text:
Are the bacteria in the stomachs of unborn babies beneficial?
Babies are born with bacteria in their stomachs. I heard on The radio that when a child is given antibiotics for the first time unique bacteria in the stomach are destroyed and cannot be replaced. Is this true, and, if so, does this have negative effects on the health of the newborn?
Closely Related, but different: What bacteria do unborn babies contain?

It's a fascinating topic! While most of the bacteria known to colonize babies comes from the vaginal tract during birth and then later, through breastfeeding, although there is evidence to suggest that microbial colonization may begin before birth.
Regarding what these bacteria are, our microbiomes are composed of probably hundreds of species of bacteria from at least four major phyla: actinobacteria, proteobacteria, firmicutes and bacteroidetes (see the review for more on them).
As for taking antibiotics, I find it highly unlikely that taking antibiotics would completely destroy any native gut flora species. I certainly can't find any evidence to suggest that that might be the case. In general, when we have to take antibiotics, the offending bacteria are a relatively small population, compared to our native species and are less well-adapted to our body environment. Antibiotics work with our own immune defenses to clear our system of pathogenic species. Antibiotics also hurt our native flora, but less so than the ones that make us sick.
As for your last question regarding health, I wouldn't exactly say that having a microbiome promotes better health, so much as that your microbiome is critical for survival and health. There are actually nutrients that we need for survival that we cannot digest without our microbiota and a wide number of diseases, from immune disorders to potentially depression, can arise from an unhealthy microbiome.
As a fun bit of trivia to ponder in parting, our bodies are composed of 90% bacterial cells by count. Sweet dreams...  :-)

The 90% bacterial cell number is most likely too high by an order of magnitude. See this paper.

I think you missed one important part of the question - the claim that antibiotics destroy bacteria in the body. They don't - not by far. They can affect the balance of bacteria (some are more affected by that particular antibiotic than others), and they reduce their populations and do a bit of selection, but they simply can't kill all of even one kind of bacteria. If they could, antibiotics would cure any bacterial infection instantly, which simply isn't the case - they just tip the fight in your favour. Not to mention that many parts of the body aren't easily accessible by antibiotics.

Interesting fact : Knowing that a baby born by caesarean is not likely to come in conatact with useful microbes of the vagina of the mother, Rob Knight, a microbiologist applied them on his baby with a swab from his wife's vagina !

Good point, @Luaan! I definitely missed that. Thanks for adding to it. In future, I'll try to keep my answers to daylight hours, when I'm most awake. ;-)

Your answer has some errors (probably just phrasing) in it. For example, babies are not born colonized with all sorts of interesting bacteria. They acquire them at birth, which is very different (also stated clearly in the paper you cite.) This is a science site. Accuracy is valued.

@anongoodnurse, which of the sources are you referring to? I'll of course correct any errors, or just remove the answer if it doesn't stand up, but in the first  reference, the authors state: "It was previously thought that the in utero environment was largely sterile and that a fetus was not colonized with bacteria until the time of birth. Recent studies suggest the presence of a microbiome within the placenta as well as fetal meconium, suggesting that the colonization process begins well before delivery." This suggests that colonization begins prior to birth.

Suggests is the key word. The preceding statement is thought to be correct: "Colonization of mucosa in the digestive, respiratory, urogenital tracts, as well as the skin begins at, or perhaps even before, the time of birth when a newborn is exposed to a mother’s microbiota." There aren't really good studies yet about in utero gut microbiomes, but a lot to suggest otherwise at this time. If you have a some good studies to support your statement (there wasn't any reference cited in that article), I'm very interested in reading them. Thanks.

@anongoodnurse - fair point. I've edited my answer to better reflect the ongoing research into pre-natal bacterial colonization. Also to address a point raised earlier, by Luaan.

@biogirl He also convinced four other moms to do the same, apparently. There is also this recent paper claiming that OR dust might seed the infant microbiome, but I always worry about contamination in these really low biomass studies.

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text:
What happens to a snail if we cut off its antennae?
First off, I don't know why snails have antennas. Are they eyes? And what if we cut those antennae off? If they are like eyes, could a blind snail survive somehow?

And by the way: how unethical would it be to find it by myself?

Super unethical. If you were obeying the three Rs you would realise that these animal experiments could be easily replaced by reading about snails. If you don't know what you're doing from a practical point of view and are not being careful to act scientifically (recording logs, testing against reasonable hypotheses, and following the three Rs) animal "experimentation" could be seen as nothing more than deliberately torturing animals without any real goal.

