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Genetics of epilepsy
Is epilepsy genetically inheritable? If yes, is it dominant?

This is going to get closed as a personal medical question as-is, but a simple edit could fix that.  That being said, there is a well-referenced section on Wikipedia: https://en.wikipedia.org/wiki/Epilepsy#Genetics

Sometimes!
The causes of epilepsy are legion.  There's a massive Wikipedia page listing various causes, and, wow, I get tired just reading the table of contents.  None of those are genetic causes, but it should perhaps therefore be not surprising to learn that the genetic causes of epilepsy, although the minority of cases, are also quite varied.  Apparently most of the causative genes involve ion channels (whether voltage- or ligand-gated), but there are a truly large number of genes that can be related to epilepsy.
This 2011 paper has quite a lot of information.  Some facts it presents on the genetics of epilepsy:

Something like 1-2% of all mutations in mice present with epilepsy symptoms.
Concordance is around 50-60% for monozygotic twins, and 15% for dizygotic

The majority of twin concordance is likely from the same (genetic) cause

Monogenic causes (versus complex causes of epilepsy) account for around 1-2% of human cases.

In direct answer to your question, there is this paragraph (emphasis added) explaining the rough breakdwn:

Monogenic inheritance is suggested by the familial aggregation of cases that share a similar phenotype and are distributed in the pedigree according to a Mendelian mode of transmission: autosomal or sex-linked, dominant, or recessive. Autosomal recessive epilepsies are often associated with structural or metabolic abnormalities of the brain and with neurologic comorbidities, so most of them are not in the category of idiopathic epilepsies. Examples of these are pyridoxine-dependent epilepsy (PDE), several progressive myoclonic epilepsies (PMEs), and some malformations of cortical development (MCDs). Most of the monogenic idiopathic epilepsies follow the pattern of autosomal dominant inheritance, implying the presence of multiple cases in successive generations and male-to-male transmission.

In short:

If it's genetic, it's likely to be complicated and controlled by many genes
If it's controlled by one gene, it's likely to be dominant

The paper also presents the following table which may be of interest, listing monogenic causes of epilepsy:

"The causes of epilepsy are legion".. did you mean lesion?

@WYSIWYG Nope.  Adjective form of the word, referencing biblical usage.  Just a fancy way of saying "a lot".


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Why are female clones more often produced
As a student of biology when ever I come by artificial cloning, I always find examples of females being cloned - Dolly the sheep, CopyCat, Daisy, etc. The only male I could see was Fibro mouse and a few more. What is the reason behind this? Is the male genome more difficult to be cloned? I am specifically looking for genetic reasons or other complications.

It might just be a case of they take the sample from the same animal they are using the eggs from for ease of access.

@SolarLunix I dont think this can be the reason. By the way, thank you.

What exactly do you mean by "cloning"? Somatic cell nuclear transfer? Making transgenics/knockouts/other genetically-modified organisms? Please [edit] your question to add additional information, as well as some literature citations supporting your observations, as currently this just appears to be anecdotal evidence. There is no difference between the male and female genomes, obviously excepting the sex chromosomes.

No there is no problem as such. However, a female can produce her own clone but a male cannot.

I mentioned this below but to be more clear: Rarely (ever?) does or can a female produce her own clone.  It still takes large numbers to get viable offspring, so at least dozens of surrogates will be used.

Female can be inseminated

@rhill45 Do you think it has any link with artificial cloning? What can be its benefit?

You can maintain some of the genetic traits in progeny if you clone a female, since it, as a female, can give birth. A male would be a more difficult model to work with if you were studying genetics. If anything, because females have more genetic content (x is bigger than y), the success rate of the micro injections for females I would be willing to bet are a little less successful. But I'm just guessing here in all honesty about my last statement. @RehanUllah

@rhill45 Wow! thats really a good point for industrial or educational cloning!!

They aren't, anymore.  It was a fair guess at the time, but first I think we should define what cloning in this context mean.
Our own cloning tag says:

The process in nature or in the lab by which a new organism is created that is genetically identical to its predecessor.

For animals - I'm going to use Dolly as an example since you do as well - when we say "cloning" we usually mean somatic cell nuclear transfer.   This image from Wikipedia sums up the process:

Basically, you take the nucleus of your to-be-cloned animal and put it inside the egg cell from another animal.  Dolly was not produced by one animal but by two - a donor and and a surrogate.  She was made using mammary tissue (another good image here) from the donor, which is important to note.
Dolly was the only one out of 277 egg cells that made it.  This is a hard technique, and we still don't understand a lot of it.  With even less information at the time, some prevailing ideas were:

Maybe there's something special about reproductive-based tissue
Maybe there's something special about female tissues

Even when using a different technique (e.g. Cumulina), early cloning attempts hedged their bets with those same tissues. That's why Fibro, the first male cloned (from tail), was a big deal - he showed that any tissue could be used, and that reproductive or female tissue wasn't inherently special.  You still need an egg and a surrogate, but if you can get the nucleus right it's just as doable.

I'd also make the case that, where the XY sex system is in place, anything genetic with a Y chromosome is inherently less stable.  But that's my opinion.

Nice explanation. Thank you for the valuable images.

@Amory A nitpick - If I understand correctly, the image from Wikipedia is somewhat misleading, as the whole somatic cell is fused with the enucleated egg (i.e., we don't use solely the nucleus of the somatic cell). See another question.

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Breakdown current for human body
If I am not mistaken, during exposure to electricity sources it is the magnitude of the current and not the voltage that kills the human body.  If so, what is the order of magnitude of current that human body can sustain, and for what duration?  How do defibrillators exploit this?

It might be better to break this into two questions, the second one being how defibrillators exploit this.  I think you've got a good answer to the first half already.

A part of the answer can be found in Skeptics question: http://skeptics.stackexchange.com/questions/1664/is-it-the-current-that-kills-you-not-the-voltage

@AtlLED I thought one who answers the first question will most likely be able address then second one continuing the explanation and for this reason I clubbed the two questions

@PradeepS The linked post is insightful, thank you for sharing.

According to Wikipedia Electric shock, the Magnitude of electric shock to a body is mainly due to current as well as voltage. Various factor of the environment will also play a major role in damaging the body while under contact. The following quote explains it:

The minimum current a human can feel depends on the current type (AC or DC) and frequency. A person can feel at least 1 mA (rms) of AC at 60 Hz, while at least 5 mA for DC. At around 10 milliamperes, AC current passing through the arm of a 68 kg (150 lb) human can cause powerful muscle contractions; the victim is unable to voluntarily control muscles and cannot release an electrified object. This is known as the "let go threshold" and is a criterion for shock hazard in electrical regulations. The current may, if it is high enough, cause tissue damage or fibrillation which leads to cardiac arrest; more than 30 mA of AC (rms, 60 Hz) or 300 – 500 mA of DC can cause fibrillation.

To give a clear picture of how various current threshold will affect human body see the image below. (Complete data is available here "Electrical Safety").

Even High Voltage also can be fatal to human body which is enough to cause damage.

High voltage electrical energy greatly reduces the body's resistance by quickly breaking down human skin. Once the skin is punctured, the lowered resistance results in massive current flow. Ohm's law is used to demonstrate the action.
  At 1,000 volts, Current = Volts/Ohms = 1,000/500 = 2 Amps, which can cause cardiac arrest and serious damage to internal organs.

Now what is the length of time that body is under electrical contact. This length of time exposure is also critical.

When muscular contraction caused by stimulation does not allow the victim to free himself from the circuit, even relatively low voltages can be extremely dangerous, because the degree of injury increases with the length of time the body is in the circuit. LOW VOLTAGE DOES NOT IMPLY LOW HAZARD!
  100mA for 3 seconds = 900mA for .03 seconds
  in causing fibrillation

(Complete detail is available How Electrical Current Affects the Human Body)

This article deals with the issue in detail.

Please write a short summary of the information in the article.

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Strange looking mushroom found in a dead tree
I'm trying to identify this mushroom my sister found at her campus' lawn. It is brown, looks somewhat like a turtle or a brain and is growing inside of a dead tree trunk. Geographically the campus is in Haifa, Israel in case that helps. Any ideas?
Images:

Is it too dark to be Boletus subtomentosus ? (another pic here)

Have you tried mycokey? Looks like there are a lot of factors that can't be seen in that picture which might be important.

Possible Species: California Fungi - Gymnopilus luteofolius

Source:
http://www.mykoweb.com/CAF/species/Gymnopilus_luteofolius.html
http://mushroomobserver.org/174362?q=28kZM


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What does 'virus prototype strain' mean?
Does the term 'prototype virus strain' mean the first virus isolated and without mutations?

A prototype virus may or may not be the first isolated virus of a group. It's essentially the same as a "reference" virus -- in fact, the International Committee on Taxonomy of Viruses
(ICTV) uses the terms interchangeably, as in the  Hepeviridae Study Group which has a column entitled "Prototype/Reference Strain".
In many cases the reference virus is the first isolate, but it isn't necessarily the case. The ICTV is the official body that determines reference strains, and they may choose a different virus as the reference/prototype. For example the first isolate may turn out to be unusual or an outlier in same way, so that a more typical strain may be chosen as a reference or prototype (I don't know offhand of examples of this though).
"Prototype" is often used in a broader sense as well, where a group of viruses can act as prototypes for a still broader group.  For example, "The genomic structure of Pencillium chrysogenum virus (PcV), the prototype of the genus Chrysovirus ... " (pdf link) uses "prototype" to refer to all the viruses in the Pencillium chrysogenum group, as compared to the broader genus.

virus strain:

Different lines or isolates of the same virus (e.g., from different geographical location or patients)

prototype:

the first example of something, such as a machine or other industrial product, from which all later forms are developed

I think prototype of virus strain is first isolated virus of that strain.
Refferences

Principles of Molecular Virology fourth edition; Alan J. Cann; page 64.
https://en.wikipedia.org/wiki/Strain_(biology)
https://dictionary.cambridge.org/dictionary/english/prototype

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Why are there two abrupt changes in the genome sequencing price curve?
In the price curve of the genome, from NIH:

NIH explained the abrupt drop at 2008 thusly:

beginning in January 2008... the sequencing centers transitioned from Sanger-based (dideoxy chain termination sequencing) to 'second generation' (or 'next-generation') DNA sequencing technologies.

