechanism. Somehow this is a clue about how telomeres appeared: Drosophila telomeres could be an intermediate between circular chromosomes and telomerase-based maintenance of linear chromosomes.

This is a complicated topic, but the scientific literature about the appearance of telomeres is fascinating. Some bacteria (Borrelia and Streptomyces taxa) have linear chromosomes, but maintenance mechanisms that have nothing to do with transposition nor telomerase.

Here are some references:

Drosophila: https://doi.org/10.3389/fonc.2013.00112
Borrelia: https://doi.org/10.1146/annurev.micro.112408.134037
Streptomyces: http://link.springer.com/chapter/10.1007/7171_2007_090

If you can read French, you will find more info in the introduction of my PhD thesis.


What is this agglomeration of pink cells I found attached to a stone? Photo taken in a garden in Singapore. The organism is attached to a stone, close to water. Many of these were there.

Size approx 3cm.

The shell of this eggs is very soft. When touched, a pink colored liquid drops out.

They are Apple snail's eggs; check the picture:

Check this.


Heat shock vs electroporation I've been transforming E. coli via heat shock in order to insert oligonucleotides (around 50 nt); however, none of my experiments have given positive results so far. I begin to question the efficiency of chemical transformation, especially for short DNA fragments. Is there such a notable difference between chemical and electro transformation?

EDIT: I'm checking for CRISPR array expansion, so my oligos have a protospacer length and structure. I'm using BL21(DE3) cells which have an IPTG-inducible T7 that I'm first transforming with a Cas1-Cas2 plasmid. Then, I induce the cells in order to express those proteins, make them competent, and transform then once again but with the oligos and an eGFP plasmid (for some sort of selection). To check for positive results, I'm amplifying the leader-repeat junction of the CRISPR array and compare its length (via electrophoresis) with a usual array that has no integrands.

How do you detect a potenially positive transfection? Short fragments might have proper teriary structures which may make them behave differently than you would expect. Also, noncircular DNA and RNA is targeted much faster for degradation in most cells if the right head or tail signals are missing.

To your question: pulsed electroporation with well prepared bacteria (state, buffer,...) is usually 5-100 x more efficient than chemically competent bacteria.


Which secondary structures of RNA are symmetric? I'm trying to understand what is the meaning of this statement.

  A088518       Symmetric secondary structures of RNA molecules with n
  nucleotides.      4

  %I

  %S 1,1,1,2,2,4,5,9,12,21,29,50,71,121,175,296,434,730,1082,1812,2709,

  %T
  4521,6807,11328,17157,28485,43359,71844,109830,181674,278769,460443,

  %U
  708840,1169283,1805291,2974574,4604363,7578937,11758552,19337489,30064037

  %N Symmetric secondary structures of RNA molecules with n nucleotides.

  %C Diagonal sums of triangle in A088855. [From Philippe Deléham, Jan
  04 2009]

  %C Number of prime symmetric Dyck (n+2)-paths with no ascent of length
  1. E.g. the a(3) = 2 5-paths are

  UUUUUDDDDD and UUUDDUUDDD. - David Scambler, Aug 27 2012

Each one of those lines has a reference to a paper which will help you to understand the calculation that was performed

Read this from your original post
https://oeis.org/A088518

Overlapping sequences


How Behind is the Human Mind (Latency of the Senses) I would like to know if there is any research into the latency of human perception.  Particulary:

What is the minimum time for various inputs (vision, touch, sound) to be recognized by the conscious mind?
How different are these times?  (Loud sound vs sense of touch in your toe)
Given the above, is there a number we can put on how many milliseconds behind reality the human mind is?

There is a huge amount research into this subject. It is vast and nebulous as such I cannot give you an overall picture of this. I can however illustrate some of the complexities to this.

Firstly I would say that what you mean by human perception is extremely complex, there are different modalities of perception. For example in terms of a visual stimulus, we may simply perceive its basic shape, outline, colour, whether or not it is moving. We then may also perceive higher levels of information such as the function of the object. Similarly there are different aspects to other stimuli.

These different components of perception are transmitted by different neurons leading to the brain and then processed by different areas of the brain suited to specific tasks and then are integrated together to give us a conscious idea of what the object is.

Therefore when measuring the latency of human perception you would first have to decide what exactly you mean by this?

The other aspect is that a lot of study has occurred in this area as we are aware that perception can be altered by states of illness (for example audio evoked responses in schizophrenia, or visual evoke responses in multiple sclerosis). The perception of pain is yet another huge area of study.

Again this is such a vast area of research that I wouldn't really know where to point you to. However for a entertaining read on how perception can change in neurology I would recommend reading the books of Oliver Sacks, in particularly "The Man Mistook His Wife for a Hat" and an "Anthropologist on Mars".

I am sorry I haven't provided you with more detail but good luck in reading around this subject. If you are more specific about what perceptions, (e.g. perception of faces, perception of danger etc..) then maybe you will receive more specific answers.


Finding out the best concentration for my plant extract to be used as drug for diabetes I am using plant extract of Ajuga parviflora and found out that it possess anti-diabetic properties by using alpha-amylase inhibitory assay. I used various concentration 250 µg/ml(29% inhibiton of alpha-amylase), 500µg/ml(37%),750µg/ml(46%) and 1000µg/ml(63%). Basically, alpha-amylase results in increase in glucose level after eating food. So  i wanted to know that how could i find out that what is the best concentration of my plant extract to be used as drug.

You have to try to determine the best concentration.

Usually there are multiple clinical trials, first in animals, then in humans to

figure out the effective dose
look for side effects
compare the new drug's efficacy with existing drugs


Have proteins been observed to come into existence through mutations and natural selection? A protein that catalyzes one reaction can theoretically be modified by mutations and natural selection and eventually catalyze another reaction completely unrelated to the original. Has this been observed, documented, or at least postulated to be where a certain protein(s) came from?

How about EWS-FLI1 and other oncofusion proteins?

One could argue that cancer progression is as close to viewing "evolution in real time" (as you say) as possible.


Hardy-Weinberg Color-blind In a city, 4% of male population have color blindness. How many of the female are (a) color blind carrier, (b) color blind? Suppose the city holds Hardy Weinberg equilibrium.

My progress: 4% of male have color blind => $p=F(cb~allele)=0.04$ and therefore $q=F(not~cb)=0.96$. Since HW equilibrium stand, we get the allele frequency among female is the same as among male. Then (a) $2pq=2*0.04*0.96=0.0768=7.68\%$ and (b) $q^2=0.9216=92.16\%$.

Am I correct?

A: wild-type allele / a: color blind allele

Because color blindness is recessive and X-linked your assumption $p=F(a)=4\%$ is correct as men do only have one copy of the allele. Subsequently $F(A)=q=1-p=0.96$ is also correct. Therefore:

a) $F(Aa)=2pq=7.68\%$ is correct and b) is wrong, a is the color blind allele and $F(a)=0.04$ therefore it's $p^2=0.04^2=0.0016=0.16\%$.

92% color blind among females seems a bit high :).


Are there antibiotics for all bacteria somewhere in the earth? When I read about Penicillin, I found that it came from a green mold to protect itself.

If all bacteria and/or molds in competition to survive,
can we believe that there is an antibiotic for each bacterium somewhere in the earth?

In other words, just like bad bacteria change themselves to resist against the existing antibiotics, could good bacteria/molds produce antibiotics against the bad bacteria?

If so, can we use them like Penicillin, or should we still develop most of them?

The number of antibiotics that remain undiscovered is huge, but is estimated to be tens of thousands of compounds.

The number of bacteria that remain undiscovered is also huge, but is estimated to be perhaps millions of species.

Resistance to antibiotics is developed by bacteria in response to other bacteria and human antibiotic use, but in theory all antibiotics should work on previously unexposed bacteria. In practice there are resistance mechanisms that operate on whole classes of antibiotics at once(drug exporters, for instance). So there might be a bacterium that happens to be actively or passively resistant to every antibiotic on the planet, but it's a question of statistics. I think it's pretty unlikely but there are a lot of bacteria, so it's theoretically possible. (It wouldn't be a dangerous pathogen, that amount of drug-resistance genes would 'weigh down' the genome and make it slow to divide, and all those transporters would be great immune system targets. The human immune system would eat it for breakfast.)

What is true is for every bacteria, there are at least some antibiotics it's already resistant to. Furthermore, some antibiotics aren't useful because they aren't selective enough and they are simply poisons. (We use them for chemotherapy agents sometimes, but they're not useful antibiotics).

Some fun examples: Vancomycin-resistant S. aureus is completely immune to nearly every antibiotic, including the last line of defense(methicillin) and the toxic really really last line of defense (vancomycin). It's susceptible to trimethoprim-sulfamethoxazole, one of the oldest antibiotics out there(~80 years old). On the other hand, the organism that causes tularemia is naturally immune to trimethoprim-sulfamethoxazole and always has been. It, in turn, is susceptible to nearly all other antibiotics.


How does the inability to produce vitamin C helped weight gain? I recently wondered how do dogs cope without vitamin C intake like us.

A few Wikipedia pages later, I learned that our dry-nosed ancestors lost about two-thirds of the gene responsible for vitamin C synthesis some 63 millions years ago. And then this passage:

  Johnson et al. have hypothesized that the mutation of the GULOP (pseudogene that produces L-gulonolactone oxidase) so that it stopped producing GULO may have been of benefit to early primates by increasing uric acid levels and enhancing fructose effects on weight gain and fat accumulation. With a shortage of food supplies this gave mutants survival advantage.

(Wikipedia: L-gulonolactone oxidase)

I'm curious about the interaction (GULO/uric acid/fructose effects/fat storage) quoted above.

