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Is there any evidence that sexual selection may lead to extinction of species?
Darwin suggested that sexual selection, especially by female choice, may counter natural selection. Theoretical models, such as a Fisherian runaway process, suggest that evolution of preference and preferred phenotypes may drive each other in ever increasing speed.
Because one male may fertilize many females, one could imagine that natural selection against preferred but energetically costly phenotypes may be weak, and the whole process may not slow down fast enough (i.e., be sufficiently self-limiting). If male mortality is high and their number is low, the random fluctuations may easily cause the extinction of population.
Is there any fossil or experimental evidence that this may really happen?

TL;DR:

There is a dearth of actual experimental evidence. However:

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

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

First of all, this may be cheating but one example is the extinction because a predator species specifically selects the species because of selected-for feature.
The most obvious case is when the predator species is human. As a random example, Arabian Oryx was nearly hunted to extinction specifically because of their horns.

Please note that this is NOT a simple question - for example, the often-cited in unscientific literature example of Irish Elk that supposedly went extinct due to its antler size may not be a good crystal-clear example. For a very thorough analysis, see: "Sexy to die for? Sexual selection and risk of extinction" by Hanna Kokko and Robert Brooks, Ann. Zool. Fennici 40: 207-219. [STUDY #1]
They specifically find that evolutionary "suicide" is unlikely in deterministic environments, at least if the costs of the feature are borne by the individual organism itself.
Another study resulting in a negative result was "Sexual selection and the risk of extinction in mammals", Edward H. Morrow and Claudia Fricke; The Royal Society Proceedings: Biological Sciences, Published online 4 November 2004, pp 2395-2401 [STUDY #2]

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

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

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

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

The first example is a study on the Japanese medaka
  fish Oryzias latipes (Muir and Howard 1999 - [STUDY #5]). Transgenic males which had been modified to include a salmon growth-hormone gene are larger than their wild-type counterparts, although their offspring have a lower fecundity (Muir and Howard 1999). Females
  prefer to mate with larger males, giving the larger
  transgenic males a fitness advantage over wild-type
  males. However, offspring produced with transgenic
  males have a lower fecundity, and hence average female
  fecundity will decrease. As long as females preferentially
  mate with larger males, the population density will
  decline. Models of this system have predicted that, if
  the transgenic fish were released into a wild-type
  population, the transgene would spread due to its mating
  advantage over wild-type males, and the population
  would become go extinct (Muir and Howard 1999).
  A recent extension of the model has shown that
  alternative mating tactics by wild-type males could
  reduce the rate of transgene spread, but that this is still
  not sufficient to prevent population extinction (Howard
  et al. 2004). Although evolutionary suicide was predicted
  from extrapolation, rather than observed in nature, this
  constitutes the first study making such a prediction from
  empirical data.
In cod, Gadus morhua, the commercial fishing of large
  individuals has resulted in selection towards earlier
  maturation and smaller body sizes (Conover and Munch
  2002 [STUDY #6]). Under exploitation, high mortality decreases the
  benefits of delayed maturation. As a result of this,
  smaller adults, which mature faster, have a higher fitness
  relative to their larger, slow maturing counterparts
  (Olsen et al. 2004). Despite being more successful
  relative to slow maturing individuals, the fast-maturing
  adults produce fewer offspring, on average. This adaptation,
  driven by the selective pressure imposed by
  harvesting, seems to have pre-empted a fishery collapse
  off the Atlantic coast of Canada (Olsen et al. 2004). As
  the cod evolved to be fast-maturing, population size was
  gradually reduced until it became inviable and vulnerable
  to stochastic processes.
The only strictly experimental evidence for evolutionary
  suicide comes from microbiology. In the social
  bacterium Myxococcus xanthus individuals can develop
  cooperatively into complex fruiting structures (Fiegna
  and Velicer 2003 - [STUDY #7]). Individuals in the fruiting body are
  then released as spores to form new colonies. Artificially
  selected cheater strains produce a higher number of
  spores than wild types. These cheaters were found to
  invade wild-type strains, eventually causing extinction of
  the entire population (Fiegna and Velicer 2003). The
  cheaters invade the wild-type population because they
  have a higher relative fitness, but as they spread through
  the population, they decrease the overall density, thus
  driving themselves and the population in which they
  reside, to extinction.

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

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

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

We test the hypothesis that response to sexual selection increases the risk of extinction by examining the fate of plumage-monomorphic versus plumage-dimorphic bird species introduced to the tropical islands of Oahu and Tahiti. We assume that plumage dimorphism is a response to sexual selection and we assume that the males of plumage-dimorphic species experience stronger sexual selection pressures than males of monomorphic species. On Oahu, the extinction rate for dimorphic species, 59%, is significantly greater than for monomorphic species, 23%. On Tahiti, only 7% of the introduced dimorphic species have persisted compared to 22% for the introduced monomorphic species.
...
Plumage is significantly associated with increased risk of extinction for passerids but insignificantly associated for fringillids. Thus, the hypothesis that response to sexual selection increases the risk of extinction is supported for passerids and for the data set as a whole. The probability of extinction was correlated with the number of species already introduced. Thus, species that have responded to sexual selection may be poorer interspecific competitors when their communities contain many other species.

Many thanks for all articles! I'll take a look on it (though it would take some time).

This answer is an inspiration to everyone on all of Stack Exchange.  Thank you!

Relating to your last comment on random fluctuations in survival, a recent theoretical paper by Lee et al. 2011 studies the effect of mating systems on demographic stochasticity in small population. No empirical data there though. Their main conclusion is that polygyny (in relation with sex ratio) can lead to high demographic variance, therefore lowering stochastic population growth rate and increasing extinction risk. The general effect is known as demographic stochasticity, a sampling effect leading to random variation in realized demographic rates due to small population size.


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Smallest viable reproducing population
What is the smallest viable reproducing population, such as in a human population. By viable I mean a population which keeps genetic defects low (enough).
A very strongly related question: what is the expected number of generations a given population can survive?

http://en.wikipedia.org/wiki/Minimum_viable_population ?

The conservation biology literature has a great deal of information, particularly with reference to developing species survival plans (e.g., Traill et al. [2007] report a minimum effective population size of ~4,000 will give a 99% persistence probability of 40 generations).
Because the question specifically mentions human populations, I'll focus my answer on the genetics of small human populations, though considerably less information is available.
Hamerton et al. (1965; Nature 206:1232-1234) studied chromosome abnormalities in 201 individuals from a total population size of 268 from the small island of Tristan da Cunha. These authors report increasing chromosome abnormalities (aneuploidy; hypo- or hyperdiploidy) with age and suggest that it may result in decreased mitotic efficiency. This population is thought to have developed from a founder population of only 15. According to Mantle and Pepys (2006; Clin Exp Allergy 4:161-170) approximately two or three of the original settlers were asthmatic, which has led to a very high prevalence (32%) in the current population.
Kaessmann et al. (2002; Am J Hum Genet 70:673-685) present a more modern study of linkage disequilibrium in two small human populations (Evenki and Saami; ~58,000 and ~60,000 population sizes, respectively) compared to two large populations (Finns and Swedes; ~5 and ~9 million). The authors find significant LD in 60% of the Evenki population and 48% of Saami, but only 29% in Finns and Swedes.
Lieberman et al. (2007; Nature 445:727-731) discuss the potential for human kin detection to avoid inbreeding. Such mechanisms have been found in other species, "from social amoebas, social insects and shrimp, to birds, aphids, plants, rodents and primates." Lieberman et al. propose mechanisms contributing to sibling detection in humans, including "maternal perinatal association" and "coresidence duration." Beyond these behavioral cues, the authors also suggest physiological cues such as major histocompatability complex as playing a role.

I suspect the answer would definitely include a parameter that would state how 'diverse' the reproducing population is to begin with - including how heterozygous each individual is (versus inbred);  as well as across individuals -  i.e. how different these individuals are from one another.

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Do any birds have established "poke a predator's eyes out" behavior?
Is there a pattern/tactics of behavior in any birds species that consists of attacking a predator's eyes with its beak?
I'm looking for established tactics, not 1 or 2 anecdotal examples.

Not that it matters, but I arrived at the question when trying to answer http://scifi.stackexchange.com/questions/87740/how-came-fawkes-know-how-to-disable-basilisk :)

From this paper about black-headed gulls responding to a hedgehog:

The gull might peck the intruder, or strike it with its feet. Pecks were
  mostly directed at the hedgehog's head and might be delivered after a
  horizontal approach with the wings partly lifted.

Although not directed at the eyes specifically, they observed the birds directing attacks to the predator's head.
There's another paper (Ratner 1975) that also looks promising, but I'm on my home computer and can't access it right now

Any luck on the second paper? Thanks!