The NIH did not give any details as to why there was a similarly precipitous drop in 2015, or why there was such a saddening (for me!) plateau after that. Please explain them to me?

This graph from the Broad's Opinionome blog (ugh) is somewhat more annotated:

As noted elsewhere, the precipitous drop in 2007 is almost certainly due to maturing next-gen sequencing (NGS), in particular Illumina.  Illumina acquired Solexa in 2007, which offered gigabase-level sequencing ability.  In 2014, President of Illumina Francis de Souza essentially said as much:

During the EmTech conference, De Souza said Illumina’s success was due to a “hard pivot” the company made in 2006, when it got into the DNA sequencing business by acquiring Solexa, a U.K. startup, and bet its fortunes “on a technology with no sales, that no one knew if it would work.”

Essentially, by 2007/2008 you had stellar technology+company hard-selling it = adoption
I'm less certain about the less-dramatic drop in 2014/2015, but I agree with Franck that it's likely largely be due to the introduction of the Illumina HiSeq X Ten in early 2014.  You can read some corporate spam, but it was indeed a big deal.  There were other technologies that probably played a role (new PacBio system released in 2013, etc.) but Illumina was and is top-dog.
None of this takes into consideration increased interest in such research, or the faster computers, larger SSDs, and expansion/normalization of multi-core systems that makes working with such data easier.

The "opinionome" is the oddest use of "-ome" I've seen so far lol

@MaudPieTheRocktorate This is likely intentionally tongue-in-cheek, but a friend and I used to keep a list of wild -omics words in published papers, and... yeah, there are some categorically absurd ones.

Would you give a few examples? For the lolz of posterity.

Some I consider begrudgingly fine — injectisome, translatome, inflammasome — while others are bad and feel like they're trying to make "fetch" happen — promoterome, ligandome, connectome — and others are just beyond — HAR-ome, imagenomics, screenome.

The graph is in contradiction with the data in the Excel spreadsheet the same webpage provides (https://www.genome.gov/sites/default/files/media/files/2019-06/Sequencing_Cost_Data_Table_Feb2019.xls (mirror)), which I plotted below:

Update on 2019-11-17: I contacted wettersk@mail.nih.gov and the graph on https://www.genome.gov/about-genomics/fact-sheets/Sequencing-Human-Genome-cost is now fixed:

https://en.wikipedia.org/w/index.php?title=\$1,000_genome&oldid=902062326#Commercial_efforts to some of the dates on the reaching the 1000 USD/genome goal, and doesn't indicate any plateau:

In January 2014, Illumina launched its HiSeq X Ten Sequencer, claiming to have produced the first \$1,000 genome at 30× coverage. Some researchers hailed the HiSeq X Ten's release as a milestone – Michael Schatz of Cold Spring Harbor Laboratory said that "it is a major human accomplishment on par with the development of the telescope or the microprocessor". However, critics pointed out that the \$10 million upfront investment required to purchase the system would deter customers. Furthermore, the \$1,000 genome cost calculation left out overheads, such as the cost of powering the machine.[25] In September 2015, Veritas Genetics (co-founded by George Church) announced \$1,000 full-genome sequencing including interpretation for participants in the Personal Genome Project.[26]
In April 2017, the newly formed European company Dante Labs started offering the WGS for \$900.[27][28] In 2017, Beijing Genomics Institute began offering WGS for \$600.[29] In July 2018, on Amazon Prime Day, Dante Labs offered it for \$349.[30] In November 2018, around the time of Black Friday, Dante Labs offered WGS for the first time less than \$200,[31][32] and Veritas Genetics for two days for the same price of \$199 offered WGS limited to a thousand customers.[33] In March of the same year, geneticist Matthew Hurles of Wellcome Sanger Institute noted that the private companies, including Illumina,[34] are currently competing to reach a new target for WGS of only \$100.[35]

Page summarizing current prices: http://arep.med.harvard.edu/gmc/genome_services.html (mirror).
Update (2019-07-03) https://www.cnbc.com/2019/07/01/for-600-veritas-genetics-sequences-6point4-billion-letters-of-your-dna.html (mirror):

Veritas is lowering the cost of a full genome sequence from \$999 to \$599 and believes within two years it will be pricing in the \$100–\$200 range.

Another price progression plot from https://youtu.be/jH87sfVD36M?t=554 ("George Church - Cognition Genes. Aging Reversal. Lab-built Brain Components"):

Illumina launched HiSeq 2000 in early 2010 after purchasing it from Solexa in 2007  http://dx.doi.org/10.1155/2012/251364

By "contradiction" do you mean the mistake in the y-axis labeling?

@tyersome yes that seems to be the issue

I'm not 100% sure, but I think Illumina launched their HiSeq machine around that time, massively increasing the sequencing output in one run. That dip might be related to that.


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Why is the head/neck of the femur at that 120-150 degree angle?
I'm just wondering why the femur is such that there is that head and neck sticking out of the top at an angle, why it isn't just straight up into the hips?

The answer to this great question lies in understanding the "Hip Index". I am afraid I will have to go into some technical details to explain this:

When we stand on one leg, the hip abductor muscles on that side have to work hard to keep the pelvis stable and prevent it sagging. In this case the femur is static and the hip abductors are actually working on the pelvis that tilts up or down around the hip centre of rotation. The abductors are represented as "Fm" in the diagram.
In order to do so, the hip abductors have to exert more force than the actual person's weight. This is because the length of the effective lever arm of these muscles "distance h linking H1 with the hip centre H" is shorter than the opposite lever arm "distance D between H and G representing the vertical line down from the centre of gravity".
The hip index represents the mechanical disadvantage of the abductor muscles and is around "2/1" in normal individuals. Therefor if the person's weight is 70kgs, then when they stand on one leg, the hip abductor muscles on that side are contracting at 140Kgs to stabilise the pelvis, and the person's own weight is pushing down at 70kgs from the other side, resulting in the head of femur coming under 210kgs of weight.
If the neck of femur angle becomes more straight as in your question (approaching 180 instead of the average 135), then the hip index goes up towards infinity due to the reduction in distance "h" which approches zero. This is a deformity called "Coxa Valga". If the opposite happens and the neck of femur angle becomes less straight (less than 120), then although the mechanical advantage of the abductor muscles improves, this is offset by the reduction of the actual length of the abductor muscles "distance from i to T", making the muscles weaker. This condition is called "Coxa Vara". In reality, Coxa Vara in humans is also associated with shortness of the neck of femur, which reduces the length "h" also resulting in an increase in the hip index, and an increase in the forces over the head of femur in spite of the abductor muscles becoming weaker.
Both conditions "Coxa Vara and Valga" result in the hip abductor muscles becoming less effective in stabilising the pelvis. In these conditions, the hip index can go up to 4-6/1. This means that a person weighing 70kgs could eventually end up with over 400kgs on the head of femur, leading to pain and early wear and tear. It also results in the pelvis sagging down when walking, which leads to an abnormal walking pattern called "Trandalenburg Gait".
Therefore, a neck of femur angle of about 135 degrees provides optimum conditions for the minimum possible hip index without compromising muscle length and power. Any variation results in reduced abductor muscle effectiveness, gait problems, increased hip joint wear and tear and eventually pain.

Then what about the knee? In my rookie eyes, the situation around the knee is pretty similar to the hip, yet the angle is 180' there.


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In vitro virus assembly
Are researchers able to assemble viruses in vitro?
For example, I imagine that a phage display library may be generated by throwing in a test tube the capsid proteins (or what have you) along with relevant DNA that will self assemble. Has this been done? If so, is it a technique readily applicable to a broad range of viruses?

Yes, and a quick search for viral in-vitro assembly will turn up tons of results. — it's a little more complicated than that! — but it's not usually done as such, which I will explain.  Basically, there are four things you might want to do:

You want to make large amounts of virus and study it. If so, then all you need to do is infect your cell culture with your virus and let it replicate.  Some are obviously easier than others — from my own experience, HIV is pretty easy but Hepatitis C is a real PITA — but that's essentially it.  This obviously presumes you already have some virus stock on hand for infection.  You could also transfect the culture with full-length viral plasmids, which leads me to...
You want to study some specific aspect of the virus.  That's cool!  Most people aren't just concocting virus.  Generally, for viruses that humans can get, it's generally recommended/heavily encouraged to only use what you need for safety reasons.  So, for example, you might transfect the one protein you think is important to see what it does by itself.  After that, you might transfect the cell culture with the full virus, but with one important gene knocked-out.  I used to make single-round HIV by using a plasmid for full-length HIV without a functioning envelope gene and another plasmid for VSV envelope; new HIV particles would be made infectious because of the VSV gene but after infecting they no longer had that gene anymore.  Basically, a limited version of the virus, which leads me to...
You want to make virus-like particles.  These are one of the better-named things in science and are just what they sound like — particles that look a lot like virus, but aren't.  Generally, they're empty shells.  We can use these for all sorts of things, from vaccine studies to other genes and diseases.  Techniques can vary, but generally it's similar to the above.
You want to introduce some other gene to a cell culture system, using a virus backbone for transduction; think "I want to fix these cells... permanently."  Generally, these viruses are usually based on adenovirus or lentivirus (aka HIV) because they will insert their genes into the cell's genome, so the gene will persist.