The effect comes indirectly since lower levels of ascorbate increases urate levels, according to

  Arthritis Rheum. 2005 Jun;52(6):1843-7.

  The effects of vitamin C supplementation on serum concentrations of
  uric acid: results of a randomized controlled trial.

  Huang HY1, Appel
  LJ, Choi MJ, Gelber AC, Charleston J, Norkus EP, Miller ER 3rd.

So the direct weight gain effect is due to increased levels of uric acid.

Further in the chain of events is that

  Recent studies show that fructose-induced uric acid generation causes
  mitochondrial oxidative stress that stimulates fat accumulation
  independent of excessive caloric intake.

according to

  Diabetes 2013 Oct; 62(10): 3307-3315.

  Sugar, Uric Acid, and the Etiology of Diabetes and Obesity

  Richard J. Johnson1,2⇑, Takahiko Nakagawa1,3, L. Gabriela Sanchez-Lozada4, Mohamed Shafiu5, Shikha Sundaram6, Myphuong Le1, Takuji Ishimoto1, Yuri Y. Sautin7 and Miguel A. Lanaspa1


The heart of a Pigmy Shrew beats 1300 per minute then why is it so fast? A pygmy shrew is such a small animal. Even with such fast heart beats their average life span is 1.5 years. So can we consider faster heartbeats to not be good for health?

There is a correlation between the heartbeat and the life expectancy as you can see below.

(source: medcan.com)

This relationship is not linear (the y-axis is on a logarithmic scale) and is negative, that is, the faster is the heart beat, the lower is the life expectancy. You'll note the outlier (human) that has a life expectancy that is twice as high as you wold expect from the regression. This shift toward the right is caused by medicine, food quality and hygiene.

Correltation vs causation

Note that correlation doesn't imply causation. Typically, you'll notice from reading the species names on the first graph that species that have a fast heartbeat (and therefore a low life expectancy) are small in size.Allometry  is the study of the relationship of body size to shape, anatomy, physiology and behaviour. You might want to have a look at the wiki page.

  can we consider faster heartbeat is not good for health?

No! it is wrong to think from from those data that the shrew (that has low life expectancy and fast heartbeat) that if they were to have a slower heartbeat, they would live longer. This is wrong. Shrews have the heartbeat they need to have. If one shrew (due to a mutation or some environmental developmental effect) had a slower heartbeat, it would die very early.

In other words, such inter/species correlation doesn't tell anything about intra-species correlation. To reuse the example of the relationship between mass and life expectancy: Body mass and life expectancy are positively correlated among species (see above) but the mass at which life expectancy is maximized in humans is average. The below graphs shows the relationship between body mass and Relative Risk (RR) of coronary heart disease.

(source: revespcardiol.org)

Health ≠ life expectancy ≠ adaptation

Life expectancy, health and high fitness (biological sense) are three concepts that are eventually related but that are very different. While life expectancy can compare health in inter-species comparison, it makes little sense to compare health of different species. Note also, that natural selection may well favour short lifespan (as suggested by @RioSiv, you might want to have a look at life-history r/K selection theory).


What motivates children to start walking? Crawling is a way we first learn to translocate but  , in all our lives, there comes a point where naturally try standing up and try to walk.. but why? What really pushes us over the edge to start walking?
When we first start walking, usually we fail many times but still we have this natural motivation learn walking despite the failure. Is this some sort 'intuitive' intelligence which babies have? To be more specific I can't imagine a baby to consider the pros and cons of walking vs crawling and then logically argue to himself/herself that learning how to walk would be something worthwhile to spend his mental resources on.

Reference video

You might be interested in Alison Gopnik's book "The Gardener and the Carpenter", where she gives thoughts on how children develop and learn. Children are very disinhibited in their behavior, and this is generally considered to be a consequence of their prefrontal cortex being immature, but she proposes that this is not a bug but a feature. That there is a tradeoff in any algorithm between "exploiting" the possibility space (incrementally improving your solution until it's as good as it can be) and "exploring" the possibility space (casting a wide net to find totally different solutions that might be even better). If you just "exploit" you are liable to stay stuck in local maxima; if you just "explore" you're never going to find a good solution because your search is too random and the possibility space is too large to examine every possibility. Good optimizing algorithms have alternations between the phases, with "explore" phases to look at many different areas of the possibility spaces, and "exploit" phases to optimize the most promising candidates. Gopnik's argument is that children are the "explore" phase of human development, and that is why they are disinhibited: they are motivated to try many different things for the sake of it, with no specific objective in mind or much thought to the consequences. (and in this view, an important job of parents is to make sure the consequences won't be fatal).
This might answer some of your question of babies thinking about "pros and cons". It might be more realistic to see them as thinking only in terms of "pros". Not, "if I do this this will be the consequences, if I do that those will be the consequences, what should I do given the consequences I want", but "what happens if I try this? And that? And that? And that? And that?"
Another factor that wasn't mentioned in the comments is imitation; children like to imitate others around them and odds are they see adults walking all the time.
In terms of walking though I'd expect instinct to play the major role. Not that walking would be hardwired per se, but there are probably movements and reflexes that babies are hardwired to try, and once they get to a physical maturity where walking is possible the odds are that they will try those movements, and find the results interesting at least, profitable at best.


Chromosomal structures in S phase and Prophase Of S Phase:

  Existing DNA molecule acts as a template to synthesize new DNA molecule. The cell doubles it's DNA, yet the number of chromosomes remain the same

Of Prophase:

  The chromatin condenses and during condensation, DNA strands untangle to form compact mitotic chromosomes

So in the S Phase, we're talking about chromosomes which contain double the number of initial DNA molecules, while the chromosomal number still being the same.
And in Prophase, there's condensation of chromosomes! But the chromosomes are already formed in the S Phase as per the sentence I have quoted from the textbook.

That doesn't make sense to me. I'm very confused.

A comment by user AlwaysConfused has answered one part of the question, but I think that the OP's confusion is related to a point of language or teaching. The number of chromosomes doubles during S phase (C number), but the ploidy of the cell does not change (N number). That's what your textbook is trying to tell you, it's just stating it fairly confusingly.

When we say that there are the same number of chromosomes before and after S phase, that's just a lie that we tell ourselves to keep from getting confused. We have invented the C vs. N terminology that AlwaysConfused mentions to try to handle this: we say that the 2N of a diploid cell remains constant across the cell cycle, while the C number alternates between 2C (before S phase) and 4C (after S phase).

For you, this confusion seems to be worse because how we represent chromosomes is not what chromosomes actually look like, and this has gotten mixed up with the definitions of chromosomes.

When we draw pictures of chromosomes we draw them neatly like they are in mitosis, but that is not at all what they look like in interphase. They are still chromosomes during that time, they just aren't pretty and neat ("condensed").

To sum it up more, here is a diagram of chromosomes in interphase (most of the time) vs. during mitosis:

It is only during a very specific part of the cell cycle (mitosis) that the chromosomes are packaged up ("condensed") in such a way that we can readily see them as discrete entities. The rest of the time they're all glommed together and are organized instead according to transcriptional activity etc. rather than according to which molecule they're part of. Remember: chromosomes are very big molecules and if they are "loose" they have a total length that is many orders of magnitude larger than the diameter of the nucleus; so the nucleus is like a big bowl of noodles in interphase.

In S phase it will just be a bowl with twice as many noodles in it as before, because there are twice as many DNA molecules ("chromosomes"; "chromatid" is a term that only applies to the condensed form in mitosis).


Are there any bacteria, in our environment, able to break down nitrate under aerobic conditions? Given a fix volume of water saturated with dissolved oxygen through aeration. Suppose that ammonium, Nitrosomonas, and Nitrobacter are always available in the water. We know that some of the ammonium will eventually be oxidized, by the bacteria, to nitrate. We also know that under anaerobic condition, some of the nitrate, through many steps, will be broken down into Nitrogen by denitrifying bacteria.

Question: Are there any bacteria, in our environment, able to break down nitrate under aerobic conditions? If there aren't, will the nitrate continue to accumulate?

My initial reaction upon reading this question was to think that the answer was: no, denitrification is a process in which nitrate is used in the absence of oxygen as an alternative electron acceptor. However I decided to check the literature, and I have discovered that there is, in fact, a lot of new evidence that many bacterial species may be able to use both of these electron acceptors simultaneously. This article is a good place to start if you want to find out more:

  Chen & Strous (2013) Denitrification and aerobic respiration, hybrid electron transport chains and co-evolution. BBA Bioenergetics 1827: 136-144

This is a review which summarises the area from the point of view of bioenergetics, but most importantly for this question, includes a Table summarising the experimental evidence for the phenomenon.  Referring to this Table, they state:

  It appears that in most cases, the evidence presented is not sufficient to support the conclusion that denitrification really proceeded in the presence of excess oxygen. It should be noted that the aerobic denitrification rates were much lower than the anaerobic denitrification rates measured for the same strain while aerobic respiration rates remain high. This implies that the major electron flow in the respiratory chain is towards complex IV rather than the NOx reductases, and that aerobic respiration is still the preferred pathway for growth. Apparently aerobic denitrification can be an auxiliary pathway next to aerobic respiration.

The last sentence answers the OP question.


What are an internal and external exons? I read the book: Essential Genetics and Genomics It has a table summarizing the properties of the "typical" human gene:

It has a gene feature Size of internal exon, what internal means in this context?

When I searched for it I found mentions about external exons, but found no definition.

I strongly suspect they mean:

External exons are the first exon right after the 5' untranslated region and the last exon just before the 3' untranslated region and all the other exons are internal exons.

As turned out this was almost right, but had a mistake which is wonderfully pointed out in the accepted answer.

Yes, the internal exons are those that aren't at the ends, which are often referred to as terminal exons1.