@DVK Sadly I don't have access to it at work either, sorry!

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Do the majority of fish lack scales on their heads?
Based on pictures, it seems to me that a vast majority of fish species that have scales do NOT have scales on their heads.
Is that fact true?
To make this properly answerable:

lets' define a "majority" as >70% of fish species. But frankly, I'm more interested in actual numerical answer than whether it passes some arbitrary threshold or not.
The universe which I'm interested in measuring the percentage are fish species that have "normal" (Cycloid and ctenoid is the technical term, I believe?) scales on their bodies.
If that's not specific enough, you can restrict the universe to species in Actinopterygii (ray-finned) that have scales.

Shouldn't a majority be 50% + 1? Also are you referring to species or to total numbers?

@Kevin - species, as the first bullet point notes. As far as 70% vs 50%+, the question came out of an argument, for which mere 50%+ would not be a convincing enough number, whereas 70% would. And without a specific number, this would be a bad SE question (too vague)

@DVK: there is really no argument that 50%+1 > 50%-1, hence it is the majority. But I'm just nitpicking.

(Should be comment, but rep=1.) This might be helpful (from Wikipedia): "The same genes involved in tooth and hair development in mammals are also involved in scale development." Mammals tend to have less hair on their face than on their bodies. If you can track down the reason for that, then you might have the same reason for fish, and then could use that to reason out your estimate.

Would also be nice to know (or at least think about) whether if this is the case it's because of synapomorphy (i.e. shared heritage) or convergence.

aren't they just much smaller and softer so harder to see clearly as scales?

A lot of fishes have scales on the opercle ("cheek"), and sometimes inferior to the orbit of the eye--but they are often very small. I'm not sure about overall patterns, or how common they might be. I could see a hydrodynamic reason for not having scales rostrally to avoid inducing drag, but not sure the literature agrees with the answer.

@Charles I was not the one who defined majority, just said that 50%+1 > 50%-1 , which is purely a math statement :)

I know Chondrichthyes (sharks and rays) have scales on hte head, their entire body is covered in tiny placoid scales. Don't know about other fish with different scale types.

I certainly agree with your general observation, but not being an ichthyologist, I can only offer a partial answer, based on a particular family of fish. Within the family Tripterygiidae, most species lack scales on their head, or have highly modified types of scales. A comparative study of 48 species showed that only 2 have "normal" scales of their head (Jawad, 2005).

The squamation pattern of the bases of the fins
  varies among species. The head is usually devoid of scales
  except for two species that have squamation with body-
  type scales (Matanui bathytaton (Hardy, 1989) and
  Norfolkia clarkei). Several species have head ctenoid scales
  modified into tiny spicules of different shapes (Acantha-
  nectes rufus Holleman & Buxton, 1993, Apopterygion
  oculus Fricke & Roberts, 1994, Axoclinus carminalis,
  Ceratobregma acanthops, Cremnochorites capensis, Ennea-
  nectes boehlkei Rosenblatt, 1960, Forsterygion malcolmi
  Hardy, 1987, Forsterygion varium (Forster, 1801), Karalepis
  stewarti, Matanui bathytaton, Norfolkia clarkei, Notoclinops
  caerulepunctus Hardy, 1989).

So far, I haven't found a broader comparative study, to support your general question. Someone more knowledge in the area and the literature can perhaps offer a more general answer. This is at least an indication that your observation might be correct.
Reference
Jawad. 2005. Comparative scale morphology and squamation patterns in triplefins (Pisces: Teleostei: Perciformes: Tripterygiidae). Tuhinga 16 (1), 137-168

Based on a lack of written evidence, in searching Google and Google Scholar, I believe fish have scales on their heads, where I'm defining 'scales' as 'solid, protective bony scales' [see below], and I'm assuming the fish heads are covered with solid protective bony Big scales.  I think a lack of scales on fish heads would be a fish fact that wouldn't be too difficult to find.

Some fish lack scales altogether, such as gobies and toadfish:
https://www.slideshare.net/gurya87/types-of-scales-in-fishes-44959366
This wikipedia article mentions scales repeatedly [examples below] but says nothing about a lack of scales on fish heads -https://en.wikipedia.org/wiki/Fish_anatomy

a.  The dermis is covered with overlapping scales.
b.  The dermis of bony fish typically contains relatively little of the connective tissue found in tetrapods. Instead, in most species, it is largely replaced by solid, protective bony scales.
c.  The outer body of many fish is covered with scales,

I can't find reference to it is not good justification.


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How to design an experiment with scent triggered memory recall in humans?
I've recently learned that scents can trigger memory recall in humans, and am thinking about setting up an experiment where I would attempt to induce memory recall through exposure to scents.
In order to help reduce the amount of experimentation required to actually trigger recall, I'm interested in - What kinds or qualities of scents have been demonstrated to trigger memory recall in humans? Are they pleasant smells/unpleasant,  sharp or subtle?
Is there any information about how long of an exposure is needed to trigger such recall? Is it 2 seconds, 15 seconds, an hour?

From personal experience and also being curious about this phenomenon I can add: Sometimes normally unpleasant smells get "pleasant" by triggering a pleasant experience. And it does work the other way round as well: specific situations can trigger "smell hallucinations" of former similar situations. All in all, this is a very tricky thing to study, so you best start by asking around how it works for different people. For me, it is instant, it does not matter if the smell is pleasant/subtle/..., the memory is more important than the type of smell and a situation also triggers a smell.

Originally I wanted to try this experiment during sleep, however, the K&R "Principles and practice of sleep medicine" 4th edition, on page 16, under "Olfactory system" mentions that both pleasant (peppermint) and unpleasant (pyridine) smells were poorly recognized during sleep:

Both well recognized during stage 1 sleep
Peppermint not consciously smelled in stage 2, stage 4 and REM sleep.
Pyridine not smelled in Stage 2 sleep
Pyridine occasionally smelled in Stage 2 and 4 sleep

It suggests that one conclusion would be that olfactory system of humans is not a good sentinel during sleep.

Scents can make memory recalls. We experience this very often, like when we repeatedly smell a good perfume in ,say a shopping mall , and when some person uses it too, we recall the memory of the shopping mall. This hqppens especially when the smell is associated with a very good or very bad incident.
For an experiment, you can expose yourself or someone to a particular smell ,either very good or very bad at any one time, like during examination or holidays for a couple of times. Next when the person again smells the scent he/she will be reminded of the previous exposure.
As regards to how long the exposure is required to trigger recall,it depends upon how strong the smell is (subtle smell takes ponger time) , how good/bad the memory is (very good or very bad memories will be recalled faster) and ofcourse on the memory associativity power of the person.


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Expected number of mismatches between two alleles of a gene in a population?
I can't find any article about the expected number of mismatches in alignment of two alleles of an assumed gene. Any reference or information about allele mismatch ratio (in a species or higher taxa) is appreciated.
suppose we have 10 alleles for a gene in a population. if we pick two of this alleles and align them, which number (percent) of positions are expected to be mismatches (not gaps and matches). Of course, I know that in conserved genes and domains mismatch number are lower and in different genes and species this numbers are different. I want some information from scientific resources talking about this numbers.

Maybe it's just me - but I am a bit confused about what you are asking. Do you mean the expected number of pairwise differences which separate two genes samples from a population (population genetics)? Or is it specifically about the error in nucleotide alignment (bioinformatics)? Or maybe neither?

@user438383 suppose we have 10 alleles for a gene in a population. if we pick two of this alleles and align them, which number (percent) of positions are expected to be mismatches (not gaps and matches). Of course, I know that in conserved genes and domains mismatch number are lower and in different genes and species this numbers are different. I want some information from scientific resources talking about this numbers. I add this comment to question for more explanation.

I think the question needs to be more specific. There are plenty of resources dealing with sequence alignments, and, as the question correctly points out, it depends on the gene, the organism, etc. It is not obvious what one wants to know: how count the mismatches? How to estimate their frequency from the mutation rate and phylogeny? Something else?

Still not sure exactly what you mean, but this question might be what you need.

