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Could a sperm be altered to contain a female's genetics?
While discussing with a friend a while back on the likelihood a futanari (a woman with both fully developed and functioning sets of genitalia) existing in real life, we got into a discussion of whether a child could carry the genetics over from 2 months.
Currently (to my knowledge), for a female same-sex couple to conceive a child and for both women to be involved, one would donate an egg, the other actually gives birth, and the sperm is donated by a third party. However, this means that the child will carry over the genetics of one women in the couple and the unknown male.
I am wondering if there is a way for sperm to contain the genetic information so that way both women in a same-sex relationship could be genetically related to the child.

Only as a comment for the moment: I remember to have read about animal experiments were it was tried to get embryos from male-male and female-female combinations. These embryos died very early due to the different imprinting of the genes and their possibility to get activated. Obviously some genes are activated from the mother while others are only activated from the father. If both copies are active or inactive due to epigenetic changes, this makes problems.

@Chris you should post an answer but remember science may not be there now it may be there later

Note that some serious epigenetics disease might come up such as Angelman syndrome, Prader-Willi syndrome and Beckwith-Wiedemann syndrome.

There are now some papers and actual proteins that imprint the genome (due to mostly X chromosome inactivation) are found. So reprogramming the gametes' imprinting should now be possible. So now two gay man can produce a child. That is going to be interesting. There is also that chimera man who have different imprintings...

You might be interested in this article. In this study they created haploid ES cells from artificially activating an unfertilized oocyte and growing the haploid cells. These cells, when introduced in the ICM, give rise to viable chimeras.
In another study, haploid androgenetic ES cells were created by injecting a sperm into an enucleated oocyte. These cells also are capable of creating offspring when fused with another oocyte. [See this post also]
Also, since these cells can be cultured, they can be genetically modified. However, they undergo spontaneous diploidization and lose reproductive potential after a few rounds of division. This is related to the alteration of epigenetic status of these cells on certain imprinted loci. Others have also indicated the importance of both paternal and maternal imprinting in the viability of embryos which might be a problem in oocyte-oocyte derived hES cell fusions (See cross references). [Check this article too].
It can be concluded that oocyte$-$oocyte-hES fusions are not observed because of same imprint status (Also mentioned by Chris in the comments). AD-hES also lose their paternal imprints on prolonged culture (but retain maternal imprints). It is to be ascertained if paternal imprints are more unstable compared to maternal imprints under these conditions. It may be possible to optimize the culture conditions such that oocyte derived hES lose their maternal marks: would that lead to incorporation of paternal marks post-fusion is debatable.

Yes, it is scientifically possible. Though a third party (male sperm donor) is still required. Scientists working for a British biotechnology company, as well as doctors at Oregon Health and Sciences University have been working on complex procedures but are fighting the ethical red tape and are not currently using the techniques on patients.
This is the basics of the procedure being used by the doctors in Britain "The nuclei from the father's sperm and the mother's egg, which contain the parents' DNA, were removed. The nuclei were put into another egg from which the nucleus had been removed, but which retained its mitochondria. This new embryo contained the genes from both parents plus a tiny amount of mitochondrial DNA from the donor egg."
The scientists in Oregon have a similar yet slightly different approach with procedure explained as "Doctors would remove the nucleus DNA from the donor eggs and replace it with nucleus DNA from the patient's eggs. So, they would end up with eggs that have the prospective mother's nucleus DNA, but the donor's healthy mitochondrial DNA."
This approach can easily be modified to fit a lesbian couples desire to have a child that is related to both of them. Scientifically it is possible for two mothers to be directly related to a child, but the sperm is still a relevant part of the equation. It is not possible, so far, to create a functioning embryo without male sperm.
Sources:
http://digitaljournal.com/article/290608
http://www.huffingtonpost.com/2012/10/24/3-person-ivf-embryos-women-man_n_2011546.html
And my reproductive biology book and studies: Trends in Endocrinology and Metabolism by Claire Bourgain.

I don't think this is what was desired. This is used to mitigate the presence of mtDNA mutations in the female line. While technically the mtDNA donating mother has some genetic relationship to the child, this is so minor - only 13 proteins are coded for in the mtDNA,and they are all involved in the ETC. I think the question is looking for nuclear DNA from two females as discussed by @WYSIWYG

authors: Валерий Заподовников


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What are the criteria for determining the origin and end of muscle anatomically?
For example the pectoralis muscle starts from sternum region and ends on the acromion or coracoid process. Why you can't say that it starts acromion process and ends on the sternum?

This is more of a convention.
The start point or origin is considered to be:

bone which is proximal
bone with higher mass
bone with higher stability during muscle contraction

The end point or insertion is:

the structure that tends to be moved by contraction
tendon
distal end of a bone

Reference: Wikipedia - Anatomical terms of muscle

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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Detecting Calcified stones and cracks in tooth
I had a dental problem when my first molar broke some months ago and after some decay and pain I am undergoing a dental treatment. The doctor was performing a root canal and kept on talking about calcified stones being formed and looking for a 'tak' sound inspite of having x-rays. Doctor did not point to the calcified stones earlier and suddenly came out with this new issue. In the mean time when looking for stones doctor actually managed to break my tooth and has blamed grinding and clenching for a crack that caused the tooth to break.
I am shocked that neither the calcified stone nor the crack showed up in x-ray and the preliminary examination. With current technology, can the cracks in tooth and calcified stones not be detected.

Cracks on your teeth are hard to detect if they are cracks on the mesial or distal surfaces (surface of the tooth closest to and farthest from the midline respectively) through x-rays. Please check this link for illustrations and very good explanations from the University of Maryland dentistry department. The different methods on the detection of cracks as well as the uses of radiographic evidence can be found in this link.
Now pulp stones can be identified through x-rays unless they are too small or not too dense. There has been researches done specifically using radiographs for detection like "A radiographic assessment of the prevalence of pulp stones in Australians". It could also be human error that your doctor was unable to detect it. A small explanation on pulp stones can be found here.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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How well does the event-driven DVS sensor approximate the rods of the retina?
There is a neuromorphic vision sensor that is generating some interesting research these days that is called the Dynamic Vision Sensor. One of the claims of this sensor is good approximation of the conventional retina. However, there's no detail on the website in what way this is true or to what degree this is true.
It does not detect colour, so obviously it isn't an accurate approximation of the cones found in the retina. Additionally, the function of the cornea is fulfilled by the lens of the camera, so this input isn't totally approximated. Consequently, the only significant component that remains to be evaluated is the rods of the retina?
What are the similarities and differences between a retina and the DVS sensor?
First, let me save you some reading by explaining how the DVS sensor is different from a typical camera. Instead of synchronously sending frames with data about every pixel, the DVS is event driven. That means, when a light intensity change occurs, an event is fired with the address of that change, a time-stamp and whether the pixel observed an increase or a decrease.
Do rods also encode changes in light intensity in the same manner? If not, what is the difference?


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Do macrophages engulf mtDNA?
Let us assume that in a human body, a mitochondrial DNA is released to extracellular environment.
We know that mtDNA inheritance is solely matrilineal.
So the question is, If your mitochondrial DNA is released to the extracellular environment (or into
cell cytoplasm) due to cellular and/or mitochondrial damage, what could be the
ramification of this released DNA if your immune system cells (such as macrophages,
dendritic cells or B cells) pick up and sense these DNA as a danger signal?
Is there any chance for mtDNA to survive by establishing a new mtDNA ?
I am thinking, macrophages engulf and destroy them but cannot provide sufficient evidence.