However, exons are sequences of nucleotides that are incorporated into the mature mRNA — i.e. they don't have to be (entirely) protein coding.

It is probably simplest to think of exons as being the transcribed regions that are not introns — i.e. they are the sequences that don't get spliced out during transcript maturation.

In other words, the 5'UTR is typically§ part of the first exon and the 3' UTR is typically§ part of the last exon.

§Note: I say typically, because sometimes introns are found within the UTRs2,3.

Reference:

1: Bolisetty, M. T., & Beemon, K. L. (2012). Splicing of internal large exons is defined by novel cis-acting sequence elements. Nucleic acids research, 40(18), 9244-9254.

2: Eden, E., & Brunak, S. (2004). Analysis and recognition of 5′ UTR intron splice sites in human pre‐mRNA. Nucleic acids research, 32(3), 1131-1142.

3: Paolantoni, C., Ricciardi, S., De Paolis, V., Okenwa, C., Catalanotto, C., Ciotti, M. T., ... & Giorgi, C. (2018). Arc 3′ UTR splicing leads to dual and antagonistic effects in fine-tuning arc expression upon BDNF signaling. Frontiers in molecular neuroscience, 11, 145.


Is MHC1 knockout sufficient to prevent transplant rejection? A few days ago I read about MHC1 knockout pigs for organ transplantation research.
I was just wondering, is it enough to knock out MHC1 in the donor (lets say from same species, pig to pig) for successful transplantation?

I understand that someone without MHC1 is more sensitive to  viruses, cancer, to NK and more. But the study pigs lived fine, so in theory it is possible to have knockout MHC1 and survive.
But is it enough for successful  transplantation from one pig (donor with knockout) to another (fully healthy, normal pig) ?

No, MHCII mismatch can also lead to transplant rejection, though through different mechanisms. CD8+ Tcells (that recognize class I) may become activated and directly kill donor cells*, and some NK subtypes can see the lack of self MHCI and also induce cell death.

MHCII mismatch on antigen presenting cells (APCs) brought along in the tissue may activate CD4+ (helper) Tcells, which do not kill directly. However, they can secrete a lot of pro-inflammatory cytokines which will make a generally hostile environment, and can also activate b-cells to produce antibodies against minor histocompatibility loci.

As to your other question, lacking MHCI entirely would be really rough on an animal in the wild, but under laboratory conditions where pathogens can be managed a bit more, it doesn't matter so much. It's the same reason we can keep mice that have gross immunological deficiencies alive, where humans with the same defects would be screwed.


Determining if a specific proline is cis or trans in the protein? While peptide bonds usually adopt the trans conformation, peptide bonds to proline can exist in either cis or trans conformation. The isomerization between cis and trans is slow, and has been shown to be the rate-limiting step in folding of certain proteins.

What methods can be used to determine the conformation of a specific proline in a protein?

Sarkar et al.(2007) Proline cis-trans Isomerization Controls Autoinhibition of a Signaling Protein. Molecular Cell 25, 413–426 (DOI 10.1016/j.molcel.2007.01.004), available here.

The authors report on the interactions between two SH3 domains of the Crk adaptor protein. Basically they find that the linker which tethers these two domains contains a proline which interconverts between the cis and trans conformations, and that this interconversion determines the interaction between the two domains. They follow isomerisation by using NMR.

Cis-trans peptidyl-prolyl isomerization is a subtle change, and I don't think that you will find a way of following it in a specific protein that is simpler than this, unfortunately.


At what stage of meiosis does "first meiotic arrest of oogenesis" occur? An exam question asked what stage of meiosis corresponds with "first meiotic arrest of oogenesis". I can't work out the answer from the wiki page - can anyone explain which step this refers to?

When females are in their mother's womb all their Oogonium (plural Oogonia) are being made, they they undergo mitotic divisions to become a primary oocyte. Then, the primary oocytes start to undergo meiosis I -  but meiosis I is arrested. This is the first meiotic arrest. Meiosis I continues when a female hits puberty, every month one or more primary oocytes undergo meiosis I and create secondary oocytes. These secondary oocytes will then  start the second meiotic division, but this second meiotic division is arrested as well. It is arrested for about 24 hours, waiting for a sperm to fertilise it in the Fallopian tubes. The only time an egg (or in medical terms - secondary oocyte) will complete meiosis II is if a sperm penetrates the egg, and then it is called an ovum, which develops into a zygote and a then foetus.

Therefore, the answer to your question will be - the first meiotic arrest in oogenesis will occur from the time the primary oocytes are created in the womb, until a female reaches  puberty. starting puberty until menopause every month one or more primary oocytes will mature and complete the first meiotic division.


Why do many DNA solutions contain additional compounds? DNA solubility data in only water is scarce.
A previous question asked for a quantification of DNA solubility in water. It seemed like it would be easily answerable, however isn't quite that simple since no data seems to exist for DNA solubility in exclusively water.
Even the small amount of data about water was in the context of washing away organic compounds from the solution. This got me thinking. DNA is in an aqueous solution in biological situations, and is usually handled in aqueous solutions in labs. So why is solubility data so scarce for pure water? What is important about organic compounds for DNA solutions?
Why are other additives important for laboratory DNA solutions?
So my question is why is DNA dissolved in exclusively water seemingly "uncommon" in laboratories? Is there something about pure water that is bad for DNA storage? Is it that functionally DNA never needs to be in water because it is inaccessible to proteins? Or have I misinterpreted the lack of solubility data; water is common-place and no data exists because there is no need?
I imagine PCR is where most of the data on DNA solutions exists. What about the polar organic solvents/compounds makes them important for DNA solutions?

DNA in pure water.
The only time that nucleic acids would encounter pure water would be in a laboratory setting--for example after an oligonucleotide is synthesized in vitro, the protecting groups are removed from the reactive atoms in the finished sequence and the final product is cleaved from the supporting matrix.  At that point you can lyophilize (freeze dry) the ammonium hydroxide solution, and resuspend the single-stranded oligo in pure water.
Additional compounds enhance heavy oligomer solubility.
However, as noted in the comments, nucleic acid solubility, particularly high molecular weight DNA, like genomic DNA,  is enhanced in solutions with dilute monovalent cations. 10 mM TrisHCl, pH 8.0, 1 mM EDTA suffices for almost every application. The EDTA inhibits any errant DNAses, and also slightly inhibits microbial growth.
Compounds act as pH buffers.
Tris is not the best biological buffer but has high solubility and is relatively cheap and stable. If the solution becomes too basic the DNA strands will melt, and if the solution becomes too acidic the purines will start to deaminate.
DNA never experiences pure water in biology.
From the moment that DNA is synthesized in a cell until that cell dies and its DNA is ultimately degraded, it does not encounter a pure water environment.


How can I measure bee and wasp population? Bees and wasps in our garden disappeared suddenly last year - I asked a question about it at Why our bees might have suddenly disappeared. This year, I see that some bumblebees are active now. I'd like to measure the population of bees and wasps in the garden over the year, and see if the numbers change when the nearby fields are sprayed.

I note the question How best to count bees entering and leaving a hive to measure hive activity? but I don't have a hive to count. Our bees come from far away, and I'm interested in multiple species from multiple nests, and wasps too. So I'd need to count the number visiting the garden. But, can I count reliably? It will vary with weather, and the number on any one plant will vary greatly depending on plant flowering dates.

Is there any established protocol for counting bees and wasps in the wild to look for population changes over time?

I can't spend too much time on this - I might manage an hour every week. Or, I could set up camera recording, if someone knows some really clever software to do the counting. But I still can't imagine how to overcome the variation.

Thanks!

Short Answer

No. You cannot appropriately examine population dynamics using the approach you've described.

You can, however, examine how foraging frequencies vary/correlate with field spraying (though this might take more effort than you're looking for).

 Long Answer

You're not going to be able to properly quantify population levels from casual observance.

Because you would be unable to effectively identify individuals, you would be unable to know if you're seeing different individuals or repeats of previous individuals.
The data are also biased toward those species or individuals that use the habitat features in your particular garden and are biased against those that do not (Parsons & Szewczak, 2009).
Further, you would have no way to identify which hives/nests that individuals are coming from (without watching them leave the nest directly), so you would not know which populations are represented at any given sighting.

Unfortunately, although the question you link to (How best to count bees entering and leaving a hive to measure hive activity?) would allow you to better examine/compare separate populations, those methods likewise suffer from the same shortcomings listed above.

What you can figure out:

Your causal observance can at best be used to quantify foraging frequency in your garden.

In other words, you would just be able to count how many bees visit your garden at any given time and compare those values at different discrete time points. You could compare this to a number of environmental variables to look for trends.

In your case, your approach would look something like the following:

You could count the number of sightings (or landings or feedings) in various random locations throughout your garden.

Each of these locations should be randomly selected, and you would preferably collect numerous random samples from each of various "habitats" (i.e., different locations, different flowers, etc.).
You must return to the same locations each time and spend the same amount of time at each location each sampling period.

You can do simple statistics on these different samples across all sampling periods to examine foraging frequency trends across time.
If you directly measure a number environmental variables (e.g., temp., precipitation, humidity, cloudiness, etc.) you'll be able to rule out variance in your data due to these factors.

Proper background research would be required to determine which variables might be important to measure.

Finally, you could do regression/ANOVA analyses to examine any correlation between nearby field spraying on your foraging activity.

However, there are a ton of variables that could affect the trends you see, so final analyses will likely be weak at best.

Measuring those aforementioned environmental variables will help with this, as will increasing your sampling rate. See Power Analysis

  Power analysis is an important aspect of experimental design. It allows us to determine the sample size required to detect an effect of a given size with a given degree of confidence. Conversely, it allows us to determine the probability of detecting an effect of a given size with a given level of confidence, under sample size constraints. If the probability is unacceptably low, we would be wise to alter or abandon the experiment.