I think that the question is difficult to answer in the current phrasing. However, I will show how it might be easier to answer by filling in some blanks and defining some terms.
I am going to define as an "allele" any nucleotide difference between two sequences. This is the molecular genetic definition more or less. I am further going to interpret "mismatch" as also including sequence gaps, as in the case of indels your alignment will include gaps. I am assuming that you are talking about aligned sequence differences, because you mention alignments. I am going to ignore the focus on "genes" because at the molecular level visible in alignments, alleles are not necessarily tied to annotated genes (even though they are usually introduced in that context).
So in this case, if you assume that most alleles consist of single nucleotide variants (probably not true, but a helpful simplifying assumption), you can deduce that nearly all "alleles" thus defined will differ from each other at a single nucleotide position. A larger and more complex genotypic difference (for example a microsatellite variant or a transposable element (TE)) will involve a proportionally larger number of mismatches (i.e. gaps).
Indeed, if we look at the wikipedia page for "allele":

At the lowest possible size an allele can be a single nucleotide polymorphism (SNP).[7] At the higher end, it can be up to several thousand base-pairs long.[8][9]

You might however mean something different. It's possible that the question is rather something like this:
How much segregating genetic variation of an organism (say humans) consists of single nucleotide variants (SNVs) vs. larger/more complex variants?
That's a somewhat different but much more answerable question. It is unfortunately limited a bit by our ascertainment bias in favor of SNVs, which are just easier to find. But the best estimates that I'm aware of suggests that there are probably slightly more microsatellite variants than SNVs, and some work suggests possibly a similarly large number of large-scale repeat variants (such as TEs).
I can imagine yet another interpretation, which might be something like:
If we align two (or 10, or however many) homologous sequences of defined length drawn from a natural population of an organism (say humans), at how many positions can we expect the aligned portion of any pair of sequences to differ per base pair?
This is more straightforward: the alignable portion of the human genome is expected to show approximately 0.1% differences. However, this is pretty much only counting SNVs. This will vary from species to species. Off the top of my head, I remember that interfertile Arabidopsis thaliana strains can differ by anything from 0.1% to 1% per aligned base.

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How does toluene inhalation damage the brain?
We just had a discussion about toluene abuse. It is known, that people inhaling toluene for a long time have significant brain damage, including  decreased intelligence.
I found that toluene is a lipid solvent, and that it can damage the myelin. However, myelin is only present in the white matter, but intelligence is related to the grey matter which does not contain myelin.
Is there any indirect damage, or did we miss some important point in this case? Second, how does toluene get to the brain? Is it able to infiltrate from the nose through the mucous membrane, or is it carried in the blood? I am just curious.

Unfortunately, saying that white matter doesn't relate to intelligence is like saying that the only factor in how long it will take to drive from New York to California is the condition of your car.

After crossing the blood-brain barrier, toluene, along with other volatile anesthetic agents, had been previously thought to inhibit neuronal transmission by causing a change in membrane or membrane protein conformation. Recent research has shown that interactions with several key brain neurotransmitters, mainly γ-aminobutyric acidA (GABA), to a lessor degree glycine, and possibly dopamine, are responsible for the clinical effects seen. Postmortem studies along with magnetic resonance imaging (MRI) findings have shown diffuse white matter demyelination and gliosis (solvent vapor/toluene leukoencephalopathy), which is postulated to be the end product by which chronic toxicity occurs, although the exact mechanism by which this occurs remains unclear

(McKeown at al. Toluene Toxicity).


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Why do dendritic cells have CD4/CD8 on their surface?
Why do dendritic cells have CD4 or CD8 antigens on their surface? What is their function without the presence of a T-cell receptor?

There is no direct connection between CD (cluster of differentiation) receptors and T-cell receptor (TCR).
CD-receptors are used to label and distinguish different cells belonging to immune system: macrophages, T- and B-cells etc. Dendtritic cells play a significant role as antigen presenting cells and belong to vertebrate (and human) immune system and thus bear certain CD receptor.
These cells participate in the process of learning a new antigen by the immune system. During the very first phase the antigen is taken up by these cells, cleaved and processed. Depending upon the antigenic properties of the molecule it can be recognized as a valid antigen. In this case dentritic cells participate in the process of antigen presentation, where this new antigen bound to the MHC receptor is expressed on the cell membrane.

TCR is the protein that binds to this complex (MHC + antigen) and as long as this binding takes place the signal about antigen is propagated further to the immune system (leading to formation or augmentation of immune response depending upon the cell type which connects to this complex).

This doesn't answer the question.
The classic explanation for the function of CD4 is that it's a co-receptor for MHC II (along with TCR), and likewise CD8 helps TCR bind to MHC I.
Since DCs don't express TCRs but do express CD4 and CD8, the function of these proteins on DCs is interesting!

I believe rather than canonical involvement in T cell activation the question was what role does CD4 and CD8 have in a non-T cell population. Here is an article that provides some interesting insight:
CD4 and CD8: an inside-out coreceptor model for innate immune cells
http://www.jleukbio.org/content/86/2/251.full

While the linked article may be useful, you should add some explanation in your answer rather than just providing a link.

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Exercise causes number of cell divisions to approach Hayflick limit faster? And hence shorten life expectancy?
A world class athlete spends a lot of time performing intense exercises.  Correct me if I'm wrong, but I assume that these intense exercises causes significant damage to the athlete's cells, but with proper nutrition, they are able replenish these cells with stronger ones.   This process of destroying and re-creating cells causes cell divisions to approach the Hayflick limit faster, and hence shorten the athlete's life expectancy.
I also heard that caloric intake causes the number of cell divisions to approach the Hayflick limit faster.  World class athletes generally consume substantially more calories than the average individual, which also contributes to a shorter life expectancy.
So for this reason, is the life expectancy of world class athletes generally shorter than the average individual? And what about casual athletes?
Edit
If world class athletes live longer lives than the average individual, why is this so despite performing activities that expedite the deterioration of telemeres, and hence, approach the Hayflick limit faster?

I don't know about the Hayflick limit in humans, but Olympic-class athletes tend to live longer than average, as long as it wasn't a contact sport: http://well.blogs.nytimes.com/2012/12/19/live-as-long-as-an-olympian/

Ok, then i guess i should revise my question to ask why despite doing things that expedite the deterioration of telemeres, they live longer lives?

not sure that exercise causes most cells to divide more - myocytes dont i think...  I think excessive exercise can shorten life due to stress and wear and tear.

As I know there are not many people can live as long to reach Hayflick limit - most of them are dying earlier as a result of heart diseases, cancer, or accidents. A world class athletes have a healthier way of life then odinary people: they have more physical activity, better food and have a visit to docter more frequent.  So I think it is a reason of their longer life.

Athletes who work too hard can actually shorten their lives, but for the most part exercise does prolong one's life.  Neither of these effects probably have to do with the Hayflick limit tho.

Following damage to muscle (e.g., as a result of strenuous activity) the injured fibers are removed (by immune cells) and then replaced by new myofibers (individual muscle cells that join to create new muscle tissue). This is why for a few days after exercise your muscles can be sore - it is the tissues being initially cleared of damaged cells and repaired.
Muscles, like other tissues, have resident stem cell populations ("satellite cells") that are used to replace damaged cells.
Stem cells have potentially indefinite replicative potential, as they express telomerase and thus do not have a traditional Hayflick limit.

Volonte D, Liu Y, Galbiati F. The modulation of caveolin-1 expression controls satellite cell activation during muscle repair. FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 2005 Feb;19(2):237–9.

I think there's another point here that the cells repaired do not divide and so the tissue in general does not have cell division as a result of exercise.  Even healing from injury probably has a minimal impact in this regard as well.

@shigeta the injured fibres (fused myogenic cells) are removed prior to "healing" (replacement with new fibres), or so I understand it. There may be degrees on damage that can be repaired without total removal, but generally I think the old is cleared to make room for new, stronger fibres (hence muscle being stronger after training (i.e. damage following exercise))


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How long does Lentivirus take to express in vivo mouse neurons?
Does anyone know how long it takes for a standard Lentivirus vector to express its genes (under a strong promoter such as CAG, CB7, etc.), after injection into the brain of a mouse?
By hearsay I think it's 2 weeks for full expression, is that true?

i also heard that it takes a week. but you should frame your question better. this looks like a survey

This depends a lot on what you are expressing (such as how stable it is), and where you need it (soma vs dendrites vs axons, and whether it is trafficked actively in the cell).
For optogenetic constructs, our lab has typically seen near-peak expression around 3 weeks, though expression may be suitable earlier, and toxic later.


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Can a brain be damaged by overstimulation?
I am wondering what, if any, long term health effects there are from high levels of brain activity.
I don't mean cases where a brain is being artificially stimulated, but rather where there is a high (as in the high end of normal, not as in shell-shock) sustained level of sensory input, or simply that the brain in question is "thinking too much".
Assuming a person could sustain high levels of neural activation, is there a chance that the brain could "strain" itself or somehow "wear out" or come to some other kind of harm?