Macrophages ingest and are activated by bacterial DNA

EDITS - I appreciate the comments and have incorporated them here.  Thanks to    @Superbest and @user22406 for raising them.  I hope this makes a better answer for the community.
Under normal circumstances, genomic (self) or mtDNA released into your cell or body cause absolutely no (known) problems.   I'll explain why that is, how the body can detect bacterial DNA, and finally the circumstances in which DNA can cause problems.
Self-DNA generally causes no problems
Almost from conception, cells in your body die.  Sometimes as part of pre-programmed sequence (eg inter-digital cells of the fetal limb paddle die and form fingers) or normal replenishment of cells such as the white blood cell (hundreds of millions of neutrophils die each day) or your gut epithelium.
Macrophages consume liberated DNA, and the reticulo-endothelial system in the spleen, liver and lungs filters the blood for cellular fragments.  This paper (from @Superbest) shows that bacterial DNA, and not normal human genomic DNA, can activate macrophages.
So your immune system develops, and is constantly being exposed to, virtually every cell type and cell component (proteins, lipids, DNA and RNA etc).  If self-DNA could spark an immune reaction, normal life would be difficult.  We don't make antibodies (from B-cells) or T-cells that react with self-components due to a process called anergy in which any developing T- or B- cells that could react to self-components during their maturation are instructed to shut down and/or die.   Yes, mitochondrial are inherited matrilinearly, but they still lyse and cause anergy, preventing an auto-immune response.
(Not all cell death is harmless- @Superbest's comment reminds us that apoptosis (involved in finger formation and other tissue remodelling and cell turnover) can package cellular components into self-contained vesicles.  On the other hand, damaged or lysed cells can liberate cytoplasmic components that can be pro-inflammatory or pro-coagulant.)
Macrophages' vacuoles contain DNAse II, an enzyme that degrades DNA it encounters following phagocytosing/endocytosing fragments of dead cells.  More about that later....
Our bodies can detect bacterial DNA.  Same DNA, different decoration
However, invaders (bacterial, viruses, worms etc) may activate a family of receptors called Toll-like receptors (TLRs).   TLRs have evolved to have specificity for antigens not seen in mammals e.g cell walls, bacterial flagella and so on.  Some TLRs do recognise DNA or RNA.  You may know that DNA contains 4 nucleotide bases, A,T,G and C.  In mammals, special sequences of two bases, C-G, (called "CpG"s) can be enzymatically modified by a methyl group.  In bacterial CpGs are not typically methylated and so a TLR (e.g TLR-9) that detects un-methylated CpGs is generally detecting bacterial DNA.
Mitochondria are different
Mitochondria have features that resemble bacteria: a cell wall, a genome and the production of proteins that begin with the amino acid N-formyl-Methionine (f-Met).  Mammalian proteins don't have f-Met at the start ("N-terminus").  Macrophages have a receptor that can recognize f-Met sequences (especially f-Met-Leu-Phe, fMLP) and activation of the fMLP receptor stimulates phagocytosis.
This 2013 paper describes the controversy whether mammalian  mtDNA is methylated (at CpGs) and offers strong evidence that it is methylated.    In contrast, the Oka paper  gives 5 citations where mtDNA is not CpG-methylated.
So..do mitochondria look like bacteria to our innate immune system?
@user22406 flagged this paper by Oka et al which cites this paper by Zhang et al as evidence that mtDNA can be pro-inflammatory.  The Zhang paper provides evidence that mitochondria can stimulate the immune system's receptors for (1) f-Met-peptides (i.e detecting mitochondrial proteins that look 'bacterial") and (2) receptors for un-methylated CpGs, the TLR-9 receptor.  The Commentary on the article has a great figure of how mito components might promote inflammation which copyright prevents me adding.
The Oka paper uses 2 key techniques: (1) surgical constriction of the aorta to cause heart enlargement (cardiac hypertrophy) and (2) a mouse strain with the gene for DNAse II deleted (noted as -/-, two minuses, both alleles gone).  In the hearts of DNAse II -/- mice, they observe higher levels of deposition of mtDNA in the damaged heart (Supplemental Fig 2), greater heart damage and many animals die.  This suggests that excessive levels of DNA (not degraded in these DNAse -/-  mice) may be driving the damage. (The general phenotype of DNAse -/- mice was studied by Kawane et al  and the mice get an arthritis).  In Oka's DNAse II -/- mice, the degree of heart damage can be reduced by blocking TLR-9 (using an inhibitory oligo).  In aortic constricted mice where the DNAse II gene is intact (+/+), adding the TLR-9 blocking oligo gave some improvement, suggesting that the level of unmethylated DNA liberated in tissue damage may stimulate TLR-9 in normal animals.
The authors also examined aortic constriction in TLR-9 -/- mice and found they had less lung and heart damage compared to controls.
In summary, the Oka paper suggests something is signalling  via TLR-9 to drive inflammation and damage in this model and implies (but does not prove) that the 'something' is mtDNA.
mtDNA in the plasma
Another Zhang paper  detects up to 1ug/ml of mtDNA in the blood following major trauma (car and motorcycle crashes, falling 4 stories etc).  Their paper shows that this level of liberated mitochondria could stimulate immune cells (via TLR-9 and f-Met receptor).
mtDNA won't get back inside the cell
Extracellular DNA and RNA is generally broken down and cleared rapidly.  DNA, being a large, negatively charged molecule, will have extreme difficulty passing through an intact cell membrane.  In the laboratory, cells need to be exposed to high voltage electric shocks to make transient 'pores' in the cell membrane to allow DNA to enter or have the DNA formulated in liposomes.  Even if endocytosed, there is no known pathway to direct endocytosed DNA to the nucleus or an new mitochondrial 'host'.  So mtDNA would be extremely unlikely to re-seed into a new cell or a mitochondria.
But self-DNA can be harmful if released in large quantities
During successful cancer chemotherapy, large numbers of tumor cells lyse and may give rise to tumor lysis syndrome.  Among the products released when a tumor is killed is DNA. A and G - the 'purine bases' - can be further metabolized into uric acid.    Uric acid can crystallize in the kidney and cause damage.
Summary
Mitochondria may be the remnants of endosymbiotic bacteria but, absent major trauma or mutations in both of your DNAse II genes, mitochondria come (and stay) in peace.

You are wrong in your reasoning about cells dying. Apoptosis specifically involves digestion of all DNA, and packaging of the cytoplasm of the vesicles, so none of it spills. In fact, spilling of the cytoplasm from necrosis is detected by the immune system, and causes inflammation.

@Superbest. Fair point re some cytoplasmic contents being pro-inflammatory or even pro-coagaulant.  Yes, cells die by a number of means including by apoptosis, autophagy and necrosis.  My point was host DNA doesn't drive meaningful immune responses.  Macrophages/RES consuming apoptotic bodies mean lots of DNA enters immune system pathways.  I'd be happy to edit the answer if you can point to data for genomic or mtDNA driving an immune response, like OP asked.

"Macrophages/RES consuming apoptitic bodies mean lots of DNA enters immune system pathways." - No, it doesn't. All the DNA in those apoptotic cells is chopped up. They are only consuming single nucleotides or small oligonucleotides. Own DNA does not appear to be inflammatory, according to the paper I linked to in my other comment.

@Superbest.  Apoptosis experiments show it generates a DNA ladder - by relatively infrequent endonuclease cuts, and not complete digestion.  Other than that, we seem to be in agreement, no?

@Superbest. Would you mind if I included your reference in my answer?  You found a nice, early and clean experiment.

Mitochondrial DNA that escapes from autophagy causes inflammation and heart failure http://www.nature.com/nature/journal/v485/n7397/full/nature10992.html


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What makes us all different and similar to some extent?
It is said that genes define how we look physically and psychologically; so for example if a male human sperm carries a certain number of genes, say x, and a female carries y, then mathematically there would be m genes from the male and n from the female, and a finite total available. Could there be people identical in appearance if the same genetic combinations recur?
Also we find similar-looking people with perhaps similar behaviour accross diferent geographic locations; does this means that they have similar genetic make-up, up to some percentage?
Please correct my biology and share the possiblity of having genetically identical people across different geographic locations.

Please see this question and answer (http://biology.stackexchange.com/questions/10474/on-average-how-many-genes-alleles-do-people-share/17292#17292)

For ease of explanation let me first tell you that the "genetic makeup" is called "genotype" and that "how we look physically and psychologically" is known as "phenotype". These are not complete definitions of the terms but this should help you understand what we're talking about. I also apologise for the lack of detail or inaccuracies which many fellow contributors may find aggravating, but the question calls for keeping things down to the most important aspects :)
Do genes define how we look?
Genotype defines to some extent the human phenotype, but we don't know exactly to what extent regarding most aspects of the phenotype. This is called the "nature vs. nurture" debate and is concerned with the effects of genotype itself on phenotype vs. the effects of non-genetic influences after fertilisation (such as chemical surroundings during embryonal growth, experiences at young age etc).
Numbers of genes from males and females
Another misunderstanding is that a sperm carries a certain number of genes which it combines with a number of genes from the egg. While this is strictly true, the number isn't what matters because we all carry the same number of genes (*). The genotype doesn't depend on the number of genes, but rather, almost all genes exist in several variants within the human population. So the genotype is actually about which variants an individual carries, not about the number of genes. In biology, we use the term "allele" to refer to variants in this context. So in other words, each gene can have different alleles.
People with identical appearance
If two people have identical alleles for all genes (i.e. identical genotype), then they can indeed look almost identical. However, because of the vast number of genes and alleles present in the human population, it is practically impossible for the same alleles to come together in two humans. With only one exception: if two individuals result from the same combination of sperm and egg cell, they will be identical, and this is exactly what happens in monozygotic twins.
Similarities by geographical region
However, the total number of genes and alleles is limited (**). This concept is what people call the "gene pool" and is the reason why humans are still always humans and share certain similarities. In particular, for most of human history our geographical movement has been limited (most of the time), creating geographical "sub-gene pools" (to keep it simple). This is why people from the same geographical region are more likely to look similar; they have a higher chance to share the same alleles of genes that determine appearance. In terms of behaviour - to whatever degree genotype influences behaviour, peopel from the same geographical region will be more likely to be similar in these regards than people from different geographical regions. However, you can now hopefully understand why this "degree of similarity" is next to impossible to quantify (lack of knowledge: which genes determine what, how many alleles exist of them, how many people have which allele, how much and how far do people travel,...).

(*) Ok, not quite - it is possible for an individual to have the odd gene actually completely missing, but for the sake of simplicity we all have the same number.
(**) Again, not strictly, because new alleles and possibly even entire genes can result from mutation, but this is relatively rare and on the large scale you can work on the assumption that they are limited in number.

It is said that genes define how we look physically and psychologically

I would be skeptical of anyone saying this. Nature vs. nurture is far from settled, especially in psychology. The trend seems to be that many behavioral traits have a large heritable component, but are far from being determined only by heritable traits.

if a male human sperm carries a certain number of genes, say x, and a female carries y, then mathematically there would be m genes from the male and n from the female

I think you are confused. If a sperm carries $x$ genes and an egg carries $y$ genes, the resulting zygote will have $x+y$ genes. If the male had $m$ and the female had $n$ genes, $x+y\approx m+n$ and $m \approx 2x$, $n \approx 2y$.