@James Thanks! Very Valuable comment, since I have no background in biology at all! I didn't even heard about 3Rs. And your answer is magnificent :)

I'm not an animal scientist so I don't have deep insight, but I know animal scientists in my institute. There is a related meta that you might find interesting. The snail answer isn't mine, it's @JordiZambrino's! I agree, it is a very good answer.

If this answer addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered.

How mean. Please don't do that. Those are fingers they use to sense the surrounding environment around them.

It really depends on which type of gastropod you are talking about, since different types of snails, have different types of eyes.

Marine gastropods could only become more mobile, when their abilities of sight had improved. This happened, when the eye cup deepened and the visual opening narrowed. An effect was the result, which in historical time was used by the so-called pinhole camera: A picture of sufficient sharpness can be displayed by reducing the camera's aperture to the size of a pinhole. The smaller the aperture, the sharper the picture. But because there is only a small amount of light falling through the pinhole, the image will be quite dark. Besides, the displayed area of the image is very limited.

From left to right: Pinhole eye of an ormer, A Roman snail's simple lens eye, A limpet's cup shaped eye
Could a blind snail survive?
There are even some types of gastropods which are naturally born blind such as:

Cecilioides acicula, common name the "blind snail" or "blind awlsnail", is a species of very small, air-breathing land snail, a pulmonate gastropod mollusk in the family Ferussaciidae.

Descriptive features:

This animal is white, there are two pairs of tentacles, but eyes are lacking. 4
  The shell is long and narrow, up to a maximum of 5.5 mm and a width of 1.2 mm.5 The shell is colorless, glassy and transparent when it is fresh, a somewhat opaque milky-white when it is not fresh.

Snails which are visually impaired are not limited in their ability to move, however, and can easily navigate their habitats through their sense of touch and smell.

Regarding the ethics of your "investigation", I'd recommend to just not do it.
Sources:

https://de.wikipedia.org/wiki/Blindschnecke
http://www.animalbase.uni-goettingen.de/zooweb/servlet/AnimalBase/home/species?id=1286
https://en.wikipedia.org/wiki/Cecilioides
http://www.molluscs.at/gastropoda/index.html?/gastropoda/morphology/eyes.html

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text:
What's the rationale behind freezing one's eggs if cells can be cloned?
It seems to me there's a lot of discussions around the topic of somebody freezing her eggs.
What I don't understand though are the following:

Why would you freeze your eggs when you know that the technology for transforming a somatic cell into an egg today exists, or doesn't it see here?
Is it proven that freezing doesn't alter biological activity and hence not diminish the chance of giving birth to a malformed child?

To me it seems way easier and safer (and less expensive) to artificially produce female gametes than freezing them and, 10 years later, unfreeze and hope for them to be still biologically active.

Cloning of humans has yet to be demonstrated. In the reference you provide on artificial gametes notice that all of the sentences use the words "may", and "could". It hasn't actually been done yet, at least not verifiably.