(This is such a difficult question to begin answering in any satisfactory manner, though I think can be addressed for pedagogical purposes in line with the aims of this SE.)
Before we address the question, I think it is prudent to think about the difference between stimulation and activity. A neuron can be self-activating without external stimulation, or it can be highly stimulated by sensory input and yet have low or inhibited activity. You do not specify, so I think the discussion must necessarily be very incomplete on this topic.
Your question is also naturally a little unclear and difficult to answer methodically, especially because 'damage' in this case is a very subjective term. As with all biological systems, there are self-protective mechanisms and reflexes and feedback circuits in place to prevent 'you' or your brain from overdoing anything. A dysregulation in neuron activation, or activity, would probably be a state of illness, such as having a seizure. I don't think it is possible for a typical person to expose themselves to sensory extremes without consequently feeling tired or bored as a result (e.g. looking into a strobe light or listening to loud music for inordinate amounts of time), which may be the result of an internal homeostasis, just like blood pH or blood sugar level, though regulated through physiologically-dependent behavior (sleep, concentration levels, apathy, etc.)
More strictly and scientifically speaking, all activity wears all tissues, including the brain. This would make 'brain activity' a process contributing to aging. However, once again, one can interpret anything as 'damaging'; breathing is damaging (oxidation! the cellular definition of wear-and-tear), but it also sustains you. Calories sustain you, but caloric restriction extends lifespan in virtually all animal models.
A recent publication in Nature (Oct 2019) suggests that the global inhibition or decrease of all neuron firing seems to be related to increased longevity which may suggest the opposite case to your question: lower neural activity may lead to extended lifespan. This suggests, though does not demonstrate, that over-activation may contribute more 'damage' and accelerated aging, compared to lower levels of activation. This conclusion is also based on evidence associated with a global - whole-central nervous system - effect, and does not indicate that one should under-stimulate parts of their nervous system to achieve the same result. Also, keep in mind that stimulation and activity are entirely separate things, so such a conclusion does not answer your question.

Thank you for attempting to answer. I have edited the question to clarify that I am asking about high levels of activation (and assuming that high levels of stimulation could be one cause).


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How strong is spider silk?
Spider silk is pretty darn strong and all sorts of comparisons are made to steel. I'm more curious about the various moduli of spider silk and how it compares to other materials. What is the Young's modulus of spider silk? What is the bulk modulus of spider silk? What is the shear modulus of spider silk? In general how do those moduli describe the material properties of spider.
A simpler way to ask the question, what does it mean when it is said that spider silk is strong?

I do recall that (at least some) spiders produce two variants of silk, one sticky and one not - the latter being used in construction of the web.


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Does precipitation influence the UV spec reading?
I have been checking my sample for Hydroxyl radical scavenging activity. I have dissolved Hydrogen peroxide in Phosphate buffer. My sample is clear and reagent is also clear but when I have mixed my sample extract with Hydrogen peroxide reagent a precipitant is formed. Control is very less than solution that is kept for reaction to proceed. So I am getting an answer in negatives (230 nm). Is that formation of precipitate affect the absorbance of the solution? Does precipitation increase the OD value compare to clear solution?
 Mine is mushroom powder. It is extracted with Ethanol. Extract is dried and finally it is dissolved with solvent above said. That has been used for Hydroxyl radical scavenging activity. Hydrogen peroxide 0.01 milli molar reagent is prepared with Phosphate buffer. First i have taken reading for H2O2 and added extract kept for ten mins and took reading. in 230 nm..

what is your sample and how is it stored ? Is it DNA dissolved in TE/water or cell extracts ?

also.. please describe your protocol so that the problem can be understood better

this question would be much more suited to Chemistry.SE

@MattDMo UV spectroscopy is a very common technique in the biolab, so this is certainly on-topic here. Migration is rather disruptive, so we try to avoid it for questions that are not actually off-topic on the source site.

Perhaps you could help us by explaining the basis of the assay? Am I correct in thinking that UV promotes OH radical formation? And that hydrogen-bonded OH radical absorbs at 230 nm? So is the UV beam from the spectrophotometer both promoting radical formation and also allowing the measurement of how much there is of it? And finally, do you get the precipitate if you leave out the peroxide?

No.. precipitate is forming when sample is added..

Yes UV promotes and it can be read in 230 nm as I have referred earlier.

The answer to the question as asked is that yes, any precipitate will affect the value that you are reading in your spectrophotometer. The basis of spectrophotometry is that light passes through a sample, and less light emerges than the amount which entered. The amount of light that has "disappeared" is used to deduce something about the solution in the cuvette. Light can be absorbed by chemical groups (this is the basis for e.g. DNA having an absorbance value) or it can be scattered by particulate material (this is the basis for measuring the cell density of a bacterial culture). If you are trying to make a measurement of the first type (absorbance) and you get a precipitate your reading will be distorted by the light scattering effect.
Precipitates are incompatible with spectrophotometry.
As the comments have noted: if you give more details of your protocol someone may be able to help. Phosphates are, of course, notorious for generating unwanted precipitates.

Thank you for response. Mine is mushroom powder. It is extracted with Ethanol. Extract is dried and finally it is dissolved with solvent above said. That has been used for Hydroxyl radical scavenging activity. Hydrogen peroxide  0.01 milli molar reagent is prepared with Phosphate buffer. First i have taken reading for H2O2 and added extract kept for ten mins and took reading. in 230 nm..


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How did the molecular machinery for recombination originate?
I'm wondering about the origins of genetic recombination. During crossover new chromosomes are created. They have different allele combinations from the original two chromosomes. This process allows the combinatorial explosion needed for biological diversity. I am puzzled by the accuracy of this very complicated process of generating new genetic information.
Starting from single cell, When did the first genetic recombination appear? How did it come to existence? In my understanding, it could not have been the result of evolutionary process since genetic recombination must be done right at the first attempt.

"In my understanding, it could not have been the result of evolutionary process since genetic recombination must be done right at the first attempt" is patently false, but the rest of your question is a good question. As far as I know a definitive answer is unknown but it is an area of active research.

If only we knew when the fundamental processes in cells arose! What kind of smoking gun did you expect for this one?

https://en.wikipedia.org/wiki/Chromosomal_crossover#Origins


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What actually are thoughts?
The human brain consists of neurons that transmit impulses like wires that conduct electricity.I am confused about where are our thoughts stored and what really are thoughts? For example if I think about space, what is actually happening in my brain, and in what form is my memory that there are black holes in space, stored?
After doing a little bit of research I somehow came to the conclusion that thoughts are nothing but the electro-chemical reactions that are triggered by external stimuli and Hippocampus is responsible for storing long term memory. But I was unable to understand what the following paragraph means:

"The hippocampus helps to solidify the pattern of connections that form a memory but the memory itself depends on the solidification of connections between the individual brain cells".

Please explain it. Am I correct so far? Please help.

In short -  it's more complicated than that ;)

@Mithoron, am I correct when I say that thoughts are nothing but the electro-chemical reactions that are triggered by external stimuli, ?

I think we don't know how thoughts arise from incredible amount of chemical reactions in brain. And of course internal stimuli are important.

@Mithoron, Can you please frame an answer explaining the above paragraph, :)?

I know nothing about neuroscience! Your question is on-topic here but I thought I would let you know that your question would also be a very good fit for CognitiveScience.SE

Not just hippocampus, but even cortex is involved.

But what are thoughts? :) I don't think the question is well defined yet. If you indicate a specific "thought" or "thought process" in mind, you may get a better answer.

I have edited the question. Please have a look.

The question is still ambiguous. Memory can be explained as done below in terms of short-term memory by @WYSIWYG. Long-term memory, and 'thoughts' are a whole other matter and involve large areas of the cortex, as mentioned by WYSIWG. This question needs work.

What does the "black holes" part mean?

@HDE226868 OP's reference to black holes isn't important. I think it should be read as "How is my knowledge of some arbitrary fact, X, stored?"

The hippocampus helps to solidify the pattern of connections that form a memory but the memory itself depends on the solidification of connections between the individual brain cells".

This refers to the phenomenon called Long Term Potentiation which regulates synaptic strength between neurons. Certain patterns of firing (high frequency) causes the post synaptic neuron to strengthen the synapses. One way of doing that is by increasing the number of receptors (Usually NMDA receptors). Due to this, the response would be stronger in the next firing event. You can imagine its effects- more number of times you read a passage better will you remember it.
Hippocampus is involved in this process (it is one region where a lot of synaptic dynamics happens) but consolidation and long term storage of memories is handled by the cortex. Essentially what happens when a memory is formed is strengthening of synapses.

Thanks @WYSIWYG, but I could not understand what "...patterns of firing.." means.

@Abdullah Pattern means the how the frequently and at what intensity is the synaptic signal given. I said patterns because in certain cases continuous firing can also cause weakening of synapses. This is called Long Term Depression.