Could there be people identical in appearance if they end up with identical combinations of genes?

Yes, we call these people identical twins. It could also occur by chance in unrelated individuals (well, everyone is somewhat related...) but this is extremely rare. There is just that too much variation in the human genome. There are literally tens of millions of points in the genome where some people have one version and others have another, and this person would have to happen to have the exact same version at each one as you do. This is an order of $10^{-8}$, if we consider humanity completely homogenous (and it isn't, so the probability is even lower).

we find similar-looking people with perhaps similar behaviour accross diferent geographic locations; does this means that they have similar genetic make-up, up to some percentage?

The genes may be different and still lead to the same phenotype. Say one person has the set of genes that result in red hair, another one has the set that results in brown hair. They are both albinos. They'd look the same, but have different genes.
Also, genes are not the only thing that determines how people look or behave.
So the fact that two people are phenotypically identical does not imply they are genetically identical. You can come up with a Bayesian probability that says they are more likely to have similar genes if they look similar, but how do you calculate the priors? Worse, how are you even going to measure how "similar" people look, or behave?


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Prenatal hyperkinetic dysfunction and its effect on endurace
Do people with an hyperkinetic dysfuntion have a better endurance?  Are they fitter in cause of their Dopamine-overdose or any other reason? I have a case, where someone does not do any sports, but has an endurance way better than most of others who does no sports. He even can compete with some amateur athletes.
Just for comprehension: He does not eat well, sits most of the time (during work, at home), does not do any other activities except eSports (onlinegames).
Maybe someone has an answer, at least I hope you have.

cross posted here: http://cogsci.stackexchange.com/questions/6429/do-people-with-prenatal-hyperkinetic-dysfunction-have-better-endurace

changed to not be a crosspost


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How many areas are there in Brodmann map?
I read Wikipedia claiming 52.
I heard that this can be extended to 54.
I see there is no limit of having more areas - just better understanding of the neuroblast migration and fibroblast too, probably.
How is this newer classification of Brodmann map done?

Bowmann or Brodmann map?

@potterbond007 Thank you for pointing out the mistake in the body! Brodmann map. I apparently have read too much about kidneys.

I am no expert on the topic, but according to an article published on the centenary of his study, it states that the microscopical structure and classification of these areas are in parallel to the evolutionary distinction between old and new cortical subdivisions. So as and when new subdivisions are deduced (based on its function, cytoarchitecture or the structure and organisation of cells) the map can be extended to include them. There was no upper limit to the number of divisions set in any article I read so it would be nice if you could provide some reference to where it says that the extension can be done to 54. If you are interested, you could have a look at the map published by Constantin von Economo in 1925.

Yes, I agree with you. This is just research talk where I heard people talking about more than 52 areas. I have no idea how they are doing the division. Probably, like you describe, by thinking parallel processes at some point at a particular point in time. I think the amount of these areas i.e. processes vary between different points under considerations.

@Masi basically with the advance of research, even minute differences in any part of an area currently designated due to structural differences or some new functional properties, the map can be further extended to include them as a new subdivision. Rest, I believe it is left to the discretion of the researcher as there is no definite compulsion to map new areas unless significant differences are found. That is my understanding on the subject


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H O N C alternatives for organic life?
Most organic structures built from hydrogen, oxygen, nitrogen and carbon. They are represent 1-,2-,3-,4- bond relations (chemical valence) which allow to build variety of chain structures.
Are there exist some replacements for these elements to create complex structures that theoretically can create life (self-reproduced or be a part of cell as organelle)?
UPDATE

Is there a common chemical model for life in the universe?
Arsenic-eating microbe may redefine chemistry of life
A Bacterium That Can Grow by Using Arsenic Instead of Phosphorus
https://en.wikipedia.org/wiki/DNA#Alternate_DNA_structures
https://en.wikipedia.org/wiki/Arsenic_DNA

For the last two references: These are, nicely spoken, highly debated. Its been a while since I read the paper, but as far as I remember they never showed a direct proof that the DNA from these bacteria contains arsenic instead of phosphorus. They can however grow in the presence of high arsenic concentration which is also interesting and impressive. See this article for example.

Its not scientifically or logically possible to say 'this is impossible' but since this is a speculative question, I'll hazard an opinion.
I'd like to argue that, at Earth standard pressure temperature and atmospheric conditions, C H O and N are not really replaceable.  Throw water into the mix as the most common liquid and replacing any or all of these elements is hard to imagine.
One can think about this by looking at the formation of long hydrocarbon chains.  Silicon can form polymers, but they tend to fall apart. Silcone-oxide polymers [SiR2-O-SiR2-O-] are more stable, but do not resemble hydrocarbon polymers as readily.
Carbon is much more versatile, capable of forming either chain, or including sulfur, nitrogen in stable chains that don't seem to really have any length limitations.
At thousands of atmosphere's pressure, temperatures of 70 Kelvin or in a sea of sulfuric acid, its easy to imagine other sorts of chemistry would dominate - phosphate , arsenic chains or germainium lattices, but on Earth most of these would fall apart.
Even if/when life is discovered elsewhere , it will certainly feature chemistry that will completely amaze us; unlike anything here.  But even so, its hard for me to imagine it being completely exclusive of these four elements.  I just want to point out that by a wide margin, hydrogen is the most common element of the universe.   Nearly all the other light elements like C, O and N are the next most common.  This is simply because they take fewer nuclear fusion events to create.  Hydrogen is pretty useful no matter what chemistry you are looking at.  These four are probably going to be there somewhere - most planetary atmospheres have Ammonia, CO2 and methane in them as well - at least as far as we've seen.


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Vitamin D oral intake, transportation and absorption
Several factors affecting vitamin D and its active form absorption and storage

acidity of stomach (not significant effect)
cytopathic effects of viruses
cytopathic effects of bacteria

where the last two reasons can be some reasons which may explain why vitamin D should be administered with bread; to make a surface covering around out vitamin D molecules.
Probably, the fibers also work in some short of transport media.
They can also partially explain why big dose of vitamin D does not last long time in the normostenic body.
Summary of procedures in administrating vitamin D orally

with bread (carbohydrates; fibers) - possible protection, better transportation and more to absorbtion
with oils (fat metabolism could help in destroying extra free radicals; but I see no other sense in administrating vitamin D with fish oils)
daily (not weekly)

Why does the lipid-soluble vitamin D not last in the body long time?


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Converting Ensembl Compara gene tree DNA alignment to corresponding amino acid alignment
I have Ensembl compara gene tree alignments (Compara.gene_trees.57.fasta.gz downloaded from ftp://ftp.ensembl.org/pub/release-57/emf/ensembl-compara/homologies/) in nucleotide format. According to documentation, it says that the file "contains the peptide alignment for every genetree in fasta format".
I was wondering what might be a handy tool to obtain the corresponding amino acid alignments from the file.
Thanks,
Ikram

The file is gzipped, so use a tool like 7zip or WinRAR to unzip it. After that, just open the fasta file in any text reader..?

Thanks Armatus for the comment. In fact I can view the file using zless in ubuntu. The problem is that the data is in nucleotide format (AGTC...) and I want it in amino-acid format (NGHIK... etc). I guess that, since the data is coding sequence, no frame shifts are needed and just a mapping from DNA-to-Protein might work (But I am not sure, and just want to confirm it before writing some code for it)

As a general rule, both within and without the world of bioinformatics, public FTP sites contain README files tat explain what each file offered by the FTP server contains. The file README.protein_trees states:

Compara.gene_trees.{release}.emf.gz
                        contains the peptide alignment for every genetree in emf alignment format
Compara.gene_trees.{release}.fasta.gz
                      contains the peptide alignment for every genetree in fasta format

This means that both Compara.gene_trees.57.emf.gz and Compara.gene_trees.57.fasta.gz contain the protein alignments. I had a quick look at the files and it looks like Compara.gene_trees.57.fasta.gz actually contains nucleototide sequences but Compara.gene_trees.57.emf.gz does indeed contain a protein alignment:
$ zgrep -m 1 AAAAASAAAT Compara.gene_trees.57.emf.gz.crdownload
SAAA-AHS-AGTAAAAA--AA--AAAAASAAAT-ASAATAI-SASSA-ASAAT-V----AAASVAA-HAFAS---ASAAASAAAAA-TIVAAAAX-SAASIYSAAAA-YAA--AASAS-ASAASAS-ASAASSSSSARS-AAS

So, to answer your question, the file you want is the .emf.gz one.


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Two-fold cost of sex and r/K selection theory
This article cites a bunch of articles (I haven't been through them) that the effect of the two-fold cost of sex is "reduced" in stable environment or in K-selected environment. It says:

[..] the infamous ‘two-fold’ cost may be reduced or, perhaps more accurately, more easily balanced in K-selected species. The ‘cost of males’ is with respect to reproduction. Abugov (1985) argued from life history theory principles that the two-fold cost of sex might be easier to pay with K-selection. The two-fold fecundity advantage of asexual reproduction is always a two-fold fitness advantage, regardless of whether it is in a K- or r-selected environment. However, a survival advantage is worth more under K-selection than under r-selection. Consequently, it is easier to balance the two-fold cost under K-selection if sexually derived genotypes have a survival advantage.