Note: Work by J.E. Eckert (1933) showed that (honey)bees can travel multiple miles from their hive/nest, so unless those fields are mutliple miles away, any pesticides could very well impact the populations visiting your garden.

Another Option:

You could perform Trap Counts to try to approach quantifying populations rather than just quantifying foraging behavior.

This method is used frequently for other insects. However, I found very few reputable sources examining bees/wasps.

One example: Danka & Gary (1987) estimated foraging populations effectively, but they did so by collecting data at the hive entrance.

Though there is an inherent issue with trap studies as well:

As Petrovskii et al (2012) point out:

  Traps are effective at providing relative counts that enable comparisons but are poor at delivering information on the absolute population size.

However, Petrovskii et al (2012) show that a ‘mean-field’ diffusion model is capable of revealing the generic relationship between trap catches and population density.

Their paper is freely available here.

Citations

Danka, R. G., & Gary, N. E. (1987). Estimating foraging populations of honey bees (Hymenoptera: Apidae) from individual colonies. Journal of economic entomology  80(2): 544-547.
Eckert, J. E. (1933). The flight range of the honeybee. Journal of Agricultural Research 47:257-285.
Parsons, Stuart and Joseph M. Szewczak (2009). Detecting, Recording, and Analyzing the Vocalizations of Bats In: Ecological and Behavioral Methods for the Study of Bats. Thomas H. Kunz and Stuart Parsons, ed. The Johns Hopkins University Press, Maryland, 2nd ed., pp. 91-111.
Petrovskii, Sergei, Daniel Bearup, Danish Ali Ahmed, Rod Blackshaw (2012). Estimating insect population density from trap counts. Ecological Complexity 10: 69-82. http://dx.doi.org/10.1016/j.ecocom.2011.10.002.


Why do plants' leaves become enlarged in low light areas? Why do almost all plants in shade have a smaller stem structure and larger leaf than that same species grown in a well lit, sunny area?

I have no idea of the biological mechanisms behind what I'm about to propose. Consider this a hypothesis.

If the purpose of the leave is to collect sunlight for photosynthesis, then the behavior you mention is predictable. I order of trying to maintain a healthy flux of light in dim conditions, the plant adapts by increasing the area of its leaves. Once back in a well-lit environment, the need for larger leaves fades and new leaves are thus smaller, but still catch as much light. Of course, there must be limits to the extent of leaf area variation that one plant can handle.

As for the stem structure, I can only guess it's because plants spend more energy on leaf building than stem maintenance when under such stresses.


What is most simple eukaryotic genome? Expressed in number of Base Pairs or Bytes, about how large is the simplest eukaryotic genome?

How much of this is 'junk-DNA' (non-coding)?

You asked about eukaryotes. The genome of the yeast Saccharomyces cerevisiae is 12.2 Mb.

The genome of the smallest free-living eukaryote, Ostreococcus tauri (a unicellular green alga) is 12.6 Mb

There are smaller eukaryotic genomes, but these are not free-living organisms they are intracellular parasites.


What species of insect is this? I saw this insect near a beach in Corsica France:

It's a mole cricket (in the family Gryllotalpidae).

Notice the cricket-like appearance of the posterior/abdominal portion of the insect, but the powerful, broad and flattened fore-legs that are designed for digging (reminiscent of a mole's digging legs). In fact, the family name literally means cricket-mole (from Latin, 'gryllus' = cricket and 'talpa' = mole).

Mole-cricket fore-legs:

Anterior mole legs:

The Gryllotalpidae are a monophyletic group in the order Orthoptera (grasshoppers, locusts and crickets). A 2015 paper by O. J. Cadena-Castañeda clarified/updated the phylogeny of this family using morphological characteristics.

The specific species is dependent on your location and morphological characteristics (and possiblly "song" differences too).
See here for a brief explanation and access to dichotomous keys to use to better ID the specific genus. Other keys exist here (SE USA), here, and likely via a google search. However, I couldn't quickly find a European key.

Here's an additional useful resource on these insects from University of Florida Entomology and Nematology Department.

Based on the OP's location in France, the European mole-cricket Gryllotalpa gryllotalpa (or one of it's closely related European allies in the Gryllotalpa genus) is probably a good initial guess at the OP's specific species. As seen from UC Berkeley's "CalPhotos" collection:


How to validate the use of an anti-virus monoclonal antibody in IHC by spiking a fresh organ with infected cultured cells? I have assessed the specificity of a particular monoclonal antibody against a virus by immunofluorescence. I'd like to further validate it by testing it by IHC. Therefore I'd like to infect cells in culture, and then inject them in a piece of fresh organ, fix in formalin, embed in paraffin and then cut slides before performing IHC. Is there any protocol or references to do so ?

Injecting into a fresh organ seems like a needless complication if you're just validating your antibody and not interested in gathering data about the interaction between the cells and the organ. (In fact, if you're using anything more complex than a flatworm I'd hope your IRB would have problems with needlessly sacrificing animals to get those organs.)

It seems like your purpose would be better fulfilled by making an FFPE cell plug and doing your IHC on that. Here's a protocol for making cell plugs:
Johns Hopkins Tissue Microarray Lab Cell Plug Protocol


What would happen if blood flow wasn't periodic? Blood pressure has its systolic and diastolic parts due to the beating heart and the body's used to that kind of thing.

What would happen to a person supported by a blood-pumping machine that applies steady blood pressure?

What would happen short term?

What would happen long term?

In fact, we see our blood pressure as periodic, and feel our arteries pulsating. But our tissues don't see that. What I mean by that, is that tissues get their blood supply ultimately through their capillaries, where the blood pressure and flow is essentially constant throughout the cardiac cycle, as you can see on this chart:

Image from OpenStax. Article on Blood flow and pressure

As for the second part of your question, what would be the consequences of having constant/non-pulsatile pressure? We can only speculate, I don't think it would have any palpable consequences in principle.

The only "real-life" examples include people who are, for instance: on a Cardiopulmonary Bypass during a cardiac surgery, on Extracorporeal membrane oxygenation (ECMO) in the ICU or have a left ventricular assist device (LVAD) for severe heart failure. It's very difficult to infer anything from these situations, because any on these patients are already very sick, and consequences following these procedures are usually due to insufficient oxygenation, thromboembolism and such, which have nothing to do with the constant pressure.


Strange white strings on cherry tree leaves What could be the cause of these white strings on the leaves of our sour cherry tree? Is it some kind of fungus or an insect?

Also, i don't know if it's related or not, but on the other side of the tree brown spots started to appear also on the leaves:

I live in Hungary, if the climate is relevant.

This sort of thing happened to one of my plants.  When I took a closer look at the plant, it was a group of white aphids.  The brown coloration of the leaves of your cherry tree was relevant because aphids can sometimes kill the entire plant that they feed off of.

I did not take a picture of the plant, but I found one online: https://entnemdept.ifas.ufl.edu/creatures/trees/shivaphis_celti03.jpg


Smoking, cancer, correlation between quitting smoking and increased immediate risk There is "proof" out there today that suggests smoking is directly linked to cancer. I cannot argue against that, for the evidence in favor appears strong, and the evidence against is lacking. I'll happily sit here and agree that smoking increases the risk of cancer. This question, however, is not about how smoking increases the risk of cancer, rather how stopping smoking might increase the risk of cancer.

Consider what I know so far:

Cancer is caused by mutant cell growth.
Mutant cell growth is believed to be caused by chemicals in the smoke
Smoking itself stunts growth, thus slowing the cell growth rate

If the growth stunt is severe enough that it will reduce the cell growth rate by 20%, one might assume this would take some weeks (let's say 8 weeks, sounds reasonable to me, though I lack knowledge of the subject) to recover. This will likely be some scale and will gradually decrease to somewhere near 0.

Further to this, the risk of cancer is not directly related to the lung, but it is believed to be caused by chemicals entering through the lung into the blood, and travelling around the body, causing cancer in various organs.

Consider that the cell growth is probably linked (in the lung, at least) to chemicals "surrounding" the existing cells, this explains why smokers run short of breath. This partially explains the growth stunt side of smoking. Perhaps this happens body-wide, I don't know.

Then consider what will happen when one stops smoking. The cell growth rate will begin to radically and unexpected increase as the growth stunt is suspended, meanwhile chemicals will still exist in the blood and organs which will be perverting cell growth causing mutant (cancerous) cells. At this point the body is unprepared and settled into its routine of slowly generating cells, but now it is generating them faster and is struggling to keep up. Energy is lacking in areas, and there is further cause of mutant cells to grow and even to be allowed.

Surely, given this reasoning, it might be understandable that stopping smoking increases the immediate risk of cancer, though reducing the long term risk?

Does anybody know, or can anybody find reasonable proof that any part of this argument is flawed? Is there any research to suggest that there is or is not an immediate increased risk? The one thing that people never mention in the side-effects of quitting is the risk of immediate body failure through a variety of means (I've known people to come with flu-like symptoms then find they have cancer weeks later). Is this really unexplored? Or is the nanny state trying to hide it from smokers to prevent them from damaging their health further?

To summarise your argument, cancer is a disease characterised by uncontrolled cell division of mutant cells. Smoking decreases cell division, thereby smoking decreases risk of cancer. Furthermore, stopping smoking increases growth rates, thus there's an immediate rise in risk following smoking cessation.

Cancer is NOT caused by cell division. Smoking does NOT cause cancer by cell division. That's the flaw in your argument. What's happening is that cell division ISN'T being controlled. Let's propose that smoking does indeed stunt normal cell growth. The carcinogens in tar from smoking are still floating around causing mutations in the DNA. Most of DNA doesn't code for very much, but some parts of it codes for genes which control cell division. If these genes mutate then cell division is no longer controlled by these genes and hence there's uncontrolled cell division a.k.a cancer. Once these cells are dividing in an uncontrolled fashion, smoking isn't going to limit their growth. That's because this cancer has developed in the presence of these toxins that limit it's growth and despite this it's still managed to occur.