Why Would You Freeze Your Eggs?
For 1, a woman may wish to freeze her eggs if she needs to delay childbirth. This page explores several reasons why, for example, "Women who want or need to delay childbearing in order to pursue educational, career or other personal goals.". Additionally, it explores some basic explanations of the process, if you are interested. If a woman has doubts about her fertility in 10 years time (using your final sentence as an example), such as if she is recently diagnosed with cancer, or needs to finish education but is ready to be committed to having a baby in more than 9 months' time, then she may decide to freeze her eggs for a time when she is more suited to have a baby, using a time when her body is more suited to producing eggs.
Does Freezing Have Adverse Effects?
As for your second question, the same page does mention successfully freezing an embryo for 10 years at -196 degrees Celsius, with no adverse effects on the eventual birth.
Regardless, exploring the risks reveals that the decision on whether the practice is seen as positive or negative is still on the fence - different parties argue for different opinions, as there appears to be no objective truth about proven adverse affects.
The risks described by this clinic are worth considering, albeit minimal compared to a risk of malformed children, however, it is still a popular choice, albeit put forward as 'experimental'. This study (2010, Rudick et al) showed how, in the US, cryopreservation was already being offered in 283 of 442 fertility clinics surveyed. 1/3 of the reasons for the choice was for women with cancer, and the other 2/3 was for women with 'advancing maternal age'.
The ACOG (American College of Obstetricians and Gynecologists), in 2013, stated that they do not endorse freezing of eggs 'for the sole purpose of circumventing reproductive aging in healthy women', however, the ASRM (American Society for Reproductive Medicine) lifted its label as being 'experimental' in 2012. The previously linked article describes a study conducted by the ASRM, which 'reviewed data from four randomized controlled trials and various observational studies that compared fertilization rates, embryo implantation rates and pregnancy rates of fresh eggs versus eggs that were frozen', and 'showed no increase in birth defects, developmental disorders or chromosomal abnormalities when in vitro fertilization cycles were conducted with frozen eggs, leading the society to declare the technique effective and safe'.
Conclusion
Your question is a slightly broad one, and can be answered by the subjective choice of the woman/women involved, however the ASRM still stresses that "we should proceed cautiously in using this as an elective technique", by making a clear line between 'need' and 'want'. However, there is no evidence to show that rates of abnormality are any higher using this method, but considering it is still a fairly new practice that is being marketed as a choice rather than a medical treatment, there is skepticism in the air around whether marketing scientific and medical designs as a mere 'choice' for older women will lead to this technology becoming better or worse.
Additionally, about your comment of it being 'less expensive', this website shows that the average cost of in vitro fertilization in the U.S. is currently about 10,000 - 20,000 USD, whereas the first website I linked (here) estimates the cost at about 10,000 USD to undergo an egg freezing cycle. Although, the prices will change from clinic to clinic. Regardless, the prices are still similar, and the choice lies in the woman choosing to pay and freeze her eggs if, for example, she has recently been diagnosed with cancer, or fears she will not be fertile in 5+ years time.
I hope this answer has been sufficient in answering your questions, and if you have any more questions, feel free to ask me :)
Sources:

http://uscfertility.org/egg-freezing-faqs/
http://www.mayoclinic.org/tests-procedures/egg-
http://www.sciencedirect.com/science/article/pii/S0015028210008009
http://www.ncbi.nlm.nih.gov/pubmed/24463693
http://edition.cnn.com/2012/10/19/health/egg-freezing/
http://www.advancedfertility.com/fertility-treatment-costs.htm

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How is the diploid chromosome number maintained at mitosis?
A normal human cell is diploid that contains 46 chromosomes in 23 pairs. Thus, when the cell undergoes mitosis, the cells still has the full chromosome with the two sister chromatids. What is it doing in interphase when it produces the other chromosomes?
I thought that the sister chromatids were pulled apart and, in interphase, the single sister chromatid grew another one. How is this possible if a human diploid cell contains 23 pairs of 2 chromosomes each?

No division takes place in interphase.

The terminology of "chromosome" during this process is confusing, but here it is:

There are 46 chromosomes in the cell (23 pairs)
Before division, each chromosome has two sister chromatids, joined in the middle (92 chromatids in total)
During division, the chromosomes split and each daughter cell gets 46 chromatids, one from each chromosome
These chromatids are now known as chromosomes
Each one of these new chromosomes only has one "chromatid"
During interphase, the new chromosomes replicate and now they have two chromatids each, joined in the middle

So whether a chromosome has one or two chromatids it is still called a chromosome. I hope this helps.
The following link contains a more complete explanation of mitosis. The first picture explains this point quite succintly: http://biology.tutorvista.com/cell/mitosis.html

Joe-can you add some references to your answer... it will strengthen the answer and allow other individuals to read more about the question/answer. I know it may seem silly when questions have a very easy answer that is based on common knowledge of those in the field, but we do have users as young as high school students (and potentially younger) that benefit from cited references. Thanks for your contribution!

Thanks for the advice, I've added a link to a more complete explanation with figures.

In a diploid cell the two sets of chromosomes are called homologous chromosomes (except in the case of XY pair) and not sister chromatids. Sister chromatids refer to the exact duplicate daughter chromosomes produced after DNA replication during mitosis.
After mitosis each cell receives a copy of all the pairs of homologous chromosomes.
I hope your doubt is clear now.