I think that k-selection, k-selected environment and stable environment describe (more or less) the same kind of environment. Let me know if this sounds wrong to you. Here is wiki for r/K selection theory
From the same article K-selection is defined as:

K-selection might favour slower development, greater competitive ability, delayed reproduction, higher survival rates, lower resource thresholds, leading to ‘efficiency’ (rather than productivity) and constant population sizes at or near carrying capacity of the environment.

It sounds really strange to me. Can you please help me to understand why the two-fold cost of sex is lower in stable environment than in unstable environment?.

r/K selection has become more of an heuristic for characterizing a species' strategy of reproduction and less a matter of predicting what sort of species will emerge from a given environment as it had originally been proposed by MacArthur and Wilson in 1967. The paper you cite tries to determine whether rotifers become more r or more K selective in different environments.
The thought here on k-selection is not almost from the definitions of the term, which is why it isn't explained in the paper.
In R-selected strategies, many more offspring are produced, but less investment is made in each one.  Think about a cockaroach laying thousands of tiny eggs.  The hatchlings might be eaten by their own mother; they are so 'cheap' the insect who layed the eggs doesn't have any anxiety about their survival.  In extreme cases, most of these hatchlings will not reproduce, they may even be a bit of food for the ones which do reach maturity.
In k-selected strategies, very few offspring are produced.  In addition to the 'cost of sex' limitation, they are invested in so heavily that the female may stop being fertile for a while.  An example would be how female mammals which are lactating are not fertile or seasonal mating like many birds do; the females turn off reproduction so that they can focus on the success of one or two produced offspring.
k-selection is advantageous over R-selection when more of their investment pays off.  If one out of ten R-offspring survive and one out of four k-selected offspring survive, then for these competing rotifers, the k-selected strategy is advantageous.
The cost of sex is that its half as efficient as asexual reproduction because males don't really reproduce - they only provide genetic material for females.  You can argue r/K selection independently of this factor, but the article is suggesting that k-selection can be so advantageous as to also give sexual selection an advantage over asexual selection.  I think asexual reproduction could be k-selected as well, but that seems to be the point being made here.
The reason that k/R has toned down in importance in the past couple of decades is that it has been found that individual species can adapt to shift their k/R strategems.

Can you elaborate upon what you mean by "individual species can adapt to shift their k/R strategems"?

There are definitely limits but if a bird or insect starts laying larger eggs or if elephants start to become smaller, then their offspring become more or less expensive to produce respectively.  this means that their k/R strategy (cheap or expensive offspring) is changing.  Humans are an extreme case.  children take 8 or 20 years to become independent depending on parental life styles...big difference!


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Can genes change as we age?
Let's say you're a 23-year-old man who impregnates a woman. Will your genes be the same if you were to impregnate another woman at age 35? Will your genes in those 12 years have changed/mutated/become smarter?

Epigenetic changes over time is certainly possible.

I believe that's amazing then...

Yes, there are some differences between the gametes that a parent produces at different ages!
Mutations in the germline during mitosis
Every time a cell replicates some mutations may occur (even through mitosis). Of course, any mutation that occurs in cells are located in your hand or in your brain, for example, will not be transmitted to the offsprings. Only mutations occurring in the germline (cells in the testis and in the ovaries whose descendent or themselves go through meiosis) are possibly passed to the offsprings. Interestingly, because of the developmental pathways of sperm cells and ovules, sperm cells go through a lot more mitosis than ovules do, resulting in more mutations in the sperms than in the ovules. Therefore, if you look at a mutation in an individual and assuming you know that the mutation occurred during the lifetime of the parents, then you are more likely that the mutation comes from the father than from the mother.
As reviewed by Cochran and Harpending (2013), mothers transmit on average a number x of new mutations to their offspring. This number x is independent of the age of the Mother. Fathers, however, transmit a number of new mutations to their offsprings that is very much dependent on the age of the father for developmental reasons.
Of course, as it has been pointed out there are various environmental factors that may increase or diminish the mutation rate (such as the mutagens (Tobacco, X-ray, ..))
Note on the process of adaptation
It is important to know that a vast majority of mutations are deleterious (impact negatively the reproductive success and survival of the individual carrying it). If we assume that no selection occurs between the cells of the germline, then no adaptation is possible. And in average sperm cells of an old guy should have lower fitness than the sperm cells of the same guy when he was younger. This process is referred to as mutation accumulation (mutation accumulation is not a concept that is specific to somatic lines mutations). However, one may argue the opposite! One might think that the cells that carry the new mutations (the mutation that occurred during the lifetime of the man) may be selected for or counter-selected. In such a case, the few beneficial mutations might be enough to make our cell lineages more fit with age. Whether the fitness of cells increase or decrease through our lifetime is dependent on the effective population size, the mutation rate and distribution of mutational effects. One can calculate the critical parameters yielding to one (mutation accumulation and fitness decrease) or the other (fitness increase through age) thanks to the mutational meltdown literature.
It is important to note however that what increase the fitness of a cell might decrease the fitness of its carrier. Knowing the joint distribution of mutational effect for both the carrier and the cells should allow us to calculate if reproducing late in life allows transmitting better genes than reproducing early in life. Intuitively, I would expect that reproducing early in life would allow a parent to transmit better genes.
Epigenetics
We have to talk about epigenetics also. Epigenetics refers to all the modification that occur "around" or "on" the DNA but which are not the modification of the sequence of nucleotides. It is possible that the transmission of epigenetic modification is dependent on the age of the parents. But I have never heard of any case where this happens.

Where do you get that info about parental transmission of epigenetics in order to speed up /slow down the baby's development? You're contradicting yourself here by saying there's nothing, and then saying what there is. Aside from that, telomerase is active in germ cells and thus the transmitted telomere length will not be affected by parents' age (http://jcs.biologists.org/content/115/8/1643.full.pdf - it would be a bit weird if it was any other way)

Thks, I removed the Telomere part. It's been a long I was waiting for someone coming with a reference on the subject. I felt that a part of my epigenetics paragraph was not relevant to the question so I removed it. I didn't get where was my contradiction so let me know if you still see this contradiction (you can copy-past the sentences that contradict). What I wrote was in relation to the hypothetical parental conflict origin of genomic imprinting.

The contradiction is gone now - it was exactly the part after "I've never heard of any case" that caused that (because you then went on to explain a case that you heard of) :)

Pre-sperm cells divide constantly, and will have more mutations in 12 years. Unfortunately, neither the genes (nor the father) are likely to be smarter. There is some evidence that children from older fathers are more prone to diseases like autism and schizophrenia.
A very nice, short overview of the current research is in this (open-source) Nature article.

Genes can get mutated in one's lifetime. They gene altering agents are mutagens. Some common mutagens are X-ray, UV-ray, tobacco.
Recent studies have yielded results which state that some behavioral actions may cause gene mutations.
So, yes in twelve years gene can mutate. Moreover as a man ages his efficiency of meiosis division is affected. So, genes may differently get expressed in his progenies.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Effects of having too much vitamin D?
I saw there was another question about vitamin D; however, I do not believe this is a repeat.
What are some of the effects/side effects of having too much vitamin D in your body?

That is a rare condition that can only occur when taking too much doses of vitamin D. It has nothing to do with sun exposure.
High levels of vitamin D stimulate hypercalcemia and all its negative consequences. It can also exacerbate liver and kidney chronic diseases.
Reference: Katherine Zeratsky, What is vitamin D toxicity, and should I worry about it since I take supplements?


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Various Genetic Loads and their Definitions
In population genetics, we talk about several types of genetic loads (also called just loads). I am asking for a exhaustive list and a short definition.
Here are for example some genetic loads that come to my mind..

Mutation load
Segregation load
Drift load
Lag load

Could add gender load - the cost of sexually antagonistic selection on traits with non-zero cross-sex genetic correlations (If SA selection affects shared genetic material then one/both sexes are constrained from reaching the optimal phenotype, this is the gender load). http://rspb.royalsocietypublishing.org/content/277/1686/1345.abstract

The genetic load is a population construct, a way of quantifying the fitness reduction in a population due deviations from the optimal genotype.
One type of load comprises all the others, namely genetic load.

Genetic load is just the loss of mean fitness relative to the ideal fitness.

You forgot to include substitution load in your list, but otherwise I think you included all the main ones.

Substitution load is the total loss of mean fitness caused because favorable alleles substitute gradually by selection rather than
  instantaneously.

As for the ones you mentioned:

Mutational load is just the accumulation of deleterious alleles in a population.
Segregating load is the decrease in fitness in a population due to homozygotes being less fit.
Drift load is the fixation of deleterious alleles due to small population size. The smaller the population, the greater the risk of
  this happening.
Lag load is the loss of fitness due to a change in environment.

Another type, mentioned by rg255:

Gender load, which is the deviation from the optimum due to an allele drifting back and forth because the version that is optimal in one sex is not the one that is optimal in another.

Different load described here Lande 1976, Barton and Partridge 2000; Standing load: standing genetic variation in fitness, Migration load: new maladaptive variation due to gene flow, selection load: natural selection within a generation. Phenotypic load (Wallace, 1970)


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Tc and Th1 interaction and viral immune response
Tc is T cell which can give T killer cells and T helper cells.
T helper cells (Th1) see the pathogen presented by antigen presenting cells (dendritic cells and macrophages).
They then secrete antigens to kill the pathogen.
If there is memory from previous interaction, then it will be easier to protect.
However, since some viruses replicate fast (RNA particularly), this memory benefit is often lost, like in the case of influenza virus A and B types.
However, I am uncertain how to explain this immunology with viruses.
How can you explain this general viral interaction better in the immune response?
I have these pictures in mind:

and

I actually don't understand your text. Can you clarify that?