And then that cell growth stunting may actually be causing cancer to occur. White blood cell function is impaired by smoking, these cells usually target cancerous cells and destroy them. Without being destroyed, there's a higher chance of cancer.

And then I could go further, usually cells grow older and die. Maybe smoking by stunting growth of these cells leads to cells that last longer than they should. These cells accumulate mutations and become cancerous, where else they otherwise would've been recycled.

Smoking however has been linked to improving the symptoms of some diseases. Just not cancer.


10 inch spider near Mexico City Four years ago I found a spider so big that I'll never forget. Unfortunately I don't have a picture but I guess there isn't a lot of big spiders in Mexico. So here are some things I remember:

It wasn't a brown spider, I think it had red legs with some parts black and others white.
Its legs were skinny and very long
The main body was tiny compered with the spam of its legs.
I found it at noon, after I moved to my new house. Unfortunately it wasn't moving when I found it
The spider didn't have any visibly hair.

That's all I can remember. I know that this may be impossible but I don't know what else to do.

It almost definitely wasn't 10 inches, but there are some pretty big spiders in Mexico. There is a species of spitting spider with a 9 inch legspan but it lives in South America not Mexico.
Scytodes globula

The cellar spider has a legspan of up to 3.6 inches and a comparatively small body with long skinny legs and no visible hair, but I can't see how that would be confused for 10 inches.
Pholcus phalangioides

The giant crab spider fits that description to some degree. It has a legspan of up to 4 inches.
Heteropoda venatoria

The golden silk spider is very large with long skinny orange and red legs.
Trichonephila clavipes


Can some human groups evolve into new species? The Sentinelese people are an indigenous people of the Andaman Islands, in the Bay of Bengal, an essentially hunter-gatherer society subsisting through hunting, fishing. There is no evidence of either agricultural practices or methods of producing fire.

Does such uncontacted people have potential to undergo peripatric speciation?
This link says

.......to the fact that the Sentinelese have lived in isolation for 60,000 years: genetically, therefore, there is a direct line between them and their pre-Neolithic ancestors.

Factors:
Geographical and Reproductive Isolation

They live in a  highly isolated and heavily forested Island in the Andaman sea.Any contacts with any other nearby Island has never been reported.

Differences with Mordern Humans
Wikipedia says that:

Behavioral modernity — a suite of changes in Homo sapiens behavior and cognition including abstract thinking, deep planning, symbolic behavior (e.g. art, ornamentation, music), exploitation of large game, and blade technology — is evident from around 40,000–50,000 years ago, and may have emerged abruptly then or may have arisen through gradual steps.

While Sentinels have been isolated for more than 60,000 years.

The Late Upper Paleolithic Model,  refers to the idea that, though anatomically modern humans first appear around 150,000 years ago, they were not cognitively or behaviorally "modern" until around 50,000 years ago. These authors note that traits used as a metric for behavioral modernity do not appear as a package until around 40–50,000 years ago. Klein (1995) specifically describes evidence of fishing, bone shaped as a tool, hearths, significant artifact diversity, and elaborate graves are all absent before this point.

Hints of Mutation:
This tribe miraculously survived 2004 Tsunami despite having small population.
This link says

Close to 150,000 people have been confirmed dead (due to Tsunami)... Sentinalese who live in the archipelago escaped unscathed because they took to the forests and higher ground well in time.
Scientists believe that because of the extreme isolation of the Sentinalese, this tribe has become biomedically valuable...... could be targeted by bio-prospectors for valuable genetic traits that may have long ago vanished in other ethnic or racial groups.

Strange courtship ritual

......this moment, a strange thing happened — a woman paired off with a warrior and sat on the sand in a passionate embrace. This act was being repeated by other women, each claiming a warrior for herself, a sort of community mating, as it were. Thus did the militant group diminish. This continued for quite some time and when the tempo of this frenzied dance of desire abated, the couples retired into the shade of the jungle....

Absolutely it is possible for the current human species to evolve in to two distinct species in the future. Barriers to reproduction, such as physical isolation, help the process along as it allows differences to accumulate. Gene flow allows hybridisation (not in a species to species sense, but sub-population to sub-population sense) which will impede the process of speciation because it allows genetic variation which is unique to one population to move to the other.

Differences occur between populations, which can lead to speciation, by the mechanisms of evolution - mutation, migration, drift, and selection. Different mutations occurring in sub-populations allows the two to become genetically incompatible, leading to speciation. Gene flow from a third population may make the first two too different to reproduce (see also ring species). Drift and selection may cause genetic variation which allows reproductive compatibility between two populations to be lost, further generating genetic differences. Selection in different directions (e.g. the environment of the two populations is very different) can hasten speciation, as seen in a classic Drosophila experiment.

Will the population you mention ever become a non-human/novel species? Who knows, but they are certainly interesting - as you've realised, their isolation by geographic barriers will help differences to accumulate between them and other human populations that could lead to speciation.

I suggest reading more about evolution and speciation here!


What Causes Shin Splints? My shin splints are clearly tied to running. Though the pain level doesn't seem to correlate  to my running intensity. So what is it about running that causes shin splints?

My real hope is that if I understand the cause clearly enough I can adjust to fix them.

By shin splints you probably mean the pain on the inner front side of the lower 2/3 parts of the shins? This is called medial tibial stress syndrome (MTSS).

Causes, mechanism, prevention and treatment of shin splints are still poorly understood.

From what I managed to find, custom-made cushion insoles are the only proven prevention that can help in some cases.

What has not been proven to help (I'm not saying it does not help, only it has not been firmly proven):

various types of shoes (supinator/pronator)
taping
stretching/strengthening exercises
various running techniques (pose-tech, chi-running, barefoot...)

Possible causes:

running downhill or on an uneven terrain with heel striking and forefoot slapping
sudden increase in running intensity, mileage or frequency
a way of running with moving the hips (left , right) forward
(my experience): running in a forced, conflicting way, like you feel you should not run and you still go...

Possible mechanism: vibration stress in the shinbone (tibia) and the pulling force of the muscles and tendons attached to it and possible local inflammation of then periosteum.

Do not try to run through the pain. The pain will go away but on the long-term, shin splints may worsen.

Source: Shin Splints (MTSS) (Ehealthstar)


Evidence of condition-dependent sex-allocation in regards to humans Coming from zero background in biology, I am looking for expert opinion on evidence regarding Trivers-Willard hypothesis (1973) and humans.

In short the hypothesis states that
if

"Condition" of offspring during their whole life are correlated
to that of their mother during pregnancy
Males have better on average better reproductive success (more genes in next generation) than female when in "good condition", and vice versa if you compare male/females in "bad condition".
Females objective is "eventual reproductive success" down the
generations.

Then it makes sense for females to vary sex ratio, more males when in "good condition" and more females when in "bad condition".

I think it is safe to say that plenty of evidence exists on assumption one. The second assumption seems more nuance in todays environment, but one would imagine that during most human history it does hold true. On the third one I think is safe to assume it is true based on the theory of evolution by natural selection.

Any (rigorous) reference (articles, researchers, journals) or comments would be superb!

Reported association that I am already aware of are:

Reduced gender ratio at times of war and famine (Ansari-Lari & Saadat, 2002; Song, 2012; Valente, 2015) and after natural disasters (Fukuda et al. 1998).
Darwin (Descent of man); Norberg, 2004; Almond & Edlund, (2007); Hamoudi & Nobles, (2014) divorce or "unmarriedness" correlated with lowered gende ratio.
Negative association between parents age and gender-ratio,  Jacobsen, Møller, & Mouritsen, (1999).

I am not aware of any such evidence in humans but I know little about this literature. If you happen to have data showing that, then it would probably be a relatively big thing! Below is a series of comments that might be of interest.

Evidence from Hyena

The evolution of the sex-ratio variation in hyena have been quite extensively studied. This very short article (not peer-reviewed) cite a number of key papers on the subject.

Logic behind the second assumption

In case clarification is needed. The variance in fitness is indeed often higher in males than in females. The reason is that females (by definition) produce the larger gametes, the one that don't leave the body and therefore often pay a much higher cost when reproducing than males do. As such, females are the limiting factors. As a consequence, males compete a lot to access females and "good males" receive a lot of mating opportunities while "bad males" receive little mating opportunity causing the higher variance in fitness among males than among females.

Statistics

IMHO, there is a tradition of horrible statistics when dealing with human sex-ratio data. It is particularly the case as these papers are often published in journals where reviewer have little knowledge in statistics (e.g. medicine). Typically, "windowing" data is generally a very bad idea and previous papers in the field have reported very bad interpretation from data due to cherry picking specific ways to classify observations. Please be cautious in your statistical analysis!

About the post

The formulation of the hypothesis is clear enough but some sentences are misleading

  it makes "natural selection" sense for females to vary sex ratio`

This sentence sounds very wrong. You should rather say "females that are able to vary the sex-ratio among their offspring will be have a higher fitness".

Note that I said "among their offspring" because while this would cause variation in sex-ratio in the population, genotypes are selected based on their ability to vary the sex-ratio among their offspring and not in the population. In fact, any given individual, would appreciate if all the other would produce the exact opposite sex-ratio than the one they actually produce among their offspring.

  better chance of reproductive success

This sentence a little clumsy as well and should be replaced with higher fitness


Are viruses more common due to modernity? Is there any evidence to say whether in the past viruses like the cold virus were less common?  I wonder if high density living and globalisation mean that the cold virus mutates and spreads much more than in the past.