Item 4 is probably closest to what you specifically meant.  Here's a free review on the use and safety of retroviral vectors in humans, and here's a nifty one in fish.  As for which viruses it's applicable to, well, that varies a lot by virus, host, culture system, and so on.

Thanks, that was very helpful! I inadvertently googled de novo virus assembly, which was a dead end. With point 4, you touched on an interesting topic. Because as I understand, in order to apply gene therapy to living organisms using CRISPR (or other method), we would still need a way to deliver the corresponding genes to the organism. I guess in the future this may be done using viruses or virus-like particles .

Viral vectors can indeed insert genes into the host genome (this is one reason why HIV is so hard to beat) but they tend to do it in a random or stochastic fashion.  This is decidedly bad, from a therapeutic point-of-view.  Viruses like HTLV have a tendancy to cause cancer for that reason.


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What is the result of modifying the reagents in the Sanger method?
If one of the dideoxynucleotides is omitted while using the Sanger method how would that affect the chain termination method of DNA sequencing?

Are you talking that you don't put in a whole base (like T) or if you have a deletion?

if by one of the dideoxynucleotides, you mean one of ddatp, or.ddctp, ddgtp, or ddttp was ommited from the process, then the sequencing would only be able to terminate for the other three dideoxynucleotides. And you would not be able to get the full sequence, and only nucleotides of whatever three you had.

@RoSiv if you have an answer then post that as an answer. Comments should be used only to seek clarification or suggest improvements.

@user18817 you would possibly benefit from familiarizing yourself with the BiologySE homework policy: http://biology.stackexchange.com/help/homework

@WYSIWYG         I was not sure if I was right. I am only an undergrad and I dont wanna give out a wrong answer to someone. Sorry.

@RoSiv Then provide a good answer with references. You are right. Just make it a bit elaborate.

If by one of the dideoxynucleotides, you mean one of ddATP, ddCTP, ddGTP, or ddTTP was omitted from the process, then the sequencing would only be able to terminate for the other three dideoxynucleotides. And you would not be able to get the full sequence, and only nucleotides of whatever three you had.
The function of ddNTPs (the dideoxnucleotides) is to stop the elongation of DNA and to subsequently be read by either fluorescence or radioactivity.
Source: https://en.wikipedia.org/wiki/Sanger_sequencing

Note that in Sanger sequencing the ddNTPs are not added together in the same mix. If you omit one ddNTP then you won't be able to sequence that particular base in the DNA. Though you may be able to infer the 4th base from the other three, the confidence of the read would be low.


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Are MHC Proteins the Most Polymorphic Human Proteins Known?
There is a paragraph titled "MHC Proteins Are the Most Polymorphic Human Proteins Known" in the "Molecular Biology of the Cell" by Alberts et al. 6th ed. 2014.
But someone has recently told me that it is not the case making an example of a set of genes helping to identify persons in forensic medicine. (I didn't remember the genes.) Is it true?
Are MHC proteins the most polymorphic human proteins known?

In addition to the excellent answer given by @Amory, it might be of interest for you that this not only applies to modern humans but also appears to be true for archaic humans (Neandertal and Denisova), even though the latter had far lower overall genetic diversity.

I don't think the markers used in forensic DNA fingerprinting code for proteins.

Are we restricting things to germ-line polymorphism, or is there some other reason to exclude immunoglobulins?

@AlexDeLarge: you mean MHC locus was also diverse in the archaic humans? Thank you for your comment.

@swbarnes2: primarily the emphasis was on genes.

@stan: Yes, looking at archaic genomes one also finds MHC genes to be among genes with highest diversity.

Yes.  There are many MHC (MHC in humans is called HLA) genes.  The classical loci — Class I A, B, and C, and Class II DP, DQ, and DR — are the most polymorphic.
Here's a table from a 2002 article which clearly shows the number of polymorphisms.  It's no contest.

It's worth me pointing out that those numbers are wildly out of date.  The IPD-IMGT/HLA can provide full lists of known HLA alleles, but the exact numbers are in the tens of thousands:

The person you spoke with was probably referring to sequences called microsatellites.  These are small regions that are polymorphic and quite variable between individuals, and using a number of these together can be useful for genetic fingerprinting, but each individual microsatellite will not be as polymorphic as HLA class I A, for example.


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Where can I find a full genealogy of human cell types?
It is said on Wikipedia, that the precursor of blastocyst is a morula, and that the precursor of morula is a zygote. This gives us the part of genealogy tree of cell types. Unfortunately, no full genealogy can be found in Wikipedia.
Where can I find a more complete picture, preferably a full tree of cell types including information about each type?

I find it strange that this Q was downvoted, without any comment. The question is valid and interesting.

Wikipedia has a page listing cell types which classifies their origin as endodermal or ectodermal.
I haven't been able to find a source for a complete lineage of all cell types, and I have gained the impression that there is no complete picture, except in some specific cases such as the haemopoietic lineage.
Here is a TEDX talk by a researcher in the field, and here is a slideshow by the same person which lays out the problem and its importance.


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How is it proved, that antediluvian people didn't live for hundreds of years?
Bible says that antediluvian people lived for 800-900 of years. Nowadays apologists say that it is possible and that we just can't know the truth.
I know that one of the basic science principles is the suggestion of similarity of laws of nature. I.e. if we see ancient human fossils, similar to modern human remnants, then we should expect they are of similar age.
But does science have some other age proofs besides this?
May be, for example, from migration data or from some other sources?
Isn't it possible in principle, that some virus epidemic in ancient times cause humans to live shorter, due to virus DNA embedded into all of the human DNAs?
UPDATE
We don't know abut the all reasons of aging and also we don't know about all means of horizontal gene transfer.
What if, a lifespan is a feature, which can be transferred horizontally by a virus or somehow else?

As @MCM mentions below, parsimony dictates assuming that the ages reported in the Old Testament are not literal years. I think an interesting variant of this question, and one that is more amenable to (anthropological) study, is why do so many ancient cultures think of their elders as having superhuman lifespans? Both Cree (indigenous to North America) and Jainists (mostly in Asia) think there are earlier epochs where humans lived multiple centuries.

Extraordinary claims require extraordinary evidence.

For my own curiosity, do you have a reference of the philosophy of science stating the role of "similarity of laws of natural" as having a key role in science?

I know that one of the basic science principles is the suggestion of similarity of laws of nature. I.e. if we see ancient human fossils, similar to modern human remnants, then we should expect they are of similar age.

Well, similar physiology. Modern humans, throughout recorded history, rarely broke the 100-years-old mark. Our evolutionary cousins rarely break half of that and in the wild reach old age at our "Middle Age" equivalent.
So, knowing that as we are is exceptionally long-lived for members of our clade, it would be absolutely incredible and far beyond expectations for an evolutionary ancestor to live 8x-9x longer than some of the longest-lived members of our tree (and would be one of the longest living complex organisms ever).
Impossible? No. We can only interpret data from the past; we do not have any records from the time period. In that way, you're entirely correct if you're looking for additional proof.

But does science have some other age proofs besides this?

This depends on what you consider 'other' proof. Most of the estimations of age of found fossils relies on comparative morphology: We assume that because our joints and teeth wear-out at a certain rate, we can compare the rate of decay of teeth and joints of fossils and get an estimate. If it's true that our extinct cousins experienced similar wear 'n tear as we do (and we don't have any reason to think otherwise; the bones may be slightly different, but they are made up of the same material), then we can use the comparative morphology as a reasonable estimate.
If we assume that their bones and teeth wore out much, much slower (it would have to be about 10x slower while also being made of similar material) then our age estimates would have to be adjusted.

May be, for example, from migration data or from some other sources?

Migration data would be incredibly difficult to produce. You would have to follow one family as they migrated, and fossils are rare enough as-is. Data like that would be practically impossible to gather.
Perhaps some Population Geneticist has run some genomic data and is capable of making a similar claim through the molecular clock hypothesis, but I am as-yet unaware of anything like this.

Isn't it possible in principle, that some virus epidemic in ancient times cause humans to live shorter, due to virus DNA embedded into all of the human DNAs?

In principle? Yes. But there isn't any evidence for that. Keep in mind that in order for the viral DNA to be integrated into all of humanity then it would have had to infect us when our numbers were very, very small. Evidence does show a bottlenecking event in humans about 70,000 years ago - but this was thought to have been caused by a supervolcano eruption which dramatically changed the environment and not a virus. Both genomic and geological evidence come together to support that hypothesis.
So, while you are correct that - in theory a population of humans could have been infected by a virus which mutated their DNA and caused a dramatic reduction in lifespan at the same time as a bottlenecking event - we have no other evidence supporting that, either genomic, geological, or evolutionary.
Given the lack of evidence, we should remember our Occam's Razor - In the absence of evidence, the simplest explanation is usually the correct one.
So it's either an exceptionally long-lived species of an already-long-living family contracted a virus at the same time a bottlenecking event occurred and didn't leave behind any evidence, or our ancestors lived about as long as our evolutionary cousins do now and it's us who are exceptionally long-lived because of evolutionarily advantageous things like The Grandmother Hypothesis and advancements in technology - which is supported by genomic evidence, fossil evidence, geological evidence, and recorded history.
We cannot ever truly know what happened several hundred thousand years ago. We weren't there and nobody was writing anything down. However, Science is evidence-based, implying that scientific opinion follows the argument with the most supporting evidence behind it.
If the evidence changes and begins to favor another argument, then so will the scientific community (ideally speaking).