I think you have most of the key elements.  With a virus, a virally infected cell may present virus antigen on MHC Class I or II and activate T-cells.  The rest looks fine, with "dendritic cells" considered the 'professional' antigen presenting cell that present antigen on their surface, migrate from skin/mucosa to secondary lymphoid organs like lymph nodes/spleen/GALT and drive T and B cell activation and maturation.  Depending on the source, a 2nd exposure may not need to an Innate first step.  Killer T-cells is a catch-all...cytotoxic T-cells may kill cells bearing virus but (cont'd)

its thought that natural killer (NK) cells (lymphoid lineage but lacking T cell receptor) might provide some immunity to nemotodes etc.  So your diagram mileage may vary based on pathogen.  A good immunology textbook should show the differences.

PlaysDice's answer:
Antigen presenting cells migrate from skin/mucosa to secondary lymphoid organs like lymph nodes/spleen/GALT and drive T cell activation and maturation.
T helper cells with CD8 and MHCII complex recognise the virus and kill it.
I think this is what is happening, for instance in HIV infection:

where

dendritic cell (ADCC) presentation of HIV infected CD4+ to MHCII and T helper cell
T helper cell activates cytokine release
Natural killer cells come and lyse the HIV infected CD4+ T lymphocyte


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What's the physical meaning of Svedberg unit?
Sedimentation coefficients, using a centrifuge, are expressed using Svedberg unit (symbol S, sometimes Sv). Wikipedia states that $S = 10^{-13}$ sec but I also saw in a book that actually $S = 10^{-13}$ sec/$\text{rad}^2$. Which of these is correct?
I know that a 50S ribosome has higher molecular weight than a 30S ribosome and for that reason the 50S would travel faster (on a test tube placed in the centrifuge) than a 30S, but if substitute S by $10^{-13}$ sec, for me it's a little bit-non intuitive, because 50S would be $50\cdot{10^-13}$ sec (and that is greater than $30\cdot{10^-13}$ sec), which means it takes more time to travel? Obviously not, so what's the physical meaning of time in this situation?
In response to Alan Boyd:
"In other words, at 1x g a 1S particle will travel at $10^{-13} m\cdot s^{-1}$" or $10^{-12}$?
Indeed 5.5h is a reasonable value but I still cannot understand the significance of the ratio between velocity and acceleration which corresponds to Svedberg units (in seconds).
Maybe $50\cdot{10^-13}$ sec is the time that our ribosome takes to reach the terminal velocity in the fluid? That would make some sense, for example, if I drop an unfolded A4 paper to the ground the time it will take to reach terminal velocity will be lower than the time a A4 folded paper will take to reach it's specific terminal velocity, which is higher than the velocity from the unfolded A4 paper, because the area is larger (the friction force acting on it will be very high) which is consistent with the observations that are made (in centrifugation objects with larger surface area will travel at a slower terminal velocity). What do you think ?

Wikipedia:

The sedimentation coefficient is the ratio of the speed of a substance in a centrifuge to its acceleration in comparable units. A substance with a sedimentation coefficient of 26S (26×10−13 s) will travel at 26 micrometers per second (26×10−6 m/s) under the influence of an acceleration of a million gravities (107 m/s2). Centrifugal acceleration is given as rω2; where r is the radial distance from the rotation axis and ω is the angular velocity in radians per second.

In other words, at 1x g a 1S particle will travel at 10-13 m s-1 = 0.1 pm s-1
Particles with higher values of S will travel proportionately faster, and increasing g force will also increase sedimentation rate.
Let's look at the example of a 50S ribosome at 100 000 g:
rate of sedimentation = 10-13 x 105 x 50 m per sec = 50 x 10-8 m s-1
So how long to travel 10 cm = 10-2 m?
=10-2/(50 x 1010-8) s
= approximately 5.5 h, which seems about right.

I edited my question, in response to your answer because my comment was too large.

You are overthinking. Our ribosome is in circular motion so is experiencing a constant acceleration, which is why the WP quotation goes on to define centrifugal acceleration. http://en.wikipedia.org/wiki/Circular_motion

I'm asking for the intuition to compare the value of 50S and 30S in seconds. I can go to the formula and say that the centriptal acceleration experienced from both objects is the same therefore to have a greater S the terminal velocity must be greater and obviously 50S expirience a greater terminal velocity, but what does that quotient mean? What does the time indicate?


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Antihistamine's effect on insulin secretion and tiredness?
Antihistamines are known to cause tiredness.
The essential hormones of the body are insulin (glucose), parathyroid hormone (calcium) and aldosterone (Na-K ATPase, sodium).
I am thinking how this tiredness symptom can come.
There are so many different antihistamines so I am confused about the mechanism how they cause tiredness.

Histamine acts on parietal cells of stomach via H2 receptors to stimulate hydrogen ion secretion - cephalic phase.
Excess of antihistamines can lead to decreased acidity of stomach so change in conversion of pepsinogen into pepsin.
So less pepsin breaking down peptides and proteins.
Body has to do something else to break those components - and this consumes much energy and makes you tired.
Small mucus food mass stays in the intestines.
Delayed absorption.
Nutrients needed so liver has to work and make essential things - amino acids and something else.
Some waste management also may happen - because of tiredness.

Changes in blood sugar level.
Delayed most probably after food intake.
Very fast and fast insulin secretion mechanism starting during wrong times - all of the sudden.
So less insulin secretion cumulatively:

very fast mechanism - change of permeability of membranes (Na-K ATPase and sodium channels) reacting during times when not suitable - long after food intake
fast mechanism (phosphorylation of different things) happening more, since sympaticus apparently is not so inhibiting here
slow and very slow mechanisms however preferable (increased permeability of amino acids and mitoses)

So I think the tiredness of antihistamines is because of the increased amount of active fast mechanisms of insulin secretion, while less very fast mechanisms.
To carry the raw food mass in the intestines also require much energy.
What is the physiological mechanism behind the tiredness of excess antihistamines?

What class of antihistamines are you referring to? (Those used to treat allergic responses act against the H1 receptor, not the H2 receptor.)

Both, since I do not understand how the tiredness can come only through the receptor H1.

Thanks to studies on animal behavior and on histamine dection in the Central Nervous System, researchers found out the "histaminergic system".
It's thought that histamine-containing neurons regulate sleep-wake cyrcle, immunity, memory, body temperature, drinking, feeding rhythms. By the way, knockout rats who lack of histamine system don't show big defects in any function.
H1-Receptors for Histamine are distributed in the CNS and in the rest of the body. H1-antagonists (such as Promethazine, Chlorcyclizine, Loratadine...) have different effects on CNS, depending on dose. At conventional doses central depression appears and patients are sedated. They can even experience an antihistamine "hangover" in the morning, even if they take these drugs at bedtime. By the way, antihistamine overdose typically shows with convulsions.
The "non-sedating" H1-antagonists, or "second generation" have a lot less effects on CNS. They have polar chemical structure: they can not cross the blood-brain barrier.
By the way, a lot of typical and atypical anti-psychotic drugs have H1-antagonism effects on the brain (with H2 and H4 antagonism): their main goal is sedation to stop the patient from hurting himself (or others) during manic episodes.
So I think the last two sentences explain that sedation is almost a totally CNS-mediated side effect of antihistamine drugs.
H1-antagonists don't suppress gastic secretion, do not inhibit salivary, lacrimal or other exocrine secretions. Older H1-antagonists have an anti-colinergic effect on muscarinic receptors: they may reduce ACh-mediated secretions, typically in mouth and in the respiratory tree.
H2-antagonists are used to treat acid-peptic desease (as PPIs, proton pump inhibitors). CNS-related side effects are not commons, and include: confusion, delirium, hallucinations, slurred speech and headaches. These effects are mostly related with IV infusion of the H2-antagonist.
I just made a very small research on PubMed. I found this:
http://www.ncbi.nlm.nih.gov/pubmed/3529778
as you can see it is a study (on only 9 patients, in 1986), about insuline-glucose-Cpeptide and ranitidine (H2-antagonist) relations. Their conclusion is "Ranitidine significantly increased the area under concentration/time curves for glucose and insulin but not that of C-peptide. Our data indicate that ranitidine does not affect pancreatic insulin release nor peripheral glucose utilization and are consistent with the hypothesis that ranitidine influences the hepatic clearance of glucose and insulin both of which undergo high first-pass liver extraction."
I think that tiredness is a typical CNS-mediated side effects of H1-antagonists (anti-allergic) but is not a side effect of H2-antagonists (anti-acid). Maybe H2-antagonists affects insulin action via hepatic effects.
*I'm italian (sorry for any english mistake) and I am a last-year medicine college student.
I wrote trying to summarize some chapters (8, 32 and 45) of:
- "Goodman & Gilman's The Pharmacological Basis of Therapeutics" - L. Brunton, B. Chabner, B. Knollman - 12th edition; McGrawth Hill 2011

This is wrong statement: [second generation] antihistamines cannot cross the blood-brain barrier. They can! Particularly, they can in the old and special medication (Montelukast).


text:
About the quality of microsatellites
I built a script to detect microsatellites in a FASTA file. However, there are thousands of possibilities.
So, my question is:
what are the markers of a "good" or "useful" microsatellite?
- How many base pairs, how many repetitions?
And, are there any other heuristics that can be run to further detect usefulness of the microsatellite?
thanks.