Perhaps in the past, owing to lower population density, slower and less frequent transport, viruses were effectively localised and isolated from the general population?  Of course that might not be true, as perhaps those things have been offset by improvements in sanitation and nutrition?  Perhaps virus frequency is always proportional to population size?

Short answer: there are a lot of viruses, and they're all different. The answer to your question is going to be "it varies by virus". Some of the ways population density and urbanisation affect virus transmission are summarised very briefly below.

Population density

Any pathogen's ability to sustain itself relies on every infection causing, on average, at least one other infection. This is called the basic reproduction number or R0. The transmission rate of a pathogen depends on its transmission mode, but with some modes of transmission (like droplet transmission, a major route of transmission of viruses that cause the common cold) population density is important. There's an excellent explanation of density- versus frequency-dependent transmission here. This means that as people live at higher densities, the potential for transmission of some viruses increases purely because of that difference in density, while it has little effect on other viruses.

Critical community size

However, transmission rate is only part of the story. Assuming infected people eventually become immune, a pathogen can burn itself out before new hosts are born or immunity is lost. Stochastic effects become more important in small communities, and there is a critical community size below which pathogens tend to go extinct. Small or isolated communities cannot sustain the virus causing measles, for example.

Urban environments and transmission (and vector-borne diseases)

Urban environments aren't just higher density, they are different in potentially important ways. For example, some viruses need to be transmitted between vertebrate hosts by arthropod vectors like mosquitoes. If you don't have the mosquito, you can't get the virus. Viruses like yellow fever virus, dengue virus and Zika virus are primarily transmitted by Aedes aegypti, which nowadays breeds preferentially in urban environments, so as urbanisation increases the potential for transmission of these diseases also increases. Without adequate sanitation, the potential for faeco-oral transmission also increases at high population densities, for example. Things like sewage treatment, air conditioning and exposure to wildlife all affect transmission in important ways.

So, basically, it's complicated.


Can plants produce oxygen at night (without light)? I accidentally clicked on a "Top n X's that Y" result in google and found Top 9 Plants that gives (sic) off Oxygen at night as well (best for indoors).
In this helpful answer I've found a nice, concise description that I'm just going to reproduce here:

Photosynthesis consists of two general steps, one that requires light and one that does not. The first step occurs in the thylakoid membrane, and splits water into oxygen, hydrogen ions, and energy. The second step is the carbon fixation step, which occurs in the chloroplasts and uses energy to convert the carbon dioxide into carbohydrates.
Step 1: $\ce{2 H2O + light → 2 H+ + O2 + energy}$
Step 2: $\ce{3 CO2 + 6 H+ + energy → C3H6O3-P + 3 H2O}$

In general, the oxygen released from plants comes from water splitting which is driven (in a multi-step process) by photons. From what I remember, the oxygen molecules ($\ce{O2}$) are usually produced and released to the air within seconds, and certainly within minutes after all of the necessary photons for it have been absorbed.
So I am asking; are there plants that really make meaningful, or even just measurable amounts of oxygen without light?
(Or is the idea here that you leave your lights on at night and so actually any plant can make oxygen at night?)

Short Answer: Any plant can produce oxygen at night, but plants cannot produce oxygen without light.

Longer Answer: It all comes down to spontaneity of a reaction i.e. whether a reaction can occur without input of energy or not.

Before we talk about spontaneity, I feel it better to first know about the process we're talking about here. In photosynthesis, the water-splitting reaction occurs in the oxygen-evolving complex through a process known as Joliot-Kok cycle (or simply, Kok cycle)1. Although, the complete mechanism of this process is not understood yet, the basic reaction can be depicted in a diagram as2:

(Pay attention that in the diagram, the time taken is in microseconds and even nanoseconds. So, at molecular level, oxygen evolution does not take minutes or even seconds! However, at larger scale, release of oxygen might take longer time since the formed oxygen has to pass through many fluids, like thylakoid membrane, stroma, chloroplast membrane, cytoplasm, etc. before finally coming out in atmosphere)

To know where the photons are required (since the above diagram doesn't talk about that), I'll let in another diagram involving the steps where photons come in (as depicted by Rutherford et al, 1989):

As you can see, Kok cycle does not get direct input of energy through photons. Rather, it is the high energy P680+ which oxidizes a redox active tyrosine (YZ), which drives the reaction forward (the actual process is much more complex, see another answer or Halverson et al, 2003 for details).

Now, talking about spontaneity of this reaction, oxidation of water into hydrogen and oxygen is an endothermic process i.e. it is non-spontaneous in nature. In fact, the process requires 475 kJ/mol energy for occurring (Wikipedia). This energy barrier is so large that in the Kok cycle too, 4 photons are required to bring about oxidation of 1 water molecule (generally, catalysts are used so that they bring down the energy barrier of a non-spontaneous reaction so that it can be performed under normal conditions). Nilsson et al, 1857 talks about free energy change ($\Delta G_0$) of the cycle. See the graph for free energy change:

As is clearly visible from the graph, a higher amount of energy is needed to oxidize water ($E_P^+, S_2 \rightarrow S_3$) and even higher for liberation of dioxygen from the complex ($S_4 \rightarrow S_0$) (though the free energy change is negative for the last step i.e. liberation of oxygen is spontaneous, still the overall energy is larger than that at S3). Thus, since the reaction requires overall energy input, plants cannot produce oxygen without light. Also, as you suspect already, the point here is the abundance of light from man-made sources which makes some plants able to produce oxygen at night.

BONUS: I'll add some details about the thermodynamics of the system (skip this part if you're not interested in maths). The basic equations I will use here are Gibbs Fundamental Equation ($\Delta G = \Delta H - T\Delta S$), Arrhenius Equation ($k = A \times e^{-E_a/RT}$) and Eyring Equation ($k = k_BT/h \times e^{-\Delta G^\ddagger/RT}$) and used data will be from Nilsson et al, 1857.

From $\Delta G = \Delta H - T\Delta S$, to make a reaction spontaneous ($\Delta G < 0$), either there should be release of heat ($\Delta H < 0$) or increase in entropy ($\Delta S > 0$). As we know now, the reaction is endothermic i.e. there is absorption of heat. So, there must be increase in overall entropy to drive the reaction forward. If you look at the graph for free energy change in different steps of reaction, it comes out to be like this:

In this, $\Delta G_0$ is overall energy change, $\Delta G_{in}$ is the required energy input (given by photons), $\Delta G_{ex}$ is final free energy change and $\Delta G^\ddagger$ is Gibbs energy of activation. Here, $\Delta G_{ex}$ (shown in blue) corresponds to only the entropy change when final products (oxygen and protons) are released from the system as there is no enthalpy change here.

In release intermediate stage, the mole fraction $x = 1$ for oxygen, whereas in dissociated product stage mole fraction for water $x_1 = 56 /( [O_2]_0 + 56)$ and for oxygen $x_2 = [O_2]_0 / ([O_2]_0 + 56)$ (assuming molarity of water = 56 M) since in the final stage, water or oxygen or both can remain binded to the active site.

For release of oxygen: $[O_2]_0 = 273~\mu M$ and $T = 298~K$

which gives $\Delta G_1 = -~T\Delta S_1 = -~314~meV$

For release of proton: $\Delta G_2 = -~T\Delta S_2 = -~516~meV$ (since there is no enthalpy change, $\Delta H$ is neglected)

Now, $\Delta G_{ex} = \Delta G_1 + \Delta G_2 = -~314 - 516 = -~830~meV$

Also $\Delta G_0 = \Delta G_{in} + \Delta G_{ex}$

Since $\Delta G_{ex} > \Delta G_0$ therefore $\Delta G_{in} > 0$ i.e. energy is supplied.

Now, for the reaction $~~P_{680}Y_Z^{ox}M_3 \rightarrow P_{680}Y_ZM_0 + O_2$ (for which we've made the above graph)

Time constant $\tau \approx 10^{-3}~s$

i.e. $1/k = 10^{-3}~s$

or $k = 10^3~s^{-1}$

Using Eyring equation $k = k_BT/h \times e^{-\Delta G^\ddagger /RT}$

We get $\Delta G^\ddagger = -~580~meV$

In other words $\Delta G_{in} \leq -~580~meV$

Again $\Delta G_0 = \Delta G_{in} + \Delta G_{ex}$

On solving, $\Delta G_0 \leq -~250~meV$

Again, from Eyring equation, we get $k \geq 10^4~s^{-1}$

The large rate constant shows that there is a strong driving force for release of oxygen from the system, which is very likely due to increased entropy of the final product.

Thus, the enzyme brings down the free energy of the reaction, but at the expense of an increased activation energy barrier. Coming back to the main point, since energy is supplied to the system for the reaction, the reaction is non-spontaneous. However, the last step of the reaction is spontaneous (as also seen in the first graph) because of increase in translational and rotational entropy of final products when they are released (in above calculations, we neglected rotational entropy because of lack of data). Also, the above calculations were only for the last step of reaction ($S_4 \rightarrow S_0$) to show its spontaneity. In all other steps, energy has to be supplied to the system to drive the reaction forward (as shown in both first and second graphs above), making the overall reaction endergonic. I hope this helps now.

References:

 1. Wikipedia contributors. "Oxygen-evolving complex." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 1 Jan. 2017. Web. 18 Apr. 2017.

 2. Oxygen Evolution - 1996, Antony Crofts, University of Illinois at Urbana-Champaign

 3. A.W. Rutherford, Photosystem II, the water-splitting enzyme, Trends in Biochemical Sciences, Volume 14, Issue 6, 1989, Pages 227-232, ISSN 0968-0004, http://dx.doi.org/10.1016/0968-0004(89)90032-7.