+1.Moving on to my original question,is it yet to be discovered what thoughts are and in which form are they stored?

@Abdullah To an extent. The term "thought", itself is quite broad.


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Help to identify this large, slow-growing mushroom?
Here in my backyard in Southern California, there appears to be this relatively smooth, mottled-colored dome-like structure a little larger than a chicken egg in the dirt. Can anyone identify it? Is it some sort of insect nest or a multicellular fungus?

Edit: After a couple weeks, I've observed some changes. It appears as though this is definitely a fungus and it has been growing taller out of the base. I also see a few feet away something that looks a little different, but not that different, which appeared even at first to be more mushroom-like. Right now the closest thing I could find online is something like a Shaggy Mane. Here are the new photos:

Edit #2: It's been about three more weeks, and the fungus has continued growing larger. Also I am pretty confident that the second one is also the same species. Both have been growing longer and have started to crack at the top.

It looks like a fungus to me. It might be some sort of stinkhorn, and in that case you should see it taking form (and smell) soon!

@picapica How are you concluding what it is? Can you give more information?

Hmm, I'm obviously not confident enough to post a proper answer. Just that it looks similar to mushrooms I've seen. Search for "stinkhorn egg" to see pictures of the early stage of the fruiting body. Unfortunately I don't see anything that looks just right. Have you tried poking it to see what texture it has?

@picapica I haven't, a little afraid to poke it.

understandable! but, nest or fungus, if you have it in your back yard you can keep an eye on it and see how it develops! i'm really curious, you must promise to keep us updated. another mushroom thought: perhaps some sort of puffball?

@picapica I'll see if it changes appearance. My brother told me that it is possible he remembers seeing it a few months ago, but I don't know for sure.

@picapica it still looks the same.

weird! hope you find out eventually...

@picapica OK it is clearly a fungus. The base has been growing longer.

Cool! Maybe you'll be able to answer your own question soon then. Or post pictures to make it easier for someone else to answer...

@picapica I'll probably add a picture. I think it looks a little like a shaggy mane mushroom, something like Coprinus comatus or Coprinus narcoticus.

This fungus is known as a puffball, although that is no longer a taxanomic order. Some of these fungi don't have small openings through which the spores disperse, but they burst open when the spores are ripe. This proces can be clearly seen in your last pictures. The brown stuff below the cracks are the spores. I think when you press it, the brown stuff will come out
Looking at the appearance, I think this is a Calvatia, but as I am unfamilair with the American fungi I can't name a species.

Is there anything else I should know about it? Should they be removed, are they edible? Does it vary?

It varies. Some are edible when young, but yours isn't any more. I see no reason to remove it.

OK thanks. But wouldn't leaving them cause more to grow?


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Species Identification: Bulbous root on plant, Southern California, USA
In Southern California, I was pulling out some roots and grasses and weeds in our backyard, and I noticed something weird. It appeared like there was a grape-sized bulb of something connected to one of the roots below the top layer of dirt. I didn't puncture it or anything, but do you have any idea what this could be?
It reminded me of two things: an air sack on kelp and a potato.
Edit: I took some more photos, and I tried to break it apart. I was able to break it in half with one hand, easier than a potato but harder than a grape. It was a little juicy inside. I took more photos too.
Edit number two: We have dandelions. Does this seem like it could be a potato dandelion?

Edit #3: So we have a lot of Dandelions and I thought these roots appeared to be connected to dandelion plants, so at first I thought they were potato dandelions. However, we I pulled out a different plant nearby, and it had very similar looking tubers connected to the roots. It was a small plant, but here's the picture, and a picture of a larger plant that I think is the same species as this one, but mixed with a bush. Can anyone positively identify it?

Edit #4: Here's more pictures of the plant I'm seeking to identify, which appears to be a more developed individual on a neighbor's property, and it even has berries:

Does it taste like a potato?

@GrahamChiu Does it look like a potato? I'd rather not taste it or touch it for that matter.

I do believe this is a potato dandelion. An answer that can confirm this would be nice.

This is an Asparagus species, and the root bulbs are storage organs. Unfortunately, I can't identify the species. There are 219 accepted species currently in TPL. I presume this is an ornamental plant. As far as I can see, the species is not recorded as naturalized in California.

Are you sure? Nothing on the plant looks like asparagus. It does appear to have berries on a more developed plant that I saw in the neighborhood.

Actually maybe you're right, I did an image search for a random one of those species on your list, "Asparagus altissimus", and that looked kinda like this and had berries too. Are the berries and tubers and plant all edible do you know?

I am aware that some Asparagus species root bulbs as well as young subterraneanous shoots are famine food in parts of Africa, but I don't know about their any of their properties, i.e. if they contain anything which might be irritating or even poisonous to humans.
[Edit: Young shoots of A. officinalis, of course, are cultivated for human consumption, as you will know.]

Those are root nodules. They grow on root of plants (primarily Fabaceae) . They aren't harmful (but I'm not recommending to eat them). They are natural adaptation that ensures the plant's survival. They are important because they store water too for the plant during periods of drought.

Root Nodule
  this is an asparagus fern. a very invasive plant.

[UPDATE]
About the plant's specie, well, I can't determine. I'm not good at determining plant specie by roots.

@rg255 His question was "... but do you have any idea what this could be?" and I answered that. About identifying the specie (which was mentioned in the title), I can't say from what plant are those "balls" because I can't identify clearly the roots/leaves in the photos. He just said "...I was pulling out some roots and grasses and weeds in our backyard..." But if you do know what kind of plant that is, then feel free to drop an answer or add it and edit my answer.


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Any evolutionary explanation for human blood groups?
What is the explanation of people having blood types from an evolutionary perspective?

I don't think blood group has any selective advantage (except for cases like duffy). IT seems like a neutral polymorphism that remains in the population.

Oh I didn't know about duffy. Thanks for sharing.

Researchers have puzzled over the selective explanation for the ABO polymorphism at least back to the 1950s. Multiple lines of more recent evidence, including the very old age of the ABO polymorphism and (perhaps) multiple convergent evolution events, suggest that the ABO polymorphism is maintained by balancing selection (E.g. Saitou and Yamamoto 1997, Segurel et al 2012). As best as I know, is no general consensus on what is driving balancing selection, though some researchers have argued that the selective agent is Plasmodium falciparum (e.g. Cserti and Dzik 2007).


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Difference between biological control and introducing species for conservation?
I have a biology assignment and we have to explain various methods and strategies for conservation, two of which are:

Biological control
  Introduced Species

What is the difference between these? I was under the impression that they are essentially the same thing – biological control being the introduction of species to predate pests (eg. the abysmal failure of the cane toad).
Any clarification would be great.

After talking to my teacher, he said that biological control is the introduction of species to control another species, however species may be introduced for other reasons (the "Introduced Species" method), such as to "assist an ecosystem cope, flourish or re-establish itself."
The example he gave was the introduction of South African veldt grass to Western Australia in order to stabilise sand dunes, so that they can later be built upon further (eg. plants which may not perform well in sandy, unstable soil can then be planted).
Hopefully this helps anyone else with the same problem.

Biological control does not have to be with an introduced species.  It can also be accomplished by either artificially inflating the number of existing predators.
E.g.  Spruce bud worm has a natural predator in the form of a tiny wasp.  But budworm can spread through a stand faster than the wasp can.  By moving popluatins of the wasp to the forefront of the budworm advance, you get most of the 2nd generation budworms.  The trees have a bad needle year but aren't killed.
It can also be done with habitat modification.  If you create conditions that favour the existing predator, then there are more predators in place.  E.g.  create places for ladybug overwintering to reduce aphid populations. (I have no idea if this would work.)
Anohter example -- although ecological controll may be better than biological -- I had a significant mosquito problem.  Lots of small puddles in spring.  I created a permanent pond.  This has resulted in much smaller mosquito population.

The pond is a local year round water supply for insectivorous birds.
The pond is by far the largest water body around, so tends to get most of the mosquito eggs.
The pond now has a permanent population of boreal and chorus frogs.  Tadpoles of these make it tough to be a mosquito larvae.

Is this species introduction?  Only if you consider immigrant species from neighborin populations to be introduction.


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What is the viability of Intelligent Design as a supplement to chemical abiogenesis and Darwinian Evolution?
First of all I am not endorsing Intelligent Design (Wikipedia link); I'm asking this because I (someone who does not have a background in biology, organic chemistry, or philosophy) got into a conversation with someone who does endorse it, and I'm trying to see his point of view as far as rationality can allow. Second of all, I apologize for any vagueness; Intelligent Design isn't well enough defined as a theory for me to help that. I also apologize if this is rehashing content already plentiful on the Internet, but for my purposes I can't simply depend on the likes of Wikipedia or Talk Origins, so what I'm looking for here instead is to take the opposite approach and see, based on your informed minds, if there could possibly be any reasonable likelihood of an ideal ID theory being adopted.