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Enzyme kinetics: Effect of immobilization on kinetic parameters
What is the typical effect of enzyme immobilization on the kinetic parameters of an enzyme's activity?
Can one assume that they'd stay approximately the same or is there a gross change? Any way to estimate the effect?
The native parameters are as follows:
kcat    0.5 1/min
Km      0.6 microM
[E0]    5   micro M
[S]     60  micro M

Could I expect to retain them after immobilization? Or are these too high for an immobilized enzyme?
If it matters, it is a 500 residue enzyme with a MW of approx. 65,000 Da

The main factor influencing the kinetics of immobilized enzymes is thought to be the rate of diffusion of substrate and product towards and away from the enzyme, respectively.
This has been discussed on ResearchGate and an article in Process Biochemistry from one of those in the discussion quotes figures for effects on immobilized laccase: approx. 100x increase in Km and 2–5x reduction in Vmax (as noted in the poster’s comment).
There are several theoretical treatments of the question:

http://www1.lsbu.ac.uk/water/enztech/summary3.html
http://link.springer.com/article/10.1007%2FBF02460071#page-1
http://www.amazon.co.uk/gp/search?index=books&linkCode=qs&keywords=9780849369872

Thanks! Those are great links. What I'd have loved to find was a study of the sort where someone had taken a bunch of enzymes, immobilized them and reported on the change in activities.

This snippet from your link is sort of what I wanted: "As expected, after an immobilization process, the apparent Km and Vmax values are significantly affected. In literature, for example, the Vmax value for immobilized laccase compared to that of the free enzyme is reduced of about 2–5 times compared to the free enzyme, due to substrate diffusion to the catalytic site, with an increase of Km value. The increase of Km can be explained as a result of diffusional limitation of the substrate or to conformational changes of the enzyme resulting in a lower affinity of the substrate for the enzyme"

Glad the links were of use. I'll flesh out my answer on the basis of your comment to improve it.

Did you get a chance to flesh out your answer? Any tips would help  a lot!

Sorry, just the reference. Been busy as was preparing to leave for a week. Currently en route to the French Alps.

Well! Lucky you! :)

Think of it as dedication to science. Effect of exercise at high altitude on human biochemistry.


text:
Why do RNAi pathway proteins exist in the nematode when they can cause them harm?
When dsRNA is injected in plant, Dicer cuts it and prevents disease.
Why would the plant parasite, M. incognita - a nematode,  die when dsRNA was injected in it? It should have saved it.
Again, to be more clear M. incognita has Argonaute protein and other RISC components for eliciting RNAi. This causes its death.
Then, why does the worm have such factors which cause its death?

There are many studies that have used RNAi against the plant parasite M. incognita. The fundamental idea is that RNAi is directed against one of the vital genes of this nematode. Since, RNAi causes downregulation of the target gene, the nematode dies (or becomes ineffective in infecting) because of the loss of function of these important genes. As you might know about the process of RNAi, dsRNA (or hairpins) are cleaved by Dicer and the small single stranded RNA products, called siRNAs, associate with Argonaute proteins to form RISC (RNA induced silencing complex). The RISC will cleave RNAs complementary to the siRNA.
If you see any of these articles you will notice that the dsRNA is not injected into the nematode; it is expressed in the plant. Nematodes (such as this one and C.elegans in which it is quite well studied) can take up dsRNA from the environment via the RNA transporters present in their cell membranes (See this post).
Now, coming to your question on "Why do RNAi pathway proteins exist in the nematode when they can cause them harm?"
endo-siRNA and miRNA mediated silencing pathways have critical roles in the nematode development and other miscellaneous functions (See this review). As you already know, RNAi can also serve as a defence against dsRNA viruses.
It is us, humans, who have exploited this pathway to develop tools for molecular biology and for targeting parasitic organisms. There is certainly a likelihood that the host plant may express the dsRNA against the nematode during the course of the evolution of its anti-parasitic defence system (it is however not the case now). Not just RNAi, there are many other examples of endogenous pathways of a pathogen being exploited to kill the pathogen.

"See This review" actually solved my problem.  Thank you. You are really great.

@AnubhavGoel "How do you get such links? "..... because of some years of experience.

@AnubhavGoel perhaps we can talk about this over chat.


text:
Why do we have oncogenes?
Oncogene is a gene which in certain circumstances can transform a cell
into a tumour cell.
Everything we have has reason and meaning.
Or there was some use in past.
What's the reason for we have oncogenes?

"What's the reason for we have oncogenes?".... Because they are essential for cell division. Please do some research before posting a question.

@WYSIWYG Implemented on 1st comment. Why are they essential for cell division? I thought they cause cancer.