 4. Halverson, Kelly M., and Bridgette A. Barry. “Evidence for Spontaneous Structural Changes in a Dark-Adapted State of Photosystem II.” Biophysical Journal 85.4 (2003): 2581–2588. Print.

 5. Wikipedia contributors. "Heterogeneous water oxidation." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 18 Apr. 2017. Web. 18 Apr. 2017.

 6. Håkan Nilsson, Laurent Cournac, Fabrice Rappaport, Johannes Messinger, Jérôme Lavergne, Estimation of the driving force for dioxygen formation in photosynthesis, Biochimica et Biophysica Acta (BBA) - Bioenergetics, Volume 1857, Issue 1, January 2016, Pages 23-33, ISSN 0005-2728, http://doi.org/10.1016/j.bbabio.2015.09.011.


Ribosomes and DNA in chloroplast Are there multiple copies of circular DNA and membrane bound ribosomes IN CHLOROPLAST ?
Are polysomes found in them ?

The chloroplast, having multiple circular copies of its chromosome and its own tRNA and ribosome genes more resembles the bacterial systems it is descended from.  See @A.Kennard comment

Polysomes being found in bacteria frequently are single mRNA to which are attached multiple ribosomes.  This paper shows that chloroplast polysomes were observed in the mid 1960s by centrifugal sedimentation.


If one of eyes is blind, can that eye still feel pain? I was wondering this when I touched my bare eye (my eye was open) and since I'm not blind I was wondering if an eye is blind, can it still feel pain?

Blindness can be due to a damage of the lens, retina, optic nerve or the visual area at the occipital lobe of the brain, for example.

Sensitivity of the eye cornea is enabled by a different nerve - the ophthalmic nerve, which is a branch of the trigeminal nerve (Yale Journal of Biology and Medicine). As long as this nerve, somatosensory cortex at the parietal lobe of the brain and other neural structures involved in pain sensation are intact, you should be able to feel pain when touching the cornea of the blind eye.


BMI limits in interpretation in people with high/low heights In a study, I measure BMI of a large sample of adult people.

Among them, there is some who have very low and very high height.

As I can read on the internet (like here or even in the wiki, for instance), BMI is not relevant for very short or very tall people.

Some math professor even wrote an article with a "better" calculation of BMI, but with a very low impact in science world (didn't find it on pubmed) so it's not really peer-reviewed.

Let's take some examples, assuming "normal BMI" is 21:

for a 110cm tall adult, ideal weight is 25kg
for a 130cm tall adult, ideal weight is 36kg

These weights appear really low to me. Note that dwarfism cutoff is 145cm in France.

My question is then the following: How could I choose a cutoff on height to exclude BMI values ?

NB: I didn't find anything on pubmed nor on google scholar, but maybe I missed an important article

The best procedure is going to depend on what exactly you're going to do with your data. Regardless, you should NOT exclude the BMI values. Just include the height, weight, and BMI. If you're simply reporting BMI as a characteristic of your study population, you can annotate that figure and let your reviewers and readers decide what to make of it. This follows the principles in Chapter 4 of Hulley's Designing Clinical Research. You want to get and maintain all the data.

If you're going run some further analysis on BMI, or if BMI is an outcome in your study, then you can evaluate the impact of a cutoff on your results, but you have to decide ahead of time how you'll do your primary analysis. I recommend using the entire data set (no height cutoff) for your primary analysis (because *there is no established practice for a BMI height cutoff in the general medical literature), and then running a secondary analysis that excludes those research subjects above some threshold (you can pick it, but depending on the size of your sample, 2 standard deviations could be reasonable). That secondary analysis would be a hypothesis generating analysis. If excluding very short and very tall people changed the results of your analysis, that's something to mention in your discussion and something to consider for the next study.

*If you're in a specialized field, then follow the practice of that field for your primary analysis.


Are “Rings” in fish like rings in a tree? A lot of fish have structures like the rings in a tree. Is the number of “rings” an indicator of age, as in a tree, or is it fixed?

It depends which structures you're talking about. However, several body parts of bony fish such as the scales and otoliths (earbones) generally contain a record of seasonal growth patterns. So in that sense yes, the process of ageing fish is similar to finding the age of a tree by counting rings in the wood. For different species of fish, different structures are used to determine ages.

https://www.nefsc.noaa.gov/fbp/basics.htm


Why don't cells double gene expression after S-Phase? In the cell cycle (G1-S-G2-M), all of the DNA is replicated during the S or Synthesis stage. The cell may then spend some considerable time in the G2 phase before splitting in the M phase. Since there is double the amount of genetic material in the G2 phase, what mechanism if any, prevents the amount of gene expression from also doubling?

When the double strand is duplicated, the old strand (or, in other terms, the template) is methylated : this modification is enough to prevent the bind by the RNApol system and, by so, the transcription.
By methylation, DNA-repair systems are able to detect which is the newer strand, to discover and fix replication errors.

Here you can find additional infos


Reverse transcription PCR optimization What is the ideal amount of RNA to use for the RT? and how much cDNA to use then for the PCR?

I did RT with a solution of RNA of 0.36 ug/ul. Then for my PCR I used 1 ul of the cDNA obtained and used 25 cycles because I was hoping to see a difference between an endogenous level and an overexpression. However, I detected no band at the expected height of 500 bp but a diffuse band at 100 bp. What can this 100 bp represent? primer dimer? I switched to 35 cycles and I used either the same amount of cDNA or add 3 times more cDNA. In both cases I got bands at the expected height (but stronger when I put more cDNA) and still big bands at 100 bp.

I see big fuzzy bands around 100bp as well. They're most likely RNA contamination. To get rid of them, digest your RT-PCR products with RNAse-H. But if you just need to visualize your band of interest, and the fuzzy bands aren't getting in the way, it shouldn't be a problem.

I usually input anywhere from 1-2 ug of RNA into my RT-PCR reaction using the Invitrogen Superscript III kit for a total volume of 20 ul. After the reaction, I use 1/10 the volume of that (2 ul) for downstream (PCR) applications. This usually gives me nice results.

To optimize RT-PCR for detection of a specific target, consider using gene specific primers (make sure to use only anti-sense primers) in your RT-PCR instead of oligo-dT or random hexamers. This enriches your target when you use them for downstream applications. When you use GSPs though, make sure to run a parallel reaction with control (i.e. beta actin) primers to prove that your RT-PCR reaction is working.


What is the difference between DNA vs RNA Editing in the context of gene therapy? As a someone with beginner knowledge on biology, I have come across the terms "RNA editing".

Take this paper for example : RNA Editing with CRISPR-Cas13

From my understanding, DNA -> RNA -> Proteins

If we use a vector for delivering a gene to a cell in-vivo, does it mean that corrections aren't permanent for RNA edits?

There are several differences, both mechanistically and functionally.

DNA edits are heritable by the daughter cells and are therefore permanent whereas RNA edits are not.
The type of Cas protein used in the editing process for DNA and RNA are different.
In the paper that you linked the authors have fused an RNA editing enzyme (ADAR) with dCas13 (a variant that does not cleave the target). So the CRISPR-Cas system directs ADAR to the sites on RNA that need to be edited. Usually when editing the DNA with CRISPR-Cas, people rely on the ability of the complex to cleave the DNA. This double strand break may be then repaired using different pathways (NHEJ and HR) during which editing happens. See these posts for more details:       How is the type of genetic manipulation determined in CRISPR-Cas9?       Mutations/deletions with CRISPR       How does NHEJ cause indels?
It is also possible to edit DNA in a way that does not involve cutting of the DNA. These techniques use similar principle as in the case of RNA editing described in the paper that you linked (see the abstract and introduction of this paper). However, if you cut the RNA, then it will be completely degraded instead of being repaired.


Starch vs Cellulose. What are the differences between Alpha and Beta glucose ring structure in them? I'm studying "Campbell Biology, 10th Edition" and in chapter 5 page 71 there's a statement I can't understand. according to book:

  In starch, all the glucose monomers are in the α configuration.

and then says:

  In contrast, the glucose monomers of cellulose are all in the β
  configuration, making every glucose monomer “upside down” with respect
  to its neighbors.

My question is if all glucose monomers of cellulose are all in the β
configuration (according to figures) why each monomer in cellulose is “upside down” with respect to its neighbors and is not just all the same as in glucose monomers.

The reason the monomer units are shown as alternating orientation in the cellulose case and not for starch is due to the angles required for the bonds between the atoms involved.

Note that in α-glucose the OH groups of the #1 and #4 carbons are shown on the same side of the ring.  When these two groups are changed into a single O joining two α monomers into starch, they have to remain in the same position.  When a single O joins them together, that oxygen requires the angle between the bond be less than 180 degrees, so the two glucoses have to be on one side of the oxygen.  That's fine in the drawing because in α glucose both OH groups are pointing down.

On the other hand, in β-glucose the OH groups of carbons 1 and 4 are on opposite sides of the glucose ring. Joining two β monomers to make cellulose requires that these two OH groups point in the same direction so that when changed into bonds to the single O, the angle which the oxygen requires can be provided.  To get the two OH groups pointing the same way requires one of the two β-glucoses to flip relative to the other.  Hence you get the monomers of cellulose alternating in orientation.

Part of the problem may be trying to visualize these 3-D relationships from the 2-D diagrams.  On this α-/β- glucose webpage there are some rotatable images of the molecules which may help visualize the relationships.


Telomerase as cancer target There are a lot of publications, starting from 2000, about using telomerase for targeting cancer cells (it is upregulated in more than 80-90% of tumor cells). Specifically using its promoter (hTERT). In all publications, researches talking about the success of this approach.
So my questions,  why there is no use of this? What is the problem? I read a lot of articles - and didn't find an answer.

http://scholar.google.com/scholar?q=telomerase+suicide-gene+promoter

http://www.spandidos-publications.com/ijo/21/3/661  (one of the newest)

With help of canadianer (thank you) I think I found the right article, so just want to share.