Try running software like Censor. If checks in the reference repeat databases and detects microsatellites. So, you can most probably be sure of the microsatellites generated. Moreover, the microsatellites have their information present in the GIRI database. So, you can get more information, if you find the microsatellite in your sequences. Hope this helps.
~Rama.


text:
What does "developmentally programmed" mean?
What does the term "developmentally programmed" mean? I can't seem to find a definition anywhere.
What would the alternative (i.e. not developmentally programmed) imply?

Where did you find this expression? That will probably help a bit.

Agreed, this phrase can mean different things depending on the context - the answer still wouldn't be pages long if it included all contexts but it would make it a lot easier if you could provide that background information :)

As in "development of secondary lymphoid organs happens during embryogenesis and is thought to be developmentally programmed"

The link to your source would help, not only the sentence.

Sorry yes I should have posted that in the first place --> doi:10.1038/nature13158

Yeah, it looks like just bad phrasing, probably caused by word count restraints.

The term could mean two things depending on the emphasis:

"developmentally programmed" would seem to emphasise the "programmed" nature of the development of something, implying that it is under specific regulation and the result of targeted energy expenditure ("Here, we describe widespread developmentally programmed nuclear destruction (PND) events that occur during yeast gametogenesis").
"developmentally programmed" would be intending to distinguish from other means of being programmed, i.e. this would go in the direction of a nature vs. nurture statement ("Hair colour is developmentally programmed and does not depend on external influences after fertilisation").

The first of the two appears to be the more common use of this phrasing if one wants to trust Google to be representative. Something along these lines might be intended in your example, though I don't see why this statement is necessary as it seems quite obvious that any organ that develops during embryogenesis is "developmentally programmed"...
I suppose the alternative ("not developmentally programmed") would imply that the development of secondary lymphoid organs is an accident which is not driven by specific mechanisms that exist for the particular purpose of developing them.
In any case, there is no magical scientific meaning to either of these two words, to me your example seems to be rather a mishap of phrasing.


text:
How can antibiotics damage the ear?
What is the mechanism by which aminoglycoside antibiotics (such as streptomycin and gentamicin) damage the mechano-sensory hair cells of the auditory and vestibular system? (Could this be seen as evidence for Lynn Margulis' theory that these cilia are descended from bacteria?)

Thanks, I added two links (but it doesn't allow new users to add more).  Maybe it will let me add another one here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2728278/

The article does describe the mechanism.  I just didn't know if it is similar to the way it affects gram negative bacteria?        "When exposed to aminoglycosides, hair cells demonstrate both morphologic and molecular features of apoptotic cell death, including condensed, marginated chromatin, and positive terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling staining (Forge and Fradis 1985; Li et al. 1995; Lang and Liu 1997; Nakagawa et al. 1998; Forge and Li 2000; Matsui et al. 2002; Mangiardi et al. 2004)."

"In addition, aminoglycoside-induced hair cell apoptosis is mediated by c-Jun N-terminal kinase (JNK), a member of the mitogen-activated protein kinase family...Furthermore, aminoglycoside exposure results in cytochrome c release from the mitochondria and caspase activation in hair cells (Cheng et al. 2002; Cunningham et al. 2002; Matsui et al. 2004; Sugahara et al. 2006)."

This phenomenon is called Ototoxicity, which literally means "toxic for the ear". Mostly the cochlea or the auditory nerve are affected and almost all these cases are connected to medications as gentamicin or cisplatin.
The reasons for this are that the cells are either driven into apoptosis or necrosis. This is caused by destroying mitochondria and releasing calcium and cytochrome c which triggers apoptosis or by deregulating the the JNK-signal transduction pathway and causing necrosis. This image gives a nice overview:

For further reading you can start with the Wikipedia page on ototoxicity and then also read these two papers which are both freely available (the figure above is from the first):

Intracellular mechanisms of aminoglycoside-induced cytotoxicity.
Gentamicin rapidly inhibits mitochondrial metabolism in
high-frequency cochlear outer hair cells.

To answer the question why this occurs in the ear, it seems that there is some genetic predisposition for this, see this paper: "Aminoglycoside-induced ototoxicity." Mitochondrial damages leading to hearing loss is also not uncommin, see here. Noise seems to play an additional role here and is probably the "last drop" to cause hearing loss.

Thank you for your very clear answer and great references!  One thing that I still don't quite understand is why the hair cells would be disproportionately affected.  Don't all cells contain mitochondria?  And if so why isn't apoptosis triggered in all cells?

Thats a good question for which I have no answer at the moment. I will look into it.

It seems that there is some genetic predisposition for this, see this paper: Aminoglycoside-induced ototoxicity.


text:
Will the increase in atmospheric carbon dioxide lead to larger insects?
From my understanding, the increase in atmospheric carbon dioxide will also increase oxygen levels. That makes me wonder if in the near future insects will grow larger than they are today, since their maximum size is limited by how deeply oxygen is able to diffuse into their body.

I haven't seen anything suggesting increased oxygen levels. If you've got a source for that I'd be interested.

There is the supported theory that insects during the Paleozoic period were larger in size because of the increased oxygen content in the air.

The study adds support to the theory that some insects were much larger during the late Paleozoic period because they had a much richer oxygen supply.
The Paleozoic period, about 300 million years ago, was a time of huge and abundant plant life and rather large insects - dragonflies had two-and-a-half-foot wing spans, for example. The air's oxygen content was 35% during this period, compared to the 21% we breathe now, Kaiser said. Researchers have speculated that the higher oxygen concentration allowed insects to grow much bigger.

This article is based on a paper published in the American Physiological Society:

It is because when the oxygen concentration in the atmosphere is high, the insect needs smaller quantities of air to meet its oxygen demands. The tracheal diameter can be narrower and still deliver enough oxygen for a much larger insect, Kaiser concluded.

There are similar papers that investigate the relationship between oxygen and maximum potential size, such as this article published in Nature (1999):

The tendency of some animals to be larger at higher latitudes ('polar gigantism') has not been explained, although it has often been attributed to low temperature and metabolism. [...] We have analysed length data for 1,853 species of benthic amphipod crustaceans from 12 sites worldwide, from polar to tropical and marine (continental shelf) to freshwater environments. We find that maximum potential size (MPS) is limited by oxygen availability.

Another paper published in Proceedings further supports this theory:

[...] A variety of recent empirical findings support a link between oxygen and insect size, including: (i) most insects develop smaller body sizes in hypoxia, and some develop and evolve larger sizes in hyperoxia; (ii) insects developmentally and evolutionarily reduce their proportional investment in the tracheal system when living in higher PO2, suggesting that there are significant costs associated with tracheal system structure and function; and (iii) larger insects invest more of their body in the tracheal system, potentially leading to greater effects of a PO2 on larger insects.

The question you propose is very interesting, although I am sure it would take thousands of years for these insects to adapt to this oxygen level change (which in itself, to reach prehistoric levels, would take a long time) and in turn become larger.
This article, based on the original APS paper, seems to think larger insects could appear in the future if the limiting factor (in this case low oxygen levels) is removed.

Image from Biotic interactions modify the effects of oxygen on insect gigantism (PNAS, Chown 2012).

I just realized an implicit assumption in my question. Is it only lack of oxygen that limits insect size today, with their current genetic makeup, or is an evolutionary change also required to take advantage of the increased oxygen?

Although these findings are all based on theory, the general consensus for the relatively large size of ancient insects seems to be linked to oxygen levels in the atmosphere.  There could be other factors related to size, however, with their current genetic makeup I would assume that these physiological changes would not happen in a short period of time - they would adapt slowly with the changing atmosphere, based on the fact that the changes in ancient insects happened over millions of years.


text:
Where can I get numerical data for the PAR (photosynthetically active radiation) curve?
I'm trying to do some rough figuring to calculating efficiencies of various light sources for growing plants.  I'm hampered, however, by the lack of a curve to multiply by the spectrum of light sources to determine the amount of photosynthetically active radiation that a typical plant will absorb and use.
I can find curves like below all over, but I can't get numerical data in the form of tables. Is there some source from where I can get such data?

plantphysiol.org/content/early/2013/06/28/… is a starting point. He cites a paper of Mcree which may have what you're looking for (pay wall for me). Evans says that photosynthesis for 400-700nm drops off quickly as function of temperature. Red/blue encourage flowering/growth, a gardening truism which may be based on Mcree's paper.

@daniel your link was cut off

This is it---http://www.plantphysiol.org/content/early/2013/06/28/pp.113.219006.full.pdf--except for the standard characters at the beginning ending with the three w's.

@daniel a safer way to provide links in comments is using markdown, e.g. [Google](http://www.google.com/) = Google.  The second link you pasted has a "--except" appended on the end that I had to manually remove.

@NickT sorry for the late comment but what do you mean here, by "numerical"

@WYSIWYG as in a table (spreadsheet, etc) of values with the wavelength then the PAR value for each one.

@NickT Is the table not available from the source of this image?