Thanks a lot! But I would like to have some "killing" argument, not Occam or Popper like :)

The substance of the question as-posed is an appeal to ignorance and is therefore fallacious. @MCM's answer is the best form you'll get. You can't 'kill' an argument that presupposes that our current knowledge is irrelevant to the proposition. It's like positing that God is beyond all physical laws, then demanding a scientific experiment to disprove the existence of God. As long as you're asking what is biologically possible (which is unknown) and not what is biologically probable (which a good biologist can contend with) the question cannot be directly addressed.

@SuzanCioc - The problem is that without some basic assumptions the current scientific understanding can't actually answer your question. What is possible is significantly different from what is supported. If you have questions regarding a specific data type - like morphology or genetic data - then you'd get a more specialized and more detailed response. Simply saying "We weren't there so how can we know for sure?" is sort of like trying to prove I'm human and not a computer program despite only communicating online. ;-) In order for things to function, basic things must be assumed 'true'.


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At what point, when connected, do DNA strands become a helix?
When synthesizing DNA strands and beginning to "connect" them, how quickly does it become a helix?
In this answer, canadianer says

The helical structure is more stable than the "straight" form (because of base stacking interactions), and so it forms spontaneously.

This then makes me think of the following scenario: say one is constructing two strands of DNA out of deoxyribonucleotides. Then, one begins connecting them with hydrogen bonds. Before the hydrogen bonds are added, my understanding is the two strands would be straight and not helical (if this is wrong, please correct me on this) so at some point as the two strands are connected, it would "spontaneously" become helical.
The question, then, is at which point. After one "connection"? Two? All of the connections necessary to complete the piece of DNA?

Yes, in general that's correct.

I will do soon, glad it helped.

@canadianer has answered your question, but you should be aware that it is of little interest to scientists because of its hypothetical nature and experimental untestability, and the fact that it does not address a problem in biological or physical sciences. DNA is polymerized by enzymes, and we understand something about what occurs in these reactions. We also know there is not the sort of folding problem that exists for proteins. We cannot add deoxynucleotides to a pre-existing helix (which involves making phosphodiester bonds) in the way you suggest without enzymes, template and primer.

In general, a single stranded nucleic acid is helical in the absence of other secondary structure. The base stacking that drives helix formation does occur  between adjacent bases in the same strand. Note, however, that such structures are dynamic and dependent on properties such as temperature and salt concentration. You can see an example of a single-stranded RNA helix in the following crystal structure (1MHK):

Note the blue helix at the bottom of the image is actually a duplex in the crystal.


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A free book/resource for learning genetics?
I took an undergrad class in genetics. I felt it was not too intensive and I do not feel prepared for grad school (if I can manage to get in.)
Does anyone know of a preferably free resource for learning genetics?
I know the field is very large, but I would like to be competent in the field, considering I also want to learn more about genomics as well. And I figure one must first have a fundamental understanding of either computer science or biology to be successful in genomics, both of which I lack.

MIT Open CourseWare?

"Not expensive" I understand, "free" doesn't make much sense: you can afford to attend a grad school, but not to buy a book? Really? Maybe that's really the case, but the odds are quite low.

@Lohoris        I said that I was thinking of grad school, if it was possible. Sometimes they give people "free rides" I heard if they are competent enough and desired enough. I doubt I fit into that category.

Doesn't matter: even if you hadn't to pay for the school at all, you would still have other expenses just to live. And if you can cover those, then you most likely can afford to buy a non-expensive book too.

@Lohoris           I guess your right, I just always like saving money though. I figure I would buy a book when I became a bit more competent.

@Lohoris: Different countries, different "grad schools". Here I am, doing my PhD and being paid (not a huge amount, but well enough to survive for sure) for teaching and working on research projects. This is how it can work in Germany. There is also stipends and whatnot.

As you said, the question is pretty broad. Genetics is a big gigantic field and it is quite hard to know what you are exactly looking for. If you could refine into one of the subfields (molecular genetics, population genetics, phylogenetics, etc..) it would be much easier to give you better advice. As you talk about both biology and bioinformatics, it might be worth to specify whether you are looking for learning more in fundamental genetics or learning more in the methodologies to analyse genetic data.
Principles of Genetics
You may want in an introductory class in genetics. Here is a course on MIT Open CourseWare, but it may be too easy for you.
Bioinformatics
You may want to take a bioinformatics course. There are so many bioinformatics course online that there is a wikipedia page to list them (there).
Side skills
Programming
You may just want to learn to code in R, Python, Perl or Shell script (to cite few examples). You'll find tons of beginner tutorial online.
Statistics
Or you might want to learn more about statistics. KhanAcademy has a very good (but very introductory) statistics class.

Great answer. Would add Perl in the side skills as it is massively used in genomics because very powerful for treating text-based data. Also understanding Linux and its command-line interface is a must-know.

@cagliari2005 Thanks! I edited the answer. One might want to add C++ eventually. I would have not thought about Perl as I personally don't use it.

I work at the Wellcome Trust Sanger Institute, one of the world's largest genomics centres. We do maintain a website for the public wanting to learn about genomics, but it might be a bit basic for you: YourGenome.org
You can get into this field without going through grad school:

learn at least one programming language (Python is probably the key one today; perl was everything 10 years ago but not much new is starting in that language now)
try getting involved in open source bioinformatics projects, such as the Global Alliance
apply for a support role in a genomics centre, such as working as a programmer within a research group, or in their IT support groups.  Genomics is a field you can learn on the job.

To give a background, I have also taken a intro level genomics course and enjoyed it. The coding was just a taste( "hello world" and the like) but my coding needs alot of more work. I was a comp sci major, but flunked out because my coding and understanding of proofs was not good enough. In the genomics course, I did a gene annotation project under the Genomics Education Partnership (http://gep.wustl.edu/curriculum/student_work) similar to the ones on that page. Is that relevant experience in genomics?

The Coursera Introduction to Genetics and Evolution is an excellent MOOC.
If I remember correctly it contains links chapters in the online version of Griffiths et al (i.e. deep links to this: http://www.ncbi.nlm.nih.gov/books/NBK21766/ )
There is also Introduction to Biology - The Secret of Life from EdX, it is not just genetics, it covers a lot of molecular biology and biochem too, but it is by far the best course of it's type I've ever taken, and I'd say you could jump in on the genetics and skip the biochem if that is your preference. The simulation "experiments" (e.g. breeding fruit flies) are superb.
If you want to get in to bioinformatics and you don't have strong programming skills then take a look at Algorithms, Biology, and Programming for Beginners. The same people also offer more advanced courses on Coursera too, if you have more programming experience. The course is language agnostic, but Python is really the main language in the field so I'd strongly suggest you do any dev work in that.


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Trouble understanding how uncouplers in the thylakoid membrane increase the rates of the Electron transport chain?
I am a undergrad in a cell physiology class and just did a learning exercise involving testing rates of the electron transport chain via the reduction of DCPIP, analyzed by spectrophotometry. ( I think...  D:   )
So from what I understand, uncouplers stop the "connection" of the ETC and ATP synthase indirectly. And in our lab period we used a hydrogen ionophore(ammonia) as our uncoupler( I think... D:  ).
So for our results I obtained this graph**(The Y axis should be absorbance(600nm)) sorry**...:

Where tube 1 through 3 was a collection of thykloid membranes isolated from spinach leaves; tube 1 being kept in foil until the 10th min mark to then measure absorbance as a control. Where tube 2 and 3 were exposed to light for the 10mins, with absorbance readings being taking every 1 min. And with tube 3 having the added ammonia(from what I understand, the uncoupler).
Therefore how does the ammonia uncoupler speed up the electron transport chain?
My thoughts after googling are that since PQ( plastoquinone) is partially responsible for establishing the proton gradient for the thylakoid mebrane, since it transports H+ ions from the stroma to the lumen upon reduction, that if there was this ammonia uncoupler, that could travel through the membrane due to its lack of charge, it could then bind with the H+ ions forming $\ce{NH4+}$ in the lumen.
So then if the lumen now has less H+ ions then the high(lumen) to low(stroma) H+ gradient would be ruined/weakened.
So this is the part I guess confused with; if there is less of a H+ gradient across the thylakoid membrane, then how does that have any bearing on the reduction of the added DCPIP or the speed at which its reduced?
Since tube 3 went the fastest to clear( ~0 absorbance), this is only when it is reduced yes? This means then that in tube 3, the reduction of DCPIP  happened the fastest.
So then does this mean that DCPIP, the artificial electron acceptor, takes over for PQ somehow? Why does PQ have trouble "doing its job" in the presence of the weakened H+ gradient?
P.S: Sorry for the rambling, but I felt including my train of thought was important for others to see where I  misunderstood.


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Why Only DNA can Contain Hereditary Material?
Well I'm well aware that it is proven that DNA contains  genetic material via transformation and Hershey-Chase Experiment of T2 bacteriophage. Still I was wondering what is the reason only DNA contains it and not protein or RNA.
What I've learned is that DNA is the most stable of all these molecules and it has the ability to replicate itself.
Other than this I can't find any solid answere.
Thanks!

RNA might contain material that you can classify as 'hereditary' (specific to that individual of the species, a subset of the species gene pool) but since the prevailing methods of meiotic gamete formation, sexual reproduction and the fact that all enzymes are formed due to transcription from DNA and not by the inherited RNA, DNA is the one that is inherited and hence acts as the heredity carrier and not RNA.