I'm looking for the most favorable consideration for what ID might be
  if it were best developed as a viable hypothesis or theory to get an
  idea of how far such a discussion is worth taking. An unbiased,
  informed Devil's advocate, if you will.

My cursory investigation of what Stephen Meyers (video link) and Michael Behe (video link) say (correct me if I'm wrong) seems to be that either the first cell was likely designed intelligently judging by the complex code of DNA and that evolution took course from there, or that the first cells were made and many instances of evolution were from some kind of intelligently guided mutations as was needed to make "irreducibly complex" cells or body functions (whether the guidance stops after the Cambrian or continued even to the point of making different types of new bacteria and different types of apes/humans or whether every single mutation and adaptive ability is being guided, I'm not sure if they're at any consensus, and that's why I don't know if I should stop my question at abiogenesis or include evolution). The person I spoke with also brought up some specific claims (everything looks designed, DNA has ordered, complex information, blood clotting is irreducibly complex, ID can and has make predictions like decades ago that "Junk DNA" wasn't junk) that I don't need you to debunk (I have Google).
But if there could be any possible support or truth to any of the above, I would appreciate knowing about that. (Again, Devil's advocate so I can be informed and understand where the points come from.) Reading an ID book alone, it would be in places hard to know where they differ from actual scientific conclusions. After all, when someone who seems to know what they're talking about and can explain something in technical detail says that something is impossible or extremely unlikely, it's hard for me to know why they would be wrong (are they ignoring other possibilities? misrepresenting facts? are they really right and just getting the cold shoulder from an atheistic scientific community because it implies a deity?). So I focus on mainstream sources, even if they don't bother entertaining ID and leave me ignorant of its possible virtues. And thus I'm hoping someone from this informed community might enlighten me to what those possible virtues might be.

Regarding "junk DNA": The claim of 80% functional DNA is using a very very broad definition of "functional". The claim is strongly debated - for a non-scientific piece see http://www.guardian.co.uk/science/2013/feb/24/scientists-attacked-over-junk-dna-claim . Even if it were true, I do not see how this supports ID.

I'm not certain that this is suitable for a Q&A since you have a large number of questions bundled into one. As it reads now it deals with an entire "theory", and this cannot be explained in a single answer. Would it be possible to narrow down to the aspects that you are most interested in (and you could ask follow-up questions afterwards)?

Oh boy. @Bitwise, that’s a pretty bad article, even the title gets it wrong – ENCODE does not claim that junk DNA is “vital to life”. The “80% is functional” claim says nothing about necessity of that function. If ENCODE had made this claim (and if it were correct) then it’s true that the ID proponents in the 60s would have made a correct prediction (albeit for the wrong reasons). As it happens, this claim is a strawman.

If you look at any actual biological systems, its pretty clear they are too complicated to have been designed! Who would design a system with so much waste, multiple receptors and multiple ligands in each system, only a handful of which seem to actually do anything. The more you look at biology, the more absurd the idea it was designed!

@KonradRudolph I completely agree, and this is the exactly my point. I am not saying that the "80% functional" claim is incorrect, just that it means something very different than what the ID people think it means, and it doesn't support ID in any case. Sorry if that was not clear.

@Nick that just disproves the idea of intelligent design :).

You may want to have a read through this wonderful post. Specifically, point 19.

@fileunderwater I suppose I may need to do that, but if there could be any support from any point, that would be fine in my book as an answer here. Everyone else, thanks for the links and insights, keep it coming.

@terdon Thanks. Point 10 was also relevant (though I'm going to have to read the thread he linked to because there he dismissed the probability argument tersely). As was point 22. Regarding point 19, this may also be explained to me as I read through the thread from point 10, but correct me if I'm wrong, but Meyers might have, at least weakly, met his first two criteria of point 19 (Criteria: Ordered information; Methodology: Sequence DNA).

@fileunderwater I was thinking more about your suggestion, and upon further consideration I think this is indeed the one question I want answered. I have found talkorigins.org to have suitable arguments against the individual points above, but the question I indeed am looking to have answered is is there any (non-specific or specific) way that Intelligent Design could be imagined to be refined and viably fit in with Evolution or Abiogenesis (short, of course, of far-fetched speculated data like God appearing to everyone).

@AL You can always go the philosophical route and claim that an omniscient god would know that by creating a universe in a certain way how the randomness would produce human life through random processes. But there would be no testable predictions from this, since its indistinguishable from a situation without the omniscient god. That's a question for philosophy.stackexchange though!

I think the issue with Intelligent Design is not so much that its patently proven wrong.  On the contrary, the problem is that it not a scientific hypothesis and so it really isn't a scientific question.
If I may, the basis of the scientific method, as formulated by Karl Popper, but commonly in use today, is that science is the putting forth of theories of cause and effect which are testable (or if we are being precise, falsifiable).
That is to say, you put forth a theory such as 'God/some diety figure made all living things' and then you perform an experiment which can differentiate whether the hypothesis or its null version (i.e. 'no intelligence is the source of life / biology is the result of accidents') is more likely true.
This question will not be testable in a way to answer enough of the reasonable skeptical questions ( or at least so far it has not).  Experiments have been tried, but they are often not acceptable to everyone.  For instance the idea that some biological structures such as the eye or the flagellar motor are too complex to have evolved through a typical Darwinian process which involves a series of small changes are almost biological theology - one can always hypothesize a more inhuman God (probably appropriate) who acts and 'thinks' in such an inhuman manner that anything you see could be created/inspired.  While I think you should feel free to believe either way, I also believe that this is not an argument that can be won or lost.  The tendency for any experiment to confirm both the hypothesis and its inverse seem inescapable.
That is to say, that biology and physics will ultimately fail where philosophy and logic also did in proving the existence of God, besides the less interesting truism that if God does exist, the deity is consistently elusive to proof.
On the other side of the coin, the proof that life has emerged from naturally occurring phenomena such as lighting strikes in a prebiotic environment are interesting since it shows that nucleotides and amino acids might have been available without metabolic pathways to synthesize them.  In its way, the molecular origins of life on earth is a question which is really testable only in theory.
Anyone who thinks they are going to re-create the event of the beginning of life itself is scientifically on thin ice - the prebiotic environment may have extended to the entire surface and atmosphere of the earth as well as down into mud and bodies of water and sat incubating for maybe hundreds of millions of years.  The idea that the fundamental moment of life generation is just going to show up on a well chosen set of conditions in a 500 ml flasks with some electrodes attached is an idea that workers in the field don't even entertain.
Until such an experiment produces life, the work will have to rely upon the idea that there was a moment in time where the necessary elements came together.
This being said, cosmology, biogenesis work has approached the moment of the genesis of life asymptotically with amazing clarity.
The RNAWorld hypothesis strongly supports the idea that an early biotic system might have been very simple - maybe only RNA and its four nucleotides.  Clearly after what Dawkins calls a replicator exists, then the pathway to living things as we know them is pretty easy to envision.
I should add that I'm not one of those people who think that science is everything - the trend that is impoverishing some humanities program is alarming to me.  Its just that some things are not science.

I totally agree on testability. Another way to put it: ID makes no predictions, so it's useless - besides being untestable, ergo unscientific.

thanks -  Its a common problem even with scientists really - I know I never got this stuff in a class. It also comes up in general with 'new' theories of evolution, relativity, and cosmology - the new theory tries to just make the same prediction as the textbook examples, but doesn't bother to look at the sometimes thousands of other experiments which confirm the established theory but might not confirm theirs.