@NickT I think you should try one of the programs that can be used to extract numerical information from images. I never used one. There is another trick that you can try using Inkscape: import your image → crop to desired region → trace path from the image → Remove unnecessary points → simplify the path → add more nodes if you want to get more datapoints (select all nodes and click add node) → Select all → resize document to selection → save as SVG. SVG doesn't store co-ordinates but you can obtain them using parsers or other tricks.

To know how to extract co-ordinates from SVG see here and here. Since you know the X/Y scale from image you can get the original data points.

This is one paper where you can get that data.

@WYSIWYG that paper just has insolation data over the year, not the spectrum of what PAR is.

@NickT Did you try obtaining the numerical data from this curve?


text:
how is the plasma membrane repaired after endocytosis?
When the vesicle is swallowed of course the lipid layer internalizes. My question is how will the top segment of membrane will bind back together when that vesicle took the membrane with it inside cytoplasm. Will the plasma of the cell decrease or they will repair back and how does the membrane know that a certain substance is outside and i have to internalize myself in order to swallow. The same thing with exocytosis: How does the membrane open itself and repair back and what will happen to the membrane of the vesicle which went out?

You have one misconception about the endocytosis: In the process no hole in the membrane is generated. It works in principle like in the figure below (it is of course more complicated, but this should explain it):

The membrane forms a vesicle around the particle which shall be integrated until it is completely surrounded by a membrane. At this point the vesicle is detached from the cell membrane and inside the cell. To accomplish internalization, the particle binds to certain receptors which regulate this process. See the Wikipedia for more details.
Exocytosis works in principle the other way round. Here are the visicles detached from the Golgi apparatus (mostly at least) and are directed to the cell membrane. Here the fuse with the membrane and form a pit which has its opening to the outside, releasing what was in the vesicle. It works like this (image from here):

In this process you have to differentiate between permanent unregulated exocytosis and regulated endocytosis (for example for the release of hormones) which are regulated by signal transduction pathways.


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What is atrial fibrillation?
I am wondering exactly what a-fib is (causes and symptoms).

I would really appreciate having a sample of an EKG with it (because in my limited research, I have found it nearly impossible to find just a sample piece of an EKG that has a-fib on it) with your answer, so I can actually get an idea of what it looks like. With the sample EKG, I would love to have a normal one beside it so I can kind of analyze the differences between the two.
Note: This is not and never was a homework question!

http://en.ecgpedia.org/wiki/Atrial_Fibrillation pretty much has exactly what you are after.

@jonsca How about linking one of the images here and make it an answer?

@Chris My point was more that this was answered quite well by the first hit on googling "atrial fibrillation ekg".  Wikipedia's chart is actually better, but I don't want to just copy large quantities of information from there.

I know this problem. But you can at least earn the reputation for that. Write a short answer, add a picture, reference to the Wikipage. I think this is perfectly fine.

@Chris I would not mind at all if you (or anyone else) wanted to take that opportunity.

This is NOT a homework question, guys! I was asking out of sheer curiosity.

A human heart can be viewed as 2 hearts, the left and the right heart, each consisting of an atrium and a ventricle. The atrium's function is to fill the ventricle with as much blood as it can and the ventricle then pump the blood away. Also there is a system of valves to control blood flow on each side. Basically this is how our heart works.
Now, to make this system work we need to have a coordinated movement of atrium and ventricle, that is, first atrium is filled, then it pumps blood into ventricle, valve closes and then ventricle compresses.
The movement of heart muscle causes currents that can be measured (this is the ECG pronounced EKG). These currents are representative of the movements of atrium and ventricles are expressed respectively as p waves (for atria) and qrs (for ventricles).
It is the case that atria are not very important and sometimes they can stop working properly. They now longer have coherent movement and stop helping to pump blood into the ventricles, but they still move. This event is called atrial fibrillation.
From this explanation one can expect that no longer p waves will be identifiable in the ecg, but instead a random noise overlapping with "normal" qrs representing normal ventricular movement. The movement is actually not exactly normal, because the ventricular contraction due to atrial fibrillation now occurs at random times, that is qrs complexes occur with random spaces between them. The explanation for this is rather more complex: there are bundles of specialized cardiomyocites with different frequencies of depolarization. The fastest ones are on SAN and basically guide the whole heart rhythm through specialized bundles. When you have atrial fibrillation, the depolarization signals no longer come from these preferential bundles, but from any part of the atria at random. This causes the ventricles to initiate motion at irregularly spaced intervals.
I've included a photo of a normal rhythm and a atrial fibrillation side by side, but I hope you can use this explanation to find better ones by yourself in the web.
Note: don't confuse atrial fibrillation with atrial flutter. Flutter is a faster paced regular (therefore organized) atrial movement. It will appear as a saw-tooth shaped wave with regularly spaced qrs complexes.

Hope this helps.
Causes of atrial fibrillation are numerous, bur mainly high blood pressure, vascular disease, heart and lung disease among others. It can be asymptomatic in most cases or presenting with the symptoms of its underlying cause.
Please refer to http://www.webmd.com/heart-disease/atrial-fibrillation/heart-disease-atrial-fibrillation-basics for a quick overview.

To add to your answer I think you mean P waves aren't visible in AF and also old age could be added as a cause in isolation - it's very very common in the elderly

Yes, thanks you are correct, it was a typo. I've corrected it now.

Good answer. I disagree only with this: It is the case that atria are not very important and sometimes they can stop working properly. Atrial kick contributes 15-35% to the volume of blood in the ventricle. This extra volume in turn increases cardiac output by a similar 15-35%. That can make the difference between living well and living with congestive heart failure.

The relationship between the HF and AF does exist, but is only partially understood (see http://circ.ahajournals.org/content/119/18/2516.full), and although atrial systole contributes to the loss of cardiac output, it is only one of the many possible reasons for it.

Remember that except for the concluding pathway through the A-V bundle, the atrial muscle mass is separated from the ventricular muscle mass by fibrous tissue. Therefore, ventricular fibrillation.
The mechanism of atrial fibrillation, except that the process occurs only in atrial muscle mass instead of the ventricular mass. A frequent cause of atrial fibrillation is atrial enlargement resulting from heart valve lesions that prevent the atria from emptying adequately into the ventricles, or from ventricular failure with excess damming of blood in the atria. the dilated atrial walls provide ideal conditions of along conductive pathway as well as slow conduction, both of which predispose to atrial fibrillation.
For the same reasons that the ventricle will not pump blood during ventricle fibrillation. Neither do the atria pump blood in atrial fibrillation. therefore, the atria become useless as primer pumps for the ventricles. Even so, blood flow passively through the atria into the ventricles, and the efficiency of ventricular pumping is decreased only 20-30 percent. Therefore, in contrast to the lethality of ventricular fibrillation, a person can live for months or even years with atrial fibrillation, although at reduced efficiency of overall heart pumping.
numerous small depolarization waves spread in all directions through the atria during atrial fibrillation. Because the waves are weak and many of them are opposite polarity at any given time, they usually almost completely electrically neutralize one another. Therefore, in the electrocardiography, one can see either no P waves from the atria or only a fine, high-frequently, very low voltage wavy record. conversely, the QRS-T complexes are normal unless there is some pathology of the ventricles, but their timing is irregular.


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Could humans choose to establish fibre digesting colonies in our guts?
Humans don't digest fibre, and nor do any animals, but some creatures have micro-organisms (bacteria, I'm guessing) in their gut which digest fibre for them.  My question is, could humans take some sort of pill and establish our own fibre-digesting colonies in our intestines?  Has this been tried?  Supposing it could be done, would you suppose it would have any negative effects on our health?  (i.e.. would those whose gut digested fibre for them be stuck on a low-fibre diet?).
Purpose of question: just wondering.  It would be cool to be able to eat bark.

Go ahead and eat it - not taking nutrients from something doesn't mean you can't eat it :P

Related: https://biology.stackexchange.com/q/59205/24354

Probably not without some substantial evolution to change our physiology, depending on what you are wanting.  If you just want to digest fibre, that might be done, but if you wanted to see nutritional value out of it, its not clear that's going to be worth it..
Soluable fibre is currently used by the human body, so you are probably be asking about insoluble fibre.
It might be possible to do a little of this experimentation - I'm not recommending this - but there would be several likely issues depending on your goals in such a project, which could vary.

the human gut microenvironment probably will not accommodate the bacteria you need and they might not grow in significant quantity.
the human gut is not physiologically arranged for digesting such fibre - ungulates generally have four stomach chambers that they can use to store some of the hard for the longer time it takes to break the fibre down.
the nutritional value of plant fibre is low XKCD has some numbers on this and a cow can eat 10kg of plant matter a day and in doing so they don't tend to move that much.  Humans have to eat a greater volume of vegetables to get the calories they need.  Is getting that last 2-5% or so of the energy from digesting fibre worth the trouble? Eat one more apple or a handful of grain.

Lastly, there would likely be some impact on human health - if you succeed then you would be modifying fibre's role in human diet as it stands - which is to help keep the intestines cleaned out.

Just to add something to the answer from @shigeta - even assuming that you did manage to establish a gut microbiome that was capable of metabolising fibre, this wouldn't be a source of glucose: in ruminants the gut bacteria ferment the sugars released from the cellulose, releasing short chain fatty acids (a.k.a. volatile fatty acids,  e.g. propionic acid).
These compounds are used to fuel gluconeogenesis in the liver of the animal: in  a lactating cow this can amount to kilograms of glucose synthesised per day. Although you wouldn't be aiming to eat that much fibre, the release of these VFAs into your bloodstream might still cause some metabolic problems.