DNA/RNA also has a relatively obvious way by which it can be replicated- having a purine base pair with a pyrimidine.

RNA has the ability to replicate itself - it could be the genetic material, but it simply isn't.  its degraded in the cell quickly. its hard to be hereditary material when you are destroyed.

@shigeta, certainly there are RNA viruses that are excellent examples of RNA functioning as hereditary materials.

that's true, but trying to respond to the question as stated as i see it, not sure its what i wanted to point out.

DNA is unable to replicate itself, a complex of protein, RNA, and DNA are involved in DNA replication.

I think any discussion of this question can benefit from a historical perspective. For a long time, it was in fact believed that proteins was the hereditary material. The Nature Scitable page on the discovery of DNA (1) starts with the following passage:

In the first half of the twentieth century, Gregor Mendel's principles
  of genetic inheritance became widely accepted, but the chemical nature
  of the hereditary material remained unknown. Scientists did know that
  genes were located on chromosomes and that chromosomes consisted of
  DNA and proteins. At the time, however, proteins seemed to be a better
  choice for the genetic material, because chemical analyses had shown
  that proteins are more varied than DNA in their chemical composition,
  as well as in their physical properties.

While perhaps easy to dismiss in hindsight, it is possible to understand the reasoning of the day. The "central dogma" of molecular biology, that genetic information flows from DNA to RNA to proteins was only described later, and explained how the production of complex proteins consisting of 20-odd amino acids can be directed by a polymer consisting of only four nucleotides. This allows great complexity and variety in phenotypes while maintaining simplicity of the genetic material. The central dogma also facilitates the seperation of the use (through protein expression) and storage (as DNA) of genetic material.
As Watson and Crick noted in their famous paper, the double helix of DNA, when discovered, immediately suggested how the genetic material could be elegantly copied. While the more complex structure of proteins would likely require a more complex copying mechanism, the specification of amino acids through three-nucleotide codons in DNA allows the regularity of the DNA material to be retained for easy replication while allowing complex proteins to be produced.
However, even though DNA is the primary genetic material today, the situation may have been different at the time life first appeared. According to the RNA world hypothesis, RNA may have been the original genetic material and that DNA is a variation of RNA, not the other way around as it is commonly seen.
For a fuller historical perspective, I recommend the book "What is Life?" by Erwin Schrödinger, which was written before the discovery of DNA as the genetic material.

In contrast to some of the accepted points in this thread. DNA is not the only hereditary material. The RNA world hypothesis remains hypothetical, but  its primary point is that RNA may have been the original hereditary material as it is slightly simpler than DNA. However, there are extant organisms that use RNA as their genomic basis.
There are many viruses which use RNA based genomes (either single stranded or double stranded, (Class IV/V and Class III viruses as described by the Baltimore Classification). There are also class VI viruses which use an RNA genome that passed through a 'DNA intermediate' phase during the infection/replication process. The latter class are "Retroviruses" as they need their genomes to be converted back to DNA. The most famous example of such is the HIV virus.
Crucially, the progeny viral particles re-package RNA, which is carried with them until the next infection cycle, making it their hereditary material.
(I realise this is an old thread at the time of my answer, but this is important for completeness)

Further, piRNAs can serve as hereditary material in animals: e.g.: Houwing, S., et al., A Role for Piwi and piRNAs in Germ Cell Maintenance and Transposon Silencing in Zebrafish. Cell, 2007

The simplest answer one could offer to this question is hidden in the structure of the DNA itself. DNA is double helix structure with the presence of 3'->5' end and 5'-3'  coiled helically in the double strand ( it is the direction in which DNA is synthesised as per formation of replication fork via the enzyme DNA dependent DNA polymerase.

The inability of the Proteins, amino acids etc to replicate themselves makes no sense to have them as genetic material ( as also concluded by Martha and chase experiment).
Now, here is the point which leads the most logical question?
Why not RNA ?
In fact it is much better in the Job that DNA does, it is very fast in replication almost have the same structure,  but the fact that the presence of OH group makes RNA very reactive and Unstable does not make it idle for transfer of hereditary material in nature, we should know that thousands of nucleotides are synthesized by DNA polymerase during the replication of DNA from the template DNA which is highly accurate and precise even slightest of error can lead to very big mutation and the presence of the Deoxyribose and complementarity principle makes the DNA best suited for Genetic material.
Although a whole of a different class of the organism exists that have RNA as genetic material, they are called retroviruses eg. HIV virus so the question that DNA is the only genetic material in all living organism is not true, although yes it is the genetic material in Humans and majority of the organism due to the above reasons.
EDIT : AS @WYSIWYG mentioned there are also many viruses which have RNA as genetic material but are not called Retroviruses, nonetheless DNA is not the only genetic material that exists.
Kapeesh !

Viruses with RNA as genetic material are simply called RNA viruses. There are many RNA viruses that are not retroviruses (for e.g. poliovirus, influenza virus).

@WYSIWYG something interesting you made me learn today. Thank you so much.


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Phenoptosis, behavior evolved for good of species?
I was reading this and felt like the argument is being made that organisms die for the good of species. Isn't this nonsense?
This especially bugged me:

"'Age-induced, soft, or slow phenoptosis'" is the slow deterioration and death of an organism due to accumulated stresses over long periods of time. In short, it has been proposed that aging, heart disease, cancer, and other age related ailments are means of phenoptosis. "'Death caused by aging clears the population of ancestors and frees space for progeny carrying new useful traits.'"

Per the selfish nature of genes, it might be okay if it was only your offspring you are dying for, but even that only when you know you can't reproduce further. And the above argument says that old age death is exactly that.

two other wikipedia links one might want to read: http://en.wikipedia.org/wiki/Evolution_of_ageing
http://en.wikipedia.org/wiki/Senescence#Theories_of_aging

I guess, programmed death for the purpose of freeing space to new individuals can be explained by: 1) kin selection (Given that aged individuals are damaged by various stress and has a lower per year number of offspring than new individuals, it might be beneficial to die if the expected relatedness to the new offspring is high enough compare to the ratio of offspring the old and the young can raise (RB>C)).
Or by 2) lineage selection: lineages (species) that dies early (so that it frees space for new individuals) have a lower extinction rate (or speciation rate).

But I think that when thinking about senescence, it is important that you know about Haldane's (and some others) work. Their hypotheses make much more sense to me than the hypothesis that individuals die to free space to others.

I don't really have an opinion on whether or not this is the main or even a reason for the evolution of senescence and death, but it is certainly not nonsense.
Death can indeed be good for a species. Diversity is always good and the death of the elders allows phenotypes that have been selected for more recently to take hold in the gene pool. If the young need to compete with the old, this will make it harder for them to grow and reproduce. In situations with a limited food supply, having to support old individuals who can no longer forage/hunt for themselves will be a strain on the species/society/pod or whatever it is we are looking at.
Therefore, genotypes that encourage the death of elders who are past the age of reproduction could be selected for. This does not contravene the selfish gene hypothesis at all, these individuals have already reproduced, the selfish gene no longer 'cares' about them. The main idea of the selfish gene hypothesis is that the genes themselves 'want' to be passed on, not that the genes 'want' to save themselves. Once their host has reproduced, they loose interest so to speak.
The selfish gene theory is just a conceptual tool, it should not be taken literally. It does not suggest that genes are actually selfish or in charge of their own evolution in any way. It is just a useful approach to take when studying evolution and was instrumental in our understanding that the gene (the nucleotide actually) and not the individual is the smallest unit of selection.
Anyway, in the strictest sense, the statement in your question is absolutely compatible with the selfish gene hypothesis. If you can no longer pass your genes along, you are useless and just a drain on the species, why should you keep living?


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Hypotonic or Hypertonic solution and why?

A doctor needed to administer 5% albumin to a patient. Albumin is normally administered dissolved in 0.9% saline solution. Since the physician did not have any 5% albumin solution, he diluted 25% albumin with water and administered this to the patient. Describe what you think happened to the blood cells of the patient as a result?

So this is what I think:
If the doctor dilutes the 25% albumin, that will make the solution have a lower concentration of solute, creating a hypotonic solution. Therefore the water will move into the cells, causing them to swell, lyse or burst.
Is this correct?

Sure sounds correct to me.   p.s. Stupid doc's solution will be (0.9/5)% saline = 0.18% saline.  Way too low.

Albumin wont form a true solution and wont affect the osmolarity greatly (colloid forming molecules like proteins can affect osmotic pressure to an extent. See oncotic pressure).. and since there is no solute the solution would be hypotonic..
But what effect it will have on the blood cells depends on how much solution was injected.


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Organelles present in sieve tubes
I know that sieve tubes do not have ribosomes, nuclei and cytoskeletal elements.
What other organelles does it not have? Does it have a cytoplasm?

A cell without a cytoplasm is not a cell.

The sieve tubes of the phloem in angiosperms consist of sieve tube elements or members. These are cells which lose their nucleus, ribosomes, and vacuoles at maturity.  They of course have cytoplasm, and it is connected by channels to companion cells (which do have these organelles).  The sieve tube elements retain mitochondria and plastids. See the Wikipedia page and this page for more details.


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What Freshwater Fish Are Affected By Magnetic Fields
I am interested in knowing which freshwater fish are affected by magnetic fields.  I've heard that Lake Sturgeon are, but would like more references. This is for a project that will have buried 3 phase power cables.

Sockeye salmon species definitely do, although admittedly the interesting salmon are those that spend significant time in the ocean.
Here's some evidence that carp can.
Raindbow trout are also capable.
Zebrafish are also able.
Japanese eels too, of which some are freshwater.