The problem with Intelligent Design is that it doesn't appreciate that the forces that shape species (and individual organism) have to be constant and ongoing or the species disappears. The past matters little, it's what happens right here, right now that keeps species in any particular form.
Biological system are not static structures like a building. You put energy into a building when you move and shape it material during construction. Immediately though, the energy in the structure begins to flow out into the ambient environment, causing the building to loose it's structure and decay. Eventually it will fall to dust.
Biological systems are dynamic, not static. A living organism is like a whirlpool.  A whirlpool is a complex ordered structure that dissipates energy caused by friction between streams moving at different velocities next to each other.  It is never composed of the same molecules of water from moment to moment and once water has passed through the whirlpool it never returns. The whirlpool is the structure, not the transitory water.
Changing the rate of flow, depth of the water, temperature etc changes the exact structure of the whirlpool instantly.
Biological systems are non-material structures like whirlpools. Matter and energy constantly flows into and out of bodies. We stop stop breathing, we die. Your body, even scars and bones are continuously begin torn down and regenerated. The average half life of atoms in your body is seven years. Even atoms that do remain in the body are moved from molecule to molecule and from tissue to tissue. Only the pattern remains semi-constant. Species and individuals organisms are the structures, not the transitory matter.
Changing the flow of matter and energy into an organism, changes it's structure instantly. Changing the flow over long periods, changes entire species.
If I show a picture of a whirlpool in water but crop it so you can't see whether it's occurring in a natural stream or a flow tank in a lab, how could tell whether the whirlpool was artificial or not?  You couldn't, because there is no structural difference between an artificial whirlpool and natural whirlpool. They look the same because the same forces and laws create them and do so continuously
The same is true of life.
You can't look at living things and determine whether they are natural or artificial because just like a whirlpool, it is the flow of matter and energy through life, at any particular moment, that defines it's structure.
Even if some intelligence, divine or material, did alter or even start life, it would have to fit into the material environment exactly like one that arose naturally. It would be indistinguishable from a natural one because the same forces would give it shape and maintain it.
So the best argument against intelligent design is that we don't need to evoke it explain how life exist now, moment to moment. If natural forces continuously create and maintain life continuously today, then they had to be able to do so yesterday and the day before, all the back.

ID addresses an obvious question which nearly everyone considers very strongly at some time. Those who don't choose to believe in God will often argue that it is a non-issue. But is it a non-issue because they are so obviously right that others have no right to voice their opinion, or because it doesn't matter? The former is a very childish view, and certainly isn't very helpful if the goal is to convince others of the "correct" view. And if it simply doesn't matter to Atheists, then surely we can all recognize that it matters quite a lot to others. I'm not suggesting that theists simply be allowed to rewrite the curriculum (which some have attempted), but this is a question which costs more time and energy to ignore than to address. And we have a lot to learn from each other in the process.
Many people, as they study evolution, very naturally begin to conclude that life could have, and therefore must have, emerged entirely by accident. This is not so different from observing that autism diagnosis has been on the rise since about the same time a certain vaccine came into widespread use, and the fact that symptoms often set in shortly after said vaccine has been given, and concluding that increased cases of autism could have been, and therefore must have been, caused by the vaccine. There is an appearance of a causal relationship, but the conclusion does not exactly follow from the evidence. In the case of the vaccine suspicions, I'm grateful that they have been solidly proved false now.
As for the true origin of life, many of us think we know the answer. Be that as it may be, this answer is not delivered to us through the study of evolutionary biology. Anyone who tells you that science has proved that we did in fact evolve without any external manipulation into what we are today, or that life emerged completely by chance, is misinterpreting the facts (or more likely, believing a rumor they heard). Anyone who tells you that science has proved the opposite, that life could not have emerged by chance, is likewise not following the logic correctly (or more likely, favors different rumors). I think that it would be a healthy exercise of critical thinking to open up this kind of discussion in a high school biology classroom, consistently reinforcing the fact that none of it on either side of the argument offers any conclusive evidence on the actual true origin of life. People who feel passionately either way on this must cringe a little at this suggestion, perhaps comparing it to the way Fox News feigns a "fair and balanced" presentation by presenting the plain and obvious truth on equal footing with an extremist view. But which is the extremist view on this issue? It depends on where you stand.
The biggest problem I foresee is that most of the instructors are so strongly biased one way or another, that they would have a hard time honestly mediating such a discussion. But, frankly, this is already the case, so I would argue that it is better to formalize this as a critical thinking exercise in the curriculum. It probably won't open anyone to new thinking on the origins of life, but hopefully, it will help them resist the next vaccine scare. And it will help them to distinguish scientific proof from speculation or belief. For many religious students, this will allow them to digest the rest of the material without feeling like it is an attack on their sacred beliefs.

If anyone down-votes for actual problems with the quality of my answer to the specific question that was asked, please educate me on my failure with a comment.

Nothing in modern science asserts that life arises by chance or accident. It arises from natural forces. You might has well say that rocks roll down hill, by "accident" and not gravity. Evolution is driven by energy from light and heat finding the maximal entropy path through organic molecules. The molecules accelerate entropy by forming complex structures dissipative structures. It's just like water turns from chaotic liquid into organized ice to shed heat or currents forming complex whirlpools to shed energy from friction of current against current. Nothing random at or chance at all.

@TechZen - Interesting conjecture, but I'm not sure how it is meant to relate to the question or to my answer.

The problem is that most curricula on evolution already point out very clearly a large amount (although encompassing only a small fraction of the total) of experimental evidence, while creationism tries to justify its assertation by pointing out the few gaps of evidence within evolutionary biology. One must also remember that the Catholic Church itself does not reject evolution as "an attack on their sacred beliefs".

@MarchHo The problem with this discussion is that too many people on both sides would rather dismiss other ways of thinking as invalid. The core of a Creationist view is not the fallacies they seek in the case for evolutionary biology, but the record of prophets. As you point out, there is not necessarily any contradiction between what is written in scripture and what science has discovered. But when you approach a person who is already certain of the truth of scripture, and begin to belittle what they know to be true, YOU CREATE opposition, and begin to convince them that evolution is a lie.

"The core of a Creationist view is not the fallacies" Yes it is. The fallacies are: circularity (codes/complexity/information/amazement necessarily implies design, while science says what design requires: brains, organs, cells, and [DNA] codes, which are complex and have information), faith (faith in in intelligence without certain parts like brains, cells, etc.), scope violations and/or faulty generalization (using biology-based intelligence as a universal truth, without bothering to explain/describe/demonstrate how non-biological intelligence can exist and function.

"science has proved that we did in fact evolve" What science has demonstrated is what intelligence needs: brains, cells, and DNA. ID totally ignores this, while hypocritically using the same cause/effect reasoning to say what codes/complexity/information needs. ID is self refuting because it inconsistently applies the same rule of cause/effect, and fails to do the same for the hypothesized cause.
"I think that it would be a healthy exercise of critical thinking" to apply the same rule you used for codes, to intelligence.

There's really two components to ID:

A No-Go Theorem (http://en.wikipedia.org/wiki/No-go_theorem) on the likelihood of spontaneously arising life, or of it reaching some threshold in evolutionary development naturally.
...which leads to "the design inference", which posits that the characteristic of intelligence is able to overcome the problem established by the no-go: that life exist, but could not allegedly have arisen from a random process.

Now certain no-go theorems claim something is physically impossible, like transmitting information faster than the speed of light, some are about the provability in mathematics like Godel Incompleteness theorem, but the ID no-go theorem is about being statistically imprlausible- but what is implausible in a Big, Old Universe? Something like 1/Number of atoms in the universe is sufficiently low (2^82), and you can demonstrate this easily by thinking of DNA code 1/4^N where N = min num of base pairs for self-replication, where N~100,000 M genitalium. This is a very naive model, but it's a start: see George Chaitan's work for better maths: http://www.youtube.com/watch?v=RlYS_GiAnK8
The design inference is really Stephen Meyer's domain, and I'll refer you to him, this is much more a philosophic argument. One thing that's important to note for people who are dismissive of ID is that this is about reasoning about intelligence in the abstract, not the manifestation in physical form, not "some being".
What's my opinion? Could I get back to you in 300 years? We'll finally have data on thousands of other planets and whether any of them have ever harbored life, and that I think would be the falsification of ID if other life was found. But I think both a barren universe, and one with other life are both plausible given what we know now. That's why I don't get why people are so staunch on this issue: it's impossible to know the one key thing we need to know in this debate in our lifetime. But in a few generations we in fact will have this answer. We get to live in some interesting times.

Stephen Meyer's explanation: http://www.discovery.org/scripts/viewDB/filesDB-download.php?command=download&id=1491

Why would finding independent extraterrestrial life disprove ID? If we find ET, it might be vastly different, perhaps not even DNA or RNA based, or based on right-handed amino acids. Or perhaps we could discover something so hauntingly similar that we could almost have expected to find it here on Earth. In either case, I don't see that it offers any evidence against ID, or even against one single Intelligence. If I discover Mona Lisa and postulate that paintings must be created by humans, later discovering The Last Supper or The Persistence of Memory proves nothing to me either way.

If we find life arose independently somewhere else (or even twice on Earth), it would substantially change the range of probability that life could arise by random process. That's the first component I described, which can be answered thru data. I think it's the second component, the inference - which you have a problem with.

No. You're already presupposing that life arises by random process; ergo finding another instance of emergence proves that such random emergence is more likely than previously assumed. But this is circular logic. If instead, you presupposed that all life was created by Intelligence, finding another independent creation of life would lead you to conclude that this same Intelligence, or perhaps some entirely other Intelligence, has created this new world full of life. If you presuppose nothing, you know nothing new about the Go/No-Go probability, nor the inference.