This study not talking specifically about telomerase, but about the same approach of using promoters that are upregulated in tumors - exactly what I looked for. Published in 2014.

http://symbiosisonlinepublishing.com/genetic-science/genetic-science03.pdf

  However, the therapeutic approach in humans is limited by
  low efficiency of delivering the suicide genes and concerns regarding
  safety. Thus the number of clinical trials in human patients has been
  limited and treatment benefits observed modest. An intensive research
  effort is necessary to overcome these obstacles and turn suicide gene
  therapy into real benefit for our patients.


Help in identifying marine specimen? I came across this specimen which I assume belongs toeither the phylum porifera or to the coelenterata.
Can someone please help me identify it?

The specimen was found in Ayodhya, India.

I am thinking it is the skeleton of a colonial large polyp stony coral. I am not certain, but I suspect a species of the Favia genus. Most likely one of these two species (see links for info and pictures):

Favia lizardensis
Favia rosaria


Worm type bug inside of stick? What is it? This bug was found on the wall of my closet in Seattle, Washington. It has been around 40-50°F lately, and it is winter. It looks like a tiny, brown, fuzzy stick/twig, but there is a hole through the middle of it. A tongue kind of thing comes out of the hole. The tongue thing is clear/tan and has a brown tip. The tongue is how it moves around and it looks like the tip sticks to the ground, and then it pulls the rest of its body/the stick part forward from there. It doesn’t seem to like it when light is shined on it (like from a phone flashlight) and goes back into the twig part when light gets shined on it. The twig part doesn’t seem to move on its own. The twig when the tongue is inside is about 0.5 cm.

It looks to me like the larva of a case-bearing moth. Despite the common name, the case is made by the larva, as seen here. What you are watching is the larva creeping out, then moving forward, bringing its case with it. Larvae of other moths make cases out of various kinds of hard materials, such as pieces of stick or grains of sand. Have a look at the possible duplicate noted above, which has helpful info.


IBD-value and IBD-fraction I have some questions about the IBD-value and IBD-fraction for two of the condensed identity states, $S_1$ and $S_7$.

My questions:

1) Is the IBD-value for the individuals i and j two (2) in $S_1$ and 2 in $S_7$ as well? (We can form the pairs aa aa in $S_1$ and the pairs aa and AA in $S_7$. The number of alleles in $S_1$ (and similarly for $S_7$) for individual i that are IBD with alleles of individual j is therefore 2)

2) Is the IBD-fraction ( or coefficient of relationship) 1 in $S_1$ and 1 in $S_7$ ? (We have the fraction 2/2 in each case since both alleles of each individual are IBD with the alleles of the other individual as described in 1) )

Picture source: http://openi.nlm.nih.gov/imgs/512/114/3579841/3579841_pone.0057003.g001.png

Edit: Comments about the figure: The dots represent alleles for one particular locus. When two alleles are IBD they are connected with a line. We look at two individuals i and j and consider the SAME locus in both individuals. There are only two persons in each of the states. In state $S_5$ individual j is homosygous and it's alleles are also IBD. One of the alleles of i is also IBD with the alleles of individual j. We therefore get the three lines between the alleles.

Definitions used:

IBD-value: "An Identical-By-Descent (IBD) value is the number of alleles which are the same because of descent from a common ancestor. Since each (diploid) individual has two alleles for a given (autosomal) gene, the number of them that are IBD with another individual can only be 0, 1, or 2."

Source:
IBD-value in pedigree with inbreeding

Coefficient of relationship: "..is the fraction of genes in two individuals that are identical by descent,..."

Source:
https://books.google.no/books?id=Q9ofvKZAmpEC&pg=PA35&lpg=PA35&dq=identicAL+BY+DESCENT+FRACTION&source=bl&ots=oOc4-PBzZg&sig=jJgJarUg36b4DbyT7sphDD6j_7c&hl=en&sa=X&redir_esc=y#v=onepage&q=identicAL%20BY%20DESCENT%20FRACTION&f=false

If I've understood the graphs correctly, then I think you are right on both questions. The difference between 1 and 7 is just that the alleles are in LD in 1 but not in 7


Is it possible to label a DNA molecule using a radioactive sulphur? The radioactive labelling of the DNA molecule is possible using radioactive phosphorus and tritium atom. But is it any how possible to label the DNA  molecule using a radioactive sulphur atom?

Yes, it is possible, and indeed this was the standard labelling procedure used in early Sanger sequencing.

You synthesise DNA using a deoxynucleotide with a sulphur replacing an oxygen on the α phosphate as shown below. This phosphate forms the phosphodiester link in nucleic acids so the sulphur is incorporated.

The image is of dATPαS

response to David's comments

Please note that:

DNA does not normally contain sulphur.
This technique is for in vitro labelling of DNA; as far as I am aware it isn't possible to label with sulphur in vivo.


Is nicotine toxic to humans? More specifically, is nicotine in the concentrations that smokers receive when smoking cigarettes toxic? I know that in great enough concentrations it can be toxic (but then, so can just about anything else, including oxygen) and I know that in plants it is used as a defense against insects and can even be used as an insecticide. However, it has always been my understanding that nicotine is irrelevant as far as the harmful effects of smoking go.

I recently had a conversation with another biologist who had just quit smoking and had done quite a bit of research on the subject. He said that nicotine itself is in fact bad for you and, therefore, that tobacco-less alternatives to cigarettes (such as electronic cigarettes) are still harmful because of the nicotine alone.

Does anyone have any more information on this? Perhaps some references? Or, even better, a detailed explanation of the pathways involved? Again, I stress, not about nicotine's toxicity in general but about its harmful effects on vertebrates (preferably human) at the kinds of concentrations one could expect to ingest when smoking.

I think its useful to say that nicotine is not very toxic to humans - cells don't die or get sick for typical smoking habits.  Secondary health effects are possible, but here is a toxicological profiles.

Nicotine is a toxin in large enough quantities and nicotine has an LD50 (lethal dose for 50% of individuals) of 0.5-1 mg Nicotine / kg of body weight.  So even a small spill on your skin of the chemical can be life threatening, but for smokers the nicotine itself is not dangerous.

Individuals who smoke intake about 1 mg per cigarette smoked.  So a small adult (110 lbs) can smoke 25 cigarettes in a short period of time (or all at once!) and just barely get to the bottom end of that limit.  Nicotine is water soluble and clears out through the urine at a fast rate though - half of the nicotine from a cigarette is cleared from  your system within 2 hours, which means that 4-5 pack a day smokers are not really killing themselves (from nicotine).

That being said, children are about 5-10 times more sensitive than adults, so even 5-6 cigarettes in an hour can be toxic.  That's quite a bit of smoking though.

Not all animals have the same relationship to the nicotinic acetylcholine receptors as humans do.  Nicotine is toxic to insects and will kill an insect in a matter of minutes or hours. Rats are about 50x less sensitive than people.

I think its comparable to the question of whether caffeine is harmful to people.  In the amount we consume it, sometimes up to grams a day, there is no obvious common side effect, but you figure that decades later it will show up as a problem - a difficult connection to prove.


Is there a biological basis for different accents? How did accents first develop? Was it climate dependent? or was it a social behavioural issue?

Is there any biological reason for the development of accents?

No. Accent is purely environmental. The ability to pick up the unique sounds of a language or variation of a language ceases around puberty: http://en.wikipedia.org/wiki/Language_acquisition

This is why adults learning a second language have trouble distinguishing the unique sounds of the second language. For learners of English, the "th" sounds and the difference between "l" and "r" can be difficult. For languages based on Sanskrit, there are a variety of aspirated/unaspirated consonants somewhere between "b" and "v" that English-speakers have a hard time distinguishing, much less imitating.


Cell-level selection and inheritance of acquired mutations I was reading about different levels of selection in Ridley's Evolution textbook (chapter on units of evolution) and saw that some organisms e.g. carrots are not Weismannist i.e. don't have separate somatic and germ lines and can make offspring with their somatic cells, and that this can in theory lead to cell-level selection because cell lines that outcompete others have a greater chance of leading to offspring and thus will be selected for. I think mutation that arises in a cell during the organism's lifetime and causes it to proliferate counts as an acquired mutation, but I've also read a lot that acquired mutations/characters aren't passed on a la Lamarck.

Is this a case where acquired mutations are passed on, and how does that fit with the usual concept that acquired characters aren't passed on? I know gene, individual, and kin selection are much more prevalent and Ridley says the cell-line selection idea is just theoretical, but what would this mean if it occurred?

Thanks :)

In any reproductive event, we transmit new mutations to the offspring. In absence of cell-line selection, whether the mutation occurred during a meiosis or a mitosis is of little interest.

In absence of cell-line selection

A big difference between acquired mutations and Lamarck's acquired inheritance is that under Lamarck's view point, characters are being adaptive. Under Lamarck's view point, individual try to perform some action, stretch their muscles and other organs toward what is optimal for their needs and this phenotypic modification is being transmitted. The classical example is the example of giraffes. Giraffes stretch their neck trying to reach for high leaves, their neck is getting longer and their longer neck is being transmitted to their babies.

With acquired mutations, in absence of cell-line selection, there is no reason for adaptive mutations to be transmitted more often than non-adaptive one.

With cell-line selection

Now, if there is cell-line selection, beneficial mutations (beneficial at the cell level) are more often transmitted. The mutational process itself stil remain "random" (see Are mutations random?) but selection will increase the ratio of beneficial to deleterious mutations. Now, mutations that are beneficial at the cell level are not necessarily beneficial at the organism level. A typical example is cancer.