@WYSIWYG Found this on wiki " Most normal cells will undergo a
programmed form of rapid cell
death (apoptosis) when critical
functions are altered. Activated
oncogenes can cause those cells
designated for apoptosis to survive
and proliferate instead." Also, >An oncogene is a gene that has the potential to cause cancer. Nowhere written for normal body functions.

Found >An oncogene is a cancer-causing gene. We have about 20 thousand genes in each of our cells, some of which are involved in fostering or promoting cell proliferation. When one of the proliferation-promoting gene suffers damage, it begins to urge the cell to proliferate uncontrollably rather than to do so in carefully measured amounts. Such a damaged growth-promoting gene is an oncogene.> on another site.   http://www.talkabouthealth.com/what-is-an-oncogene-and-what-does-it-have-to-do-with-cancer

A hyperactive allelic variant of a proto-oncogene is an oncogene (except for the virally encoded ones. It is all a stupid nomenclature). Highly expressed proto-oncogenes can also cause cancer. Since it is a variant, it cannot be grouped separately. Basically a good gene gone rogue. You have these genes that help cell proliferate which can mutate to become hyperactive. I cannot blame you here. It is a bad definition.

Whatever be the definition (of either oncogene/proto-oncogene), please clarify your question. Perhaps something like "what functions do (proto-)oncogenes have in a normal cell?" But please include some research in the question. Do not use comments to provide that clarification.

From wikipedia

A proto -oncogene
   is a normal gene  that could become an oncogene due
   to mutations or
   increased expression. The
  resultant protein encoded by an
  oncogene is termed oncoprotein.
  Proto - oncogenes code for
  proteins that help to regulate cell
  growth and differentiation.

So, we actually do not have oncogenes. Instead we have proto-oncogenes.
Due to mutation or virus, these are converted into oncogenes.
Since, proto-oncogenes are required for normal cell division and differentiation, they are necessary. Also, these can change to oncogenes any time. So, we always have to live with probability of this conversion.

Given that you wrote and answered your own question so close in time I'm suspecting this is just a rep grab. This post should be a community wiki, and you should also credit material, rather than just stealing it.

Credit must be properly given where it is due, regardless of the source.


text:
Can difference in the expression potential of alleles lead to dominance?
Several hour ago I was in thoughts what allele dominance really means on molecular level. As we know from basic genetics, if the organism had Aa type of some gene so trait is controlled by this gene would be equal to AA case. And we see it only when our organism is growing up. I'd like to know, how it works on molecular level, why Aa = AA in phenotype? I suggest, that expression level of A locus is greater than a locus and if so, why? Is that because of chemical structure of dominance allele that RNA polymerase interact with it more frequent?
Please, help me to understand. Thanks.
P.S. I don't consider different gene interactions as epistasis etc. just give you simplest example to describe what I want to know, but any useful considerations are appreciated.

Related posts: http://biology.stackexchange.com/q/1294/3340 and http://biology.stackexchange.com/q/20398/3340

Thanks, i've just read it, but i didn't find full answer. Would be grate if someone describes how RNA - pol chooses allel, or it can be by chance and it's not about chemical structure just depends on size of alleles (i mean, the bigger size allele has, the bigger chance to interact with RNA-pol etc.). Sorry if it sounds simple, don't have biological background.

Dominance is not commonly known to occur because of higher expression level, per se of one of the alleles. It can certainly be a factor but usually dominance is mostly known to arise because of a slight difference in function (or in other words activity) of the gene product (which may be a protein or an RNA).
Note that a change of function doesn't mean the alleles would have a totally different function. It just means that the alleles can be different in the way they function. For example two variants of an enzyme may have slightly different kinetic properties (such as Vmax Km and kcat). While change of activity may generally refer to Vmax (maximum enzyme activity), mutations can also change the other constants. Some mutations can make the enzyme sensitive to temperature by affecting the stability of the overall structure. The extreme would be a functional allele and a non-functional allele.
While concentration of the product does affect its activity, it does not change its specific activity, which may change in the presence of a mutation.
Moreover, even if one allele is actually has a higher expression than the other, the resultant trait can be differentiated from that of the aa homozygote only if the two alleles have slightly different functions or if the difference in expression level between of the gene product in Aa and aa is great enough to elicit different biological effects. In the second case there would be no change in the gene function and the effect of dominance is purely based on gene dosage. This review by Veitia and Birchler (2010) explores the possibility of stoichiometric alterations of macromolecular complexes or cellular networks being responsible for dominant phenotypes*.
Now, how can a mutation lead to a difference in expression level without changing the activity of the product?
There are three cases here:

The mutation is in the expressed region (exonic) but doesn't lead to change in activity (for e.g. synonymous mutations)
The mutation is in the transcribed region but in the intron.
The mutation is in the non-transcribed DNA regions such as promoter/enhancer etc. Exceptions: certain downstream promoter elements are actually transcribed.