The key to the Go/No-Go idea is to somehow prove INDEPENDENTLY that the probably either is or is not within reach of reasonably happening by chance, without Intelligent manipulation. If we knew that it was astronomically improbable even in this vast ocean of galaxies, then the more times we find life, it would only be more evidence that this Intelligence must be out there creating it.

You can't calculate the probability of some pattern occurring without understanding mechanism that creates the pattern. Calculating the odds that molecules would form into certain patterns, without known the electron dynamics that force atom into specific configurations under specific conditions, would show that every clump of matter in the universe was fantastically improbable. But once you know the rules of chemistry, it looks deterministic,not improbable. The same applies to evolution. Once you understand the thermodynamics, improbability disappears.

@TechZen ...and then someone asks how the mechanisms came to be that way, why the universal constants are so tuned to allow the universe to work this way. It's the scientists place to persistently explore and discover more. And it's the philosopher's place to humble the scientist by reminding him how much he still doesn't know, none of which has anything at all to say about what Gods may be. Science is magnificent, but must be careful not to overreach beyond what it can prove. Good science states what we have learned precisely, and leaves the mystery to the mystics.

@MarkBailey -  I don't see the relevance of your comments to my argument. You seem to be making a "God of the Gaps" argument, which is tedious. By that reasoning, since we will never know everything, we never know anything. My comment merely focused on what is known about the formation of organic molecules and the thermodynamics of their evolution into living structures. It's not a random process at any level or stage so calculations based on the premise it's entirely random are automatically false.

@TechZen Evolution is a heavily stochastic process. Don't ruin your credibility. Your previous comment however, was great. I'm not arguing against it, but hoping to complete it. Your understanding of thermodynamics will never be complete enough to conclude with any confidence that life emerged by itself. If you disagree, then "God of the Gaps" is indeed an appropriate concept to consider. If anyone thinks they can jump from a solid understanding of organic thermodynamics to a claim that Life emerged without any Architect or Director, then they are inserting quite a lot into those Gaps.


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Amplified Fragment Length Polymorphism (AFLP) primers
I am trying to blast AFLP primer sequences to the genome to find the locations of the AFLP markers. However, I can't seem to find full alignments for the primers on the genome.
For example, in the paper "AFLP fingerprinting of the human genome", Human Genetics,  108(1):59-65, Table 1 reports 100's of location of each primer pair:

Now the MseI primer is GATGAGTCCTGAGTAA. So the M-CAA primer should be GATGAGTCCTGAGTAACAA. When I blast this on the reference human genome at NCBI, the results show the best alignment only covers 6-21 of the query:
Homo sapiens chromosome 7, GRCh38.p2 Primary Assembly
Query  6          TGAGTCCTGAGTAACA  21
                  ||||||||||||||||
Sbjct  148723256  TGAGTCCTGAGTAACA  148723241

However, there should be close to a thousand matches for MseI-CAA across the genome according to the table. Does AFLP not require the whole primer to be matched?
According to the original AFLP paper, "AFLP: a new technique for DNA fingerprinting", NAR 1995, the figure 1, the whole primer is being aligned.

Cross-posted to Biostars.
Update: One needs to use the digestion enzyme recognition site to map the AFLP markers. Example: http://insilico.ehu.es/AFLP/info.html

@TalhaIrfan please see these guidelines on tags - you've been adding a lot of very narrow and new tags

@rg255 Thanks RG! I would dare to disagree a bit and I still believe Biology SE needs more tags (I haven't added any of tag blindly). Like BCI wasn't even a tag week ago. Similarly ncRNA and lncRNA must be tags as many researchers want to work with them. GRCh37 and GRCh38 maybe narrow to biologists, but they are important for a bioinformatician.

@rg255 Having said that, I have still revised the guidelines in order to ensure I am serving the community. Thanks again!

Just that things like ncrna and lncrna are likely to be better served under a more broad tag like rna or noncoding-rna - people don't follow hundreds of tags but may subscribe to a handful of favorites (e.g. I follow evolution but wouldn't follow the tag evolution-in-the-jurassic-period if it existed)


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Are wild cats the same species as house cats?
I thought that the definition of species is "can interbreed"
From Wikipedia:

The wildcat (Felis silvestris) is a small cat found throughout most of
  Africa, Europe, and southwest and central Asia into India, China, and
  Mongolia. Because of its wide range, it is classed by the IUCN as
  Least Concern. However, crossbreeding with housecats is extensive and
  has occurred throughout almost the entirety of the species' range.[2]

So why does it have a different name than the house cat?
From Species at Wikipedia:

A species is often defined as a group of organisms capable of interbreeding and producing fertile offspring. While in many cases this definition is adequate, the difficulty of defining species is known as the species problem.

While I understand that sometimes problems arise, what makes biologist mark the wild cat as a distinct species from the house cat? If they are genetically different, how different?
Donkeys can breed with horses. The result is sterile. Tigers can breed with lions with lots of complication. Wildcat seems to interbreed with housecat without problem whatsoever. Or does it? That's actually the essence of the question.

There are many definitions of species - look at the wikipedia page for an overview (this is a large and tricky subject). Some hybridization is not uncommon between "proper" species (often in narrow contact zones), also with fully or partially fertile hybrids. Definitions of species in these cases often comes down to genetic similarity/dissimilarity of populations. Even though hybridization is taking place it usually does so at very low rates, so the gene pools stay relatively distinct. The biological species concept (which is what you are referring to) is also problematic when it comes to e.g. ring species.
As for wild cats and domestic cats, my feeling is that modern evidence (e.g. molecular studies and phylogenies) places domesticated cats firmly as a subspecies of wild cats (Driscoll et al. 2007, 2009), with the domesticated cat as Felis silvestris catus. In the study by Driscoll et al. (2009), domesticated cats fall in the same mtDNA clade as F. silvestris lybica. However, domesticated cats were traditionally described as a separate species (by Linnaeus), and this has stuck and some still label them as separate species (as does Mammal Species of the World). I can imagine that some who argue for species status now might use a mixture of ecological, phenetic, and biological species definitions.
From Driscoll et al. (2009):

In contrast, the world's domestic cats carried genotypes that differentiated them from all local wildcats except those from the Near East. Domestic cats show no reduction in genetic diversity compared with the wild subspecies (37), thus giving no indication for a founding genetic bottleneck. Multiple genetic analyses produced concordant results, in each case tracing the maternal origins of cat domestication to at least 5 wildcat lines (A through E, Fig. 2B) originating in the Near East. The domestic cat is referred to as a sixth subspecies, F. silvestris catus, although it is clear that domestic cats derive very recently from F. silvestris lybica (37).

   ... the vast majority of sampled domestic cats fall into the same mtDNA clade, which also includes F. silvestris lybica...

There is also evidence that hybridization can help adaptation by facilitating gene transfer (even though hybrid fertility/viability might be low), so you might want to check out e.g. results from the Heliconius Genome Consortium (2012).

Am I (an Asian) within the same species of whites and blacks? I can interbreed with white or black females though I haven't really tried that. What makes the wild cat a different species?

@JimThio That is not a very useful analogy (for many reasons). For one, genetic differences between human populations are much smaller that within population variability, while wild and domesticated cats have relatively separate gene pools and hybridization is rare. However, hybridization can become a problem in small threatened wild cat populations (e.g. when they have a problem to find mates), which will dilute their gene pool.

@JimThio See the paper by Driscoll et al (2009) for molecular evidence for placing domesticated cats as a subspecies.

@JimThio you are attaching way too much importance to the ability to interbreed. Donkeys can breed with horses, as can zebras, tigers can breed with lions, and various other feline combinations are also possible. The ability to interbreed is not suffiecient to describe a species. In fact, defining what makes a species is still the subject of many PhD theses.

Donkeys can breed with horses. The result is sterile. Tigers can breed with lions with lots of complication. Wildcat seems to interbreed with housecat without problem whatsoever. That's actually the essence of the question.

The "species" concept is an attempt to fit a simple human conceptual category onto a reality that is not that simple.  The reality is a continuum of reproductive compatibility between an individual and any other organism rather than a binary compatible/incompatible relationship which would actually be a basis for defining "species".

@JimThio fileunderwater has given you an answer by the way. He cites a study that shows that they are not different species but one is a subspecies of the other.

@mgkrebbs Agree, and to look for the definition of species is a lost cause if you consider the multitude of modes of life. However, I dont think it is just a human construct - it is essential to understand evolution and biodiversity.

@fileunderwater, Yes, species is useful for thinking about how groups relate and evolve; when you want to look closely, though, it's good to remember the species boundaries are gray, not black-and-white.