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What is the evolutionary cause for various finger lengths?
Why are the lengths the way they are with middle finger the longest?

I'm no expert but the relative length of fingers perhaps represents functional significance. It's always helpful in the question to mention what you have found on the topic so far so people can have a constructive input/answer.

When you bend your fingers, they all arrive at the same height. I would tend to think that their lengths differ when you keep them straight because they need to have similar length when you bend them. And I guess that there is some optimal length (when bended) for fingers to grasp things.
It is nothing but a quick hypothesis. But it sounds quite plausible to me.
As @JordiZambrino commented, it is possible also that middle fingers evolved to be longer in reaction for the need for throwing things.

Very interesting angle. Never thought of this. Thank you for your answer.

with the middle finger, I read somewhere that hominid lineage began when a group of  apes began to throw rocks at  their antagonists/rivals, and that this behaviour provided procreative advantages for  a long time, and thus driving natural selection for improved throwing. Also, I think that the hand grip  was/is vital and that a longer central finger is biophysically helpful.

This is interesting. I'll add your comment to the answer. Would be great if you could find the reference.

@Remi.b I'll try to find the reference.

@Remi.b I'm leaving a citation notice on this 5 year old post due to it getting new traffic from this post. If you can, please update with a bit more referenced substance if you've learned or explored this topic further since posting your answer. Thanks!


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How best to count bees entering and leaving a hive to measure hive activity?
This is my first question here, so I apologize for all mistakes I could have possibly made.
I'm a high school student in East-Central Europe and I need to complete some research for a biology contest (asking for advice is accepted, so I'm not cheating). My task is to analyze the influence of certain environmental factors (temperature etc., it's not that important for my question) on the activity of bees. The method is pretty simple: once a week I record the entrance to the bee hive (I do it on four hives), play it in slow-mo (It's impossible to count them properly without doing so) and simply count the number of bees entering or leaving.
Problem is, I don't know how long the observation should take. I play it in like X1/8, you need to play it twice (entering/leaving), so it takes a lot of time to gather one piece of information for a certain day. Till now I've been doing it for one minute - and there seems to be some kind of pattern to their activity analyzed that way. Yet, I'm not sure if it's actually eligible. I can't do the observation for hours - I still need to learn and have other duties.
So, what should I do? Could anyone give me some advice? Is one minute (several, like 6 times a day per hive) legitimate enough?
Thank you in advance.

I know of a person who used to do these experiments. They mentioned that they also used to mark each bee to track exactly.

One minute a day sounds far too short. Several one minute measurements throughout the day would be one way, or measuring a day in full, and then using a representative time-point would also be neat. I think it depends on the question you're answering. "hot bees are more productive" and "Hot bees hives have more bees" could look like the same result in your setup. @WYSIWYG I heard a similar story - painting moving bees sounds a bit precarious to me!

I'm no expert at this but these are some of the things that I would consider thinking about. How practical is it for you to count the total number of bees in the hive, based on lets say hive weight or the number of bees on one rack in the hive (then multiply by the total number of racks to give you an estimate of the total bee numbers in a hive) before you start collecting video data? This will at least put your influx/outflow number into some sort of prospective if you are counting in different times of days or if there are different wheather conditions in different days. This is easily achieved if you divide your influx and outflow numbers by the total (estimated) number of bees. This gets you two numbers (ratios) which you plot on the Y-axis. On the x-axis you can plot the passage of time and even colour code different days based on average (lets say) temperature to see if temperature had an obvious effects on your observations. But obviously all your instances of recording and time intervals between recordings needs to be constant!
So in many fly behavioural or locomotion function assays, scientists record fly movements at certain fps and analyse the videos. Now most of this video data analysis  is done using scripting in Matlab which is (I know to be) the tool choice for motion analysis. Now since you say you are at high school, this would probably be quite a challenge since the program is costly and scripting is not that easy (at least for me), so see if you can utilise the help of someone to get over this barrier. Once you do then you can analyse much longer videos at much higher frequencies, which will give you a better resolution on your data. If you could't then consider looking through web sites using search engines such as google for Matlab codes for motion tracking analysis scripts. I did this some time ago and there are wealth of information out there and once you do that you can get the communities help in websites such as stack overflow to help you refine your codes or any problems you may have with it, so long as you show evidence of your work. This is a great option since you can add variety of data (or different data aspects) to your project such as what is the average speed/velocity which your bees travel at in different times when entering/exiting the hive, is there a pattern to their travelling (e.g. straight line, zig-zag etc) and much more. I'm aware that this is beginning to sound like a PhD project and not a high school project but these are some things to consider. If programming is totally out of the question then you can look on internet to see what free programs are out there to aid you with your data collection. I briefly looked and saw this (http://www.youtube.com/watch?v=jWD8CHW06Ks) and this (http://www.researchgate.net/post/Does_anyone_know_of_FREE_software_for_motion_capture) just by simply typing into google "video motion tracking software" so look around and see if you can find anything which you can tailor for your own need.
Now regarding video length time, as correctly mentioned in Armatus response (if I'm not wrong and correct me if I am) it shouldn't matter for how long or how frequent you are recording so long as you keep the variables (i.e. time of recording, frequency of recording etc) to the minimum (i.e. not change them), or in other words keep your observation methodology constant through time, and try to come up with a practical schedule and if you explain your thought rational (experimental design) in your report, even a professor (i dare to say) wouldn't be able to argue with it but you always have to talk about the limitations of your study and that is key and that's where peoples project falls apart when an expert reviews it and finds holes and criticises claims made, which can not be backed up by the data/types of analysis gathered/performed!!
EDIT: Just to address some statistics issues, I would make your recordings from minimum of three hives per recording time-interval/point since in science n (number of observations) should be >= 3.
Anyways I hope my ramblings have been somewhat useful.

One thing that's certain is that the activity of bees varies according to time of day, so more important than how long you record for is probably at what time you record. If you always record at the same time of day, this should allow a reasonable comparison between results of different days. For example, recording from time 14:30 to 14:35 every day could be fine. You could then record conditions at this time each day (temperature, weather, etc.) along with this.
As for the exact length of your recordings: Of course, the longer they are, the better. More samples usually increases reliability and representativeness of your results. However, more importantly you want a practically useful time as well. This really depends on the actual number of bees entering into the hive within different time frames, as well as the baseline variability between days irrespective of the conditions you are investigating. I don't know anything about either of these :)
You want the number of entrances in your recording to be at a level where you will notice if there is a meaningful difference between days, and the only way of going about this is usually to start with a guess and then change if you notice that you can't really make sense of your results.

To further reduce the time it takes you, you could start out counting both entrances and exits from the hive - but then check if you get the same results if you only consider entrances. As a measure of bee activity, I would expect entrances and exits to be equivalent and thus it shouldn't matter whether you count either one or both.

Ideally, you would gather preliminary statistics to design the experiment. If you have a high variability, and your observation window is short, then small effects will be swamped by the variability. However, if what you are looking for has a big effect in the number of bees, then counting for a shorter time is going to be fine.
A rule of thumb would be to try recording 5 to 10 segments of 1 minute analysis and see what the variability is. If the standard deviation is small compared to the effects you are seeing, then 1 minute is fine.
If you want a more theoretical justification, Poisson distribution could be used as a first order approximation of the distribution. I don't know much about statistics specific for this kind of insect behaviors though.


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Does digit 1 have an extensor sheath?
Extensor digitorum and extensor digiti minimi both insert into the extensor hoods of digits 2-5 (or just 5 in the case of e. digiti minimi).  In every source that I can find, extensor pollicis longus & brevis insert directly into the base of the distal and proximal phalanxes respectively.
Does this indicate that the thumb does not have an extensor sheath as the remainder of the digits do?

From $n=2$ textbooks, the results are equivocal.
Moore et al. (2013)

There is no mention of an extensor expansion associated with the pollex.
EPL and EPB are listed as inserting on the distal and proximal phalanges, respectively.

Rohen et al. (2010) (p. 394)

"Extensor expansion of extensor of thumb" The label points to the middle of the diaphysis of the proximal phalanx. It's odd that extensor is singular here, given that there are two extensors.

However, Abdel-Hamid et al. (2013) present data from dissection of 95 limbs.
Extensor pollicis longus:

"EPL tendon was attached to both proximal (PP) and distal (DP) phalanx through the extensor expansion in 94.7% of specimens (Figs. 1A, B; 2A). In 5.3% of upper limbs, the EPL tendon was attached to the DP through its extensor expansion (Fig. 2B; Table 2)."

Extensor pollicis brevis:

In 55.8% of upper limbs, [EPB] was attached distally to the base of the [proximal phalanx] of the thumb (Fig. 1B). While in 41%, EPB tendon was attached to the extensor expansion of the thumb at the level of the base of [proximal phalanx] (Fig. 2A). However, in 3.2% of specimens its tendon was inserted into the extensor expansion of the thumb at the level of the base of [distal phalanx]."

And the answer appears to still be equivocal.
Abdel-Hamid GA, El-Beshbishy RA, Abdel Aal IH. 2013. Anatomical variations of the hand extensors. Folia Morphol 72:249–257.