Only mutations in the promoters/enhancers can affect transcription by affecting the recruitment of RNA-polymerase. However, you should note that mutations in the non-transcribed regions, especially in the distal regulatory elements are not considered a part of the gene in consideration. Since, such complex modes of regulation were unknown during the time of Mendel, the classical genetics does not explain these effects. Hence, these mutants would not be called alleles of the considered gene.
Mutations in the transcribed regions may affect the elongation rate of polymerase (especially if it leads to formation of stable DNA secondary structures). This is just a theoretical possibility and I have not come across any study that has reported something like this.
However, mutations in the untranslated regions of the mRNA can change the expression of the protein. These mutations may affect post-transcriptional regulation of the protein expression or even the RNA localization.
Synonymous mutations in the coding region can affect the rate of translation and hence the protein concentration.

*(quoted verbatim)

Good answer +1. However, you start saying Dominance is generally not because of higher expression level. I am not so sure about this generalization. Do you have a reference for saying that most often dominance is not mediated by variation in expression level? I think we know too little about the mechansims of dominance and its evolution to make such claim.

@Remi.b I didn't mean most common in statistical terms. By common I mean commonly perceived or commonly known. I'll edit the answer.


text:
Does our immune system react on all bacteria?
In our body we carry a lot of bacteria. Some of them are bad for our health, but others are beneficial. For example bacteria may protect us against other pathogenic bacteria.
But is our immune system reacting to all bacteria, i.e. the good and the bad, or does it selectively target the bad? If yes, how does it differentiate between beneficial and pathogenic bacteria?

I believe we have commensal bacteria on and inside our body that are considered part of the innate immune system. And those flora can try to predate on the foreign flora that try and attack us.

@RoSiv I think the question is why our immune system doesn't attack those bacteria which help us i.e. although they're considered part of innate immune system, what differentiates them, from pathogens, for our immune cells?

Just because there's no answer here after 9 hours, yes the immune system would typically lash out at everything. Commensals have ways of redirecting all that anger, however, and I'll provide two reference here and here that outline some ways they accomplish this. In short: they resist some mechanisms and exert influence on others.

I don't have time to answer right now, but do some reading on immune tolerance and the microbiome. There is a lot of work going on right now to try and understand the exact details of this very process, and it's not yet clear how exactly it happens across the board. Basically, though, we and our microbiome have evolved together over millions of years, and can signal back and forth to each other. It also involves some specialized immune cells, and very complex reactions between many different species of microbiota. You could also look up "biofilms" if you're interested in that aspect.

Perhaps you should have a look at this review. It is quite extensive and relatively recent as well (2014). I am myself reading it; if you end up reading it before me then you may ask specific questions about the article.

I've found too that CD4 T-cells can become regularity suppressor T-cells that suppres effector T-cells. See at 1:17 https://www.youtube.com/watch?v=xDvQI9ynl1Q

The immune system is capable of recognizing pathogenic ("bad") bacteria, either by components of the innate (non-specific) or adaptive (specific) immune system. Pathogenic bacteria will have antigen on their surface that mark them as 'foreign', leading to an immune response targeted to the bacteria. In contrast, the immune system tolerates the normal flora of the body. The precise role that the human immune system takes in tolerating and regulating the populations of the normal flora is not known, it is currently a hot area of research.
Current research suggests that microbiota induces host immune tolerance to commensal bacteria directly via a microbe-associated molecular pattern (MAMP) and polysaccharide (PSA) signalling. The immune system continuously monitors the resident microbiota, and certain antimicrobial mechanisms are constitutively engaged to prevent overgrowth of the colonizing microbes: this maintains what is loosely called immune homeostasis. The mechanisms that control (intestinal) tolerance include those that:
1) minimize exposure to and 2) immune recognition of intestinal microbiota, and 3) those that down-regulate immune responses through intra-cellular and inter-cellular mechanisms.
Research has shown that he tolerance of the normal microbiota of the