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molecular indicators of apoptosis: clarification needed
I understand that DNA fragmentation is a molecular indicator of apoptosis. What distinguishes this as a hallmark of programmed cell death, versus one of necrosis?

Although both involve DNA fragmentation, the pattern produced is very different.  During apoptosis, DNA fragmentation is done in a regular, controlled pattern, which if run on a gel produces a characteristic "ladder" pattern.  Necrosis, on the other hand, is a more stochastic process, and will produce a smear.  This details the difference rather nicely, including different ways to assay for either one in table 18.3.1 such as morphological staining or flow cytometry.
Here's a nifty image from the link.  Figure 18.3.2.  M is the marker, and in panel A, a conventional gel, lane 1 is apoptotic DNA, lane 2 is unprocessed DNA, and lane 3 is necrotic DNA.  In panel B, a pulsed-field gel, lanes 1 2 and 3 are untreated, apoptotic, and necrotic, respectively.

I understand that DNA fragmentation appears as a regular pattern on a conventional gel. However, I wonder how can the experimenter distinguish apoptosis from necrosis on a typical FACS experiment using propidium iodine DNA staining?


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Mammal body density
Human body density is approximately 1 kg/l (same as fresh water) - which is not surprising (at first) given that we are 70% water, and is surprising (on a second thought), given that the other 30% can be just about anything (from the air in the lungs to the relatively heavy bones).
How remarkable is that?
Consider other mammalian species.
For each species, compute the average body density of an adult.
Thus, for each species we have the number - the mean body density.
How are these numbers distributed?
Mostly heavier than water? Lighter?
It is unlikely that this kind of research has been done, so I would settle for something simpler: what are the densest/lightest mammals? (or, in general, vertebrae)
PS. As you can guess, I am a mathematician, not a biologist :-)
PPS. Given abundance of water of Earth's surface (70%, same as above!), it makes a lot of sense to be as dense as water: not heavier (to avoid drowning), not lighter (to be able to dive for food), so natural selection should favor the density of 1.  Are there exceptions?

Great question! Never gave much thought to it. Human body have nearly 985$kg/m^3$ nearly equal to sea water(1020 $kg/m^3$)

Lightest have got to be bats, right?

@Oreotrephes: it would make sense that flying requires lower body density, but what it the actual number? how light are the bats?

This might help you or another answerer: http://epub.ub.uni-muenchen.de/12010/1/zitteliana_2008_b28_08.pdf and works it cites; although as far as I can tell they only give figures for birds, not bats / other mammals.

I would be careful how you measure this. Do lung insides count? Do the air sacs in bird bones count? Maybe those frogs that inflate their throat sacs would win, but only for like half a second at a time? (most importantly, do bats float?)

@JeremyKemball: mean body volume over, say, 24 hours: lungs average out; bone air sacs count; throat sacs do not.

Why do throat sacs not count?  I'm actually thinking of aquatic mammals that can purposefully adjust buoyancy with gas exchange/ retia mirabilia / etc.

@AtlLED: air sacs average out over 24 hours. E.g., what is the density of a human during inhale vs exhale?

Until someone has a better method to determine this, and I'm willing to go with idea of that this question is not answerable, I put forward the two likely forms of selection criteria:
Which mammal has the highest percentage of keratin in it's body for the highest density, and which has the highest percentage of gas (over the day) for the lowest.
I also want point that measuring the density of mammals is tricky because we can change our "volume."  Perhaps this doesn't seem like much for humans, but a small mammal with a large tongue stuck out could have an appreciable different density than one with the tongue in.  Same for retractable limbs (which are generically cool).
This article gives us an estimate for the density of keratin at "1.283 g/c.c. for cow horn to 1.335 g/c.c. for echidna quill tip" which putts it solidly more dense than water.  This means we're looking for a small heavily armored mammal, which leads me to suspect the pangolin.  I don't readily know it's density, and I would be fine with others taking the time to calculate it (I'm not interested in getting that specific).
I have fewer ideas on which mammals are least dense.  Going by this article I would guess rodents have the least dense skeletons. In particular I was surprised by this graph:

But also don't know that means we should exclude something like a sperm whale which has a lot of fat (lower density than water) and has enough lung capacity to dive for hours in deep water.  But on the off chance that the skeletal density is the best bet, I'm going to guess the least dense animal is a rodent, and if I have to pick one species I'm going with the least massive, the shrew.
Doubt any one has really researched the displacement of many of the animals that should be in the running for this, so I'm not convinced a more exact answer could be reached.

Rodents don't have air-filled bones. Birds do however.

@kmm that has been my experience as well (no air) when harvesting bone marrow in mice.  I'm going to remove that because I'm now looking at what I think is conflicting statements.


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Ancient DNA of ancestors or existing species?
Ancient DNA appears to be at most "several hundred thousand years" old.
Do we have an aDNA sample which we can reasonably confidently attribute to a species which has at least two modern descendants?
PS. This question is much less interesting than I originally thought: there are modern species which are proven ancestors of other multiple modern species (lake Victoria Cichlids).

@AlwaysConfused: the problem is that we do not have DNA sample of the common ancestor.

@AlwaysConfused: yes.

Assuming you mean by "modern descendants" "two different species that are also different from the ancient DNA", then to the best of my knowledge, no; the large vertebrates (bear, horse, humans, mammoths) that have been focused on for the most ancient DNA samples have common ancestors that are outside the range of ancient DNA isolation. I'm not very familiar with plant ancient DNA; maize DNA from a few thousand years ago is the oldest I'm aware of, but I might easily have missed some.
However, it's important to point out that the way this question is phrased makes it merely trivia, with no scientific significance.
Assuming (from the poster's other questions) that he believes this is somehow relevant to questions about speciation, I would point to modern genomes from ongoing speciation.  For example, Heliconius butterflies are speciating, and there's some work looking at the genomic components of that speciation:

Highly conserved gene order and numerous novel repetitive elements in genomic regions linked to wing pattern variation in Heliconius butterflies.
Genomic islands of divergence in hybridizing Heliconius butterflies identified by large-scale targeted sequencing.
Divergence with gene flow across a speciation continuum of Heliconius butterflies

Stickleback fish also show a number of examples of incipient evolution, and again genome studies have been done:

(Genomic landscape of early ecological speciation initiated by selection on nuptial colour.](http://onlinelibrary.wiley.com/doi/10.1111/mec.13774/abstract;jsessionid=DB86FB85259118805B95C1C52138D3EA.f03t03)
Genomics of Rapid Incipient Speciation in Sympatric Threespine Stickleback.

Since, as I say, the question as phrased is simply asking for scientifically unimportant trivia, I'll leave it that as far as guessing as to what the actual point is.

DNA is "lego-like" structure from "lego"-blocks
ancient DNA is just a name of more or less long lego DNA sequence
let's say someone in the future finds a box of lego block but does not find any of lego-blocks built toys of our times
or finds sequences only of a few blocks
what would it mean?
another thing - lego blocks are made from a pretty sturdy material (actually like DNA). However, DNA is not the only molecule that can be a template for the protein assembly - RNA can do similar job. However, RNA is extremely fragile and degrades in minutes, and therefore cannot be found in fossils. Have you seen a cake made from lego blocks made from dough and cream?  How long such cake will last?
If you don't find a dough lego, can you say that it never existed?
ps
i agree with these words from the first answer
"However, it's important to point out that the way this question is phrased makes it merely trivia, with no scientific significance."

Please add some references and, if possible, some more scientific points to your answer.


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How do processes of one osteocyte establish contact with processes of the adjacent cells within the mineralized matrix?
Are the processes and canaliculi formed and contacts established after the osteocytes are embeded in the matrix or are they formed during the embedding process itself. Is there any evidence to suggest either?

Osteocytes attach to each other by cytoplasmic extensions through gap junctions [1]. The connections between these cells are formed since they were osteoblasts and osteoid-osteocytes (type II preosteocyte) [1]. Osteoblasts have a greater volume than osteocytes and the lack of extracellular matrix favors their adhesion. As they begin to synthesize extracellular matrix, their volume is reduced and this matrix takes space between cells, but with respect to the existent intercellular junctions around which matrix forms canaliculi.
"Osteoblast Organization" by Physio Muse - I drew this figure in drawperfect, printed to .pdf, and converted to .jpg
Previously published: Not published in any form, including not used on any website. Via Wikipedia.
Osteoblasts are connected via gap junctions mediated by connexin43 protein [2]. Mature osteocytes attach to the bone matrix by integrins (alphavbeta3) [3].

References:

Wikipedia contributors, "Osteocyte," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Osteocyte&oldid=618657480 (accessed July 27, 2014).
Civitelli R. Cell-cell communication in the osteoblast/osteocyte lineage. Arch. Biochem. Biophys. 2008 May 15;473(2):188-92. doi: 10.1016/j.abb.2008.04.005. PubMed PMID: 18424255.
McNamara LM, Majeska RJ, Weinbaum S, Friedrich V, Schaffler MB. Attachment of osteocyte cell processes to the bone matrix. Anat Rec (Hoboken). 2009 Mar;292(3):355-63. doi: 10.1002/ar.20869. PubMed PMID: 19248169.


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Is telomere shortening consistant over consecutive cell divisions from zygote to a differentiated cell?
Considering the complexity of embryogenesis, a temporal referance would be helpful to coordinate the developmental sequences during embryogenesis and fetal development which is to be completed within the gestation period. Can telomere shortening if consistant be used as a reference by every cell to do what it is destined to do at particular time frame? This is without considering the influence of telomerase etc.
This is also without prejudice to the role of DNA directed molecular signalling.
To repeat the question is telomere shortening consistant over consecutive cell divisions from zygote to a differentiated cell? If so can it function as temporal control of embryogenesis?

It is not consistent, and so cannot function as a temporal or generational signal. Not because the telomere shortening is unpredictable, but because of telomerase activity in the embryo.
If it did, gamete production in specialized tissues like the ovaries or testes would have shorter telomeres than the zygote they originated from. Each generation would have shorter telomeres than their parents. They would be genetically 'older', which can't go on forever.
Development is incredibly complicated and mediated by a large number of genes. Try homeobox genes for developmental layout.


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How is it that the WI-38 cell line isolated by Hayflick in 1962 is still very much around and not affected by the 'Hayflick Limit'?
I have searched the net and I have not been able to come up with an clear answer.
Edit: Here is the para quoted from Nature http://www.nature.com/news/medical-research-cell-division-1.13273
"So began WI-38, a strain of cells that has arguably helped to save more lives than any other created by researchers. Many of the experimental cell lines available at that time, such as the famous HeLa line, had been grown from cancers or were otherwise genetically abnormal. *WI-38 cells became the first 'normal' human cells available in virtually unlimited quantities to scientists and to industry and, as a result, have become the most extensively described and studied normal human cells available to this day".*

I essentially answered this here, pointing out that telomerase negates the supposed "limit," which stem cells and cancers usually express.

@ Amory - I doubt if your comment is relevant here. WI-38 is considered to be a 'normal human cell' line. I could not find it described as a stem cell. So where does the telomerase come from? The question is a genuine one and I am looking for a serious answer or comment.

Did some digging, are you sure they actually do?  ATCC seems to disagree

From your own article: "...they so reliably stop replicating after about 50 divisions..."

Yes but the original cell line is still there and is commercially available. I just want to know how they keep it going.

The answer is that the majority of the cells were frozen from very early in their Hayflick lifetimes e.g. after 9 population doublings. They have been thawed out judiciously and only as needed thus preserving a lot of frozen stocks.  When an ampule of cells frozen at, for instance 9 population doubling, is thawed, the cells pick up where they left off and still have 41 doubling a to go.  So the magic of exponential growth combined with the fact that they keep dividing after being thawed has made for a decades- long supply . Does this answer the question to your satisfaction?

Is this Meredith Wadman of Nature?

WI-38 are the cell lines which led to the proposal of the Hayflick limit and are the classic example of cells which will only divide ~40 times.  they are not exempt - they are the example that proved the rule.
Lots of cell lines are commonly available, but have to recultivated regularly from animal/tissue source.  If they can be frozen, then the extraction of new cells doesn't happen so often without exceeding the limit of divisions.  This allows the cell lines to be used widely for experiments despite the limitations on their division in culture.
Other cell lines like HeLa and other tumor cells or Stem Cells can, under the proper conditions, divide without limit and are easier to culture in large volumes, but are often inappropriate for a given research project.


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Is the human body composition real?
In Fullmetal Alchemist when Ed goes to disprove to Rose the Sun God's "miracle" to bring humans back to life by proving that science (in the form of Alchemy) can create people by saying

Water (35 L), Carbon (20 kg), Ammonia (4 L), Lime (1.5 kg), Phosphorous (800 g), Salt (250 g), Saltpeter (100 g), Sulfur (80 g), Fluorine (7.5 g), Iron (5 g), Silicon (3 g) and trace amounts fifteen other elements.

I am wondering, is this composition true in real life? if so what are fifteen trace elements?

You'd probably get better answers at [biology.SE]. See also Composition of the human body - there's more than 15 trace elements thought to play a significant role in human physiology.

The composition of the human body has already been linked in the comments above. It takes a bit more than to mix a few buckets of elements together to get a human.

@Chris - That's actually one of the major plot points of this particular anime.  Just because they can describe the body in terms of ingredients doesn't mean they can transmute those ingredients into a human.  Bad Stuff happens when they try.

@Bobson Ah, ok. I was not aware of that :-)

@Chris - I figured, given the question got migrated out of its original context. It's a good anime, if you're into such things.

@Bobson I will have a look at it some time in the summer. Its always interesting to see new things.

No, it's only a very rough approximation.
I actually made a spreadsheet to figure this out.

The rows represent the composition as described by the quote.  I translated each into its appropriate chemical formula and converted all measurements to grams.  Then I found the atomic weight of each.  The gray area represents the grams of each element made up from that particular description, which are summed up in the first summary line.  The second summary line are the values as specified in The Last Word's link, which are based on a 70 kg (154 lb) person.
You can see that while some of the numbers are in the right ballpark, most are still off by significant amounts (the bottom row is percentage error - negative means the anime was too low, positive that it was too high).

It's been a long time since my high school chemistry.  Please let me know if I made any glaring errors in the process.

Really this is just a comment towards Bobson. The only things that I notice is that you have saltpeter as NaNO3, sodium nitrate, but that's Soda Niter. Wouldn't Saltpeter be KNO3, potassium nitrate. Also, you have no column for potassium which is said to make up .35% of the human body. Hope you see this because I'm not a high enough reputation to actually comment...

@user8184 - Nice catch.  I've updated the chart to properly use K.  Thanks!

@Bobson. Good job +1. You could improve the presentation of the table though. We can barely read the numbers for the moment.

@Remi.b - I don't think I have that spreadsheet anymore, but if you click the image, you'll get the full-sized version.

Indeed "right-click > open in a new tab" is the solution then :) Thanks

Alright, so this answer is partially based off the ideas presented by Bobson above. What i did was take his Excel spreadsheet idea and put that into the upper section. Then, I used the amounts used on the website he linked to check the proper amounts needed in the body. I then used those numbers to reverse engineer how much of each compound would be needed for the measurements to be correct.  Some of the measurements added up while others didn't. The red and blue text are the measurements used for sodium and chlorine, respectively, because they worked against each other. Also, the oxygen and hydrogen didn't add up exactly with the water so that's what the green and yellow text is. From this we see that most of the measurements are off by substantial amounts. This also shows that certain elements exist beyond the compounds stated in the show throughout the body. So although the show is simpler and fun to quote, it's not scientifically correct.

(Full size image)
If you notice anything that stands out or that I missed, feel free to leave a comment and I'll try to correct myself or see your perspective. And sorry the Excel sheet may seem a bit sloppy, I tried to work quickly late at night.

Is it possible to put a link for the spreadsheet and upload it somewhere so that we could get an enlarged version of it. Currently as it is, it is hardly visible.

You can open the image in a separate tab by right clicking and selecting "Open image in new tab". You can magnify that image easier. I don't really know how to link the spreadsheet but hopefully that works.

yes it does.. that bit skipped my mind.. thx

No problem. I realized that the other day when I was trying to view Bobson's spreadsheet

I edited in a link directly to the image, so you can just click it for the full size version.

The Internet can be such a beautiful place sometimes :P

Water can be essentially split into hydrogen and oxygen. Also the amount of salt content can be split into calculating the composition of both sodium and chlorine. Almost 99% of the mass of the human body is made up of six elements: oxygen, carbon, hydrogen, nitrogen, calcium, and phosphorus. Only about 0.85% is composed of another five elements: potassium, sulfur, sodium, chlorine, and magnesium. The remaining elements are trace elements, of which more than a dozen are thought to be necessary for life, or play a role in good health (e.g., fluorine, which hardens dental enamel). A straightforward elemental composition of the human body with the elements given by weight can be found here. I would also suggest going through the wikipedia article linked in the comment section.

funny that down-voters have nothing really to say about what is wrong with the answer. :)

I think it might be the tone of your answer.  Interpreting the anime's proportions also results in 99% of the body made up of oxygen, carbon, hydrogen, nitrogen, calcium, and phosphorus, and ~0.62% other stuff.  The content of the answer is good, but downplaying the source isn't useful.

@Bobson probably what it is. Will edit it


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Many spermatozoa, but just one ovulum
Why do men produce so much spermatozoa, that will get discarded, but women, just one ovulum, which is a good one.
Couldn't men produce good spermatozoa as a limited edition?
Where is the evolutionary advantage of things being like they are?

The way which the spermatozoa have to travel is long and relatively dangerous. So you want to make sure that at least one is reaching its final goal. Having many ovums would mean that you get more than one embryo...

There surely some room for lower spermatozoa concentrations. But since there are reports about fertility problems in men with lower spermatozoa counts, I doubt there is much room.

I think the asymmetry allows for a stronger selection process.  Sperm competition is a powerful force in evolution.
This is useful since sperm vary wildly in quality - for healthy human males only 50% might not be normally motile. Other animals can have a higher percentage, but there are always a significant number of floaters... This means that the fertilization via sperm takes out a lot of the less functional sperm.  Since these are in many cases the same genes we use as diploid organisms later, sperm competition really tames a lot of problems which might be produced in meiosis.
Many animals have multiple mating events from multiple males at just about the same time - when the female is in heat.  This gives a larger role for sperm competition - literally different sires are competing as sperm to fertilize the egg.
In females it is a different process of choosing the cells.  Ova are mostly eliminated in women by the time they reach reproductive age.  I think that this is not well understood biologically... references are hard to find.
The differences in the morphology and roles of the gametes, which goes back to the most primitive of animals has a strong role in selection of healthy offspring through a diverse set of mechanical and biochemical conditions experienced during fertilization.
Added Note: I ran across this reference for how ova are selected for presentation by the ovaries.  Its not really a review, but maybe a lead reference on how selection works in the female reproductive system - its also picky:

In mammals, ovarian folliculogenesis is a process regulated by complex networks composed of various endocrine, paracrine and autocrine factors that interact coordinately.

Its no cake walk to being an egg either...

In addition to motility - up to 70% of sperm can be abnormal forms and this is still considered normal.

that's interesting!  I wonder if they end up fertilizing the egg?

I'm not sure to be honest, some definitely wouldn't (for example loss of the acrosome) whilst others could potentially make it with reduced chances (minor tail defects etc.)

morphology isn't always fitness, though for diploid human beings it seems to be important.

Shigeta's answer is excellent.  I also agree with Chris in his discussion of ova, upon which I want to expand.
This is in part speculation, but I believe that the answer to producing (usually) only one ovum lies in the development of animal viviparity.
Many animals (especially aquatic animals) currently and historically have reproduced via oviparity - the female producing a multitude of ova and allowing the male to shower them with spermatozoa.  The general style of males producing a large number of spermatozoa seems to not have changed greatly (aside from location of sperm deposition) through evolution.
However, viviparous animals must by necessity have some sort of limit on the number of simultaneous offspring, as the females carry offspring within their own bodies.
In animals who reproduce with hemotrophic viviparity, the embryos are provided nutrients from the mother through a placental organ that interfaces with the maternal bloodstream; the biological cost of having many offspring depends on how long they are carried and how large they are at term.
Most mammals carry a litter and develop small, underdeveloped young, but hominids evolved to carry (usually) one.  There's an interesting discussion to be had on the different reproductive strategies (very careful rearing of one versus attention divided over many) but I don't have sources at the moment for those.
But the cost of having more than one embryo must have been significant enough in our own past evolutionary process to have eliminated most women who produced multiple ova.  Maternal mortality rates have historically been MUCH higher than they are now, and risk is higher with twins (or more).  There are still times when more than one ovum reaches maturation and ovulates, resulting in dizygotic twins, but it's fairly rare (between 6 and 14 per thousand births).

As spermatozoa need to be transported therefore in order to increase the chances of successful transportation (and fertilization) the number may be high.
Also, there is only one ovum probably because more cytoplasm is required in the creation of an ovum, which is evident from its size.


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What does this sentence about angina mean?
I do not understand this sentence

Angina can be treated ambulatory (in out-patient) in stable angina.

I think ambulatory refers to ambulatory ECG monitoring.
So I understand this that you can treat stable angina based on ambulatory ECG.
How do you understand this sentence about "ambulatory" angina?

Ambulatory means there is no emergency and refers to where the patient is and not to the disease itself (here the patient is out of hospital): for example there is no need to perform urgent PTCA or other procedures related to unstable CAD (coronary artery disease).
Another option is - to hospitalize the patient to perform urgent or planned procedures if the patient is unstable and there is deterioration in his/her status which may worsen and threaten the life.
The key word in this sentence "stable".


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Animal identification (larva)
I found a tiny, white animal in my mouth on the morning of June 28, 2015, in Toronto, Ontario. Luckily I don't seem to have hurt it. I was eating some sunflower and pumpkin seeds at the time. I believe that's how it got there.
The pictures include a toothpick and a Canadian cent to give an idea of its size.
I also took a video of it crawling around. I will post it if the pictures are not sufficient for identification.

Did you see any dots on it?

@Ilan I don't see any dots on it. It looks very much like the picture you posted. I still have it. I might try to keep it until it molts.

Oh, is it still alive? So keep it, it would be nice to see the actual moth!

This animal is moth larva. The images presented are blurry, but if there are no any dots on the larva my first suggestion is:
pantry/Indian meal moth larvae -

"They are a common grain-feeding pest found around the world, feeding on cereals and similar products."
(picture source)


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Toronto spider identification
I found it in Toronto, Ontario, during early June, 2015.
When prodded it seemed to jump around, or at least to move very fast.
I can also post a short video of it if needed.

That jumping spider is a Jumping Spider! (That is, family Salticidae, commonly called Jumping Spiders).
There's a lot of diversity in the family, but your pictures look similar to the Zebra Jumping Spider.


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Butterfly identification: Dorset England, July.
Can you please identify this butterfly. It was seen in Dorset England 9th July. I think it is a female Silver Studded Blue.

see similar species at the bottom of this page - http://butterfly-conservation.org/50-781/silver-studded-blue.html

see this site too http://www.natureofdorset.co.uk/species/common-blue

by the way its a lovely image

Thank you for the response rg255. After continually looking at images on the sites you advised, I finally concluded that it is a Silver-Studded Blue. The spots have worn a little and should be a dominant black like wise the band of orange spots should be more dominant.

The silver-studded blue is frequently found feeding on this plant, cross-leaved heath. There are good numbers of this species to be found on the heaths of Dorset in July and I would suggest that this is certainly silver-studded blue.

Peter, it would be great if you can add some references.


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GULO only for mammals?
I am not a biology student, but just want to know if GULO gene are present only in mammals or all species possess it ?
And is GULO gene active in human fetus?

On Genecards it is mentioned that the GULO pseudo gene being expressed in humans in many major tissues. In that case the gene might be active although not encoding for a functional enzyme.

GULO encodes L-gulonolactone oxidase which catalyses a step in the biosynthetic pathway to ascorbic acid (vitamin C).
I did a BLAST search at NCBI using the mouse GULO protein as probe, excluding mammals, and I saw highly significant hits in reptiles, birds, sea urchins, fungi and bacteria. I conclude that this enzyme, (or very close relatives) is ubiquitous.
Humans (and other primates; also guinea pigs and the Dalmatian coach hound) have a defective GULO gene and so require dietary ascorbate.
Since the gene is non-functional in humans it isn't expressed in the foetus.

Wrong in regard to "Since the gene is non-functional in humans it isn't expressed in the foetus." See my answer.

De Tullio writes

We know from other studies that pseudogenes are not inert, but can have a significant role in epigenetic control of gene expression (Poliseno et al. 2010). Could this also apply to the human gulonolactone oxidase pseudogene? Time (and much research) will tell.
De Tullio, M. C. (2010) The Mystery of Vitamin C. Nature Education 3(9):48
https://www.nature.com/scitable/topicpage/the-mystery-of-vitamin-c-14167861/

On Genecards it is mentioned that the GULO pseudo gene being expressed in humans in many major tissues. In those cases the gene might have an epigenetic role.

This is just another example of Stack Exchange not working. I wrote the same thing as in this answer in a deleted answer. It was not reopened.


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How the vaccine based on "non replicating viral vector" is produced?
As I understand, this kind of vaccine is a virus that can infect the cell, start synthesis of  proteins encoded by its genome, but cannot finish the replication cycle till the proper end. It can have extra genes in its genome, encoding proteins that cause the wanted immunity to develop. Some important vaccines against COVID-19 are based on this approach.
The question is, how such an "incomplete virus" could be produced in large amounts? It would be logical to assume that it was replicating during the manufacturing process, but then why does it cannot any longer? The only hint I found is the usage of the "helper virus" that infects the same cell, so the "incomplete virus" can borrow some parts from the healthy "coworker". However this raises another question: the helper virus obviously replicates also itself, and how to discard it later without inactivating the "non replicating" one? It would just cause infection without any use if not discarded.
I have done some search over web and article databases but was not able to find a short and clear explanation of this method. The main focus of the works I found is always somewhere else. I understand that exact technology may be secret, but it is likely at least remotely based on some research work anyway.
How is a "non replicating vector" replicated to produce enough of it, for making a vaccine out of it?

Complementing cell line (or complementary cell line) is a cell line which has been genetically modified to produce proteins necesary for non-replicating virus replication. It is designed to express exactly the genes which had been deleted from virus to render it non-replicating. The non-replicating viral vector can replicate only in complementing cell line and not in other cells.

I have learned this in a lecture. I have tried to find some comprehensive reference for this answer but found only use cases.

do you have any other good sources for "complementing cells lines? I upvoted your answer. By the way, does a Adenovirus vector for covid-19 vaccine carry the spike protein - as an experienced user would you think that's a good question to publish? How can Adenovirus be replicated in vitro without "expression" of the implanted mRNA for the spke protein? It should carry it.

@Peter Bernhard Sorry only sources would be what I would google. I wouldn't call myself experienced user and I try to stay out of judging questions. You can ask the question but be careful to not conflate expression of protein with virion packaging. The host cell expresses and contains a lot of different proteins. Only specific proteins assemble into 3D structure to form a virion.

Thank you. Good yo said "expression of protein", now up above "expression of genes" seems better in formulation. However, this  improves ma understanding - the "cell line" as a helper adds the proteins, not the genes (correct me if I am wrong, please) that are necessary for a virus to still be an intact virus, for the purposes of vaccination, to be specific. So, "packaging" seems to be very illuminating: maybe packaging genes have been deleted, and the helper cell lines add that stuff, to build viruses that last their life time only.


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How does epigenetics affect the birth conditions via alcohol?
Recent study has shown that epigenetics can play role in male-caused infertility and it cites for example studies which showed an enhancing of silent genes when drinking alcohol. Since the study argues this as a reason to the negative newborns' conditions, it has to act negatively on the organism somehow.
I would call an epigenetic influence on the fetuses an influence that is meant to prepare the fetus on the change in the conditions. Does the evolution of the enhanced genes any relate to the alcohol consumption, or is it just a negative coincidence?

You need to rephrase your question. The "study" you mention is a review. Like pretty much it reviews, it proves nothing. In general we have very limited abilities to change the epigenome in controlled, experimental conditions - a requirement in order to prove anything. Also, I searched with Ctrl+F, in the paper you mentioned, "enhance", "silent", "infertility", and did not find any mention. Can you give an example of gene that you are thinking of?

I mean the conclusions from the chapter: Effects of environmental exposure on parental epigenetics: alcohol             Sorry I can't get to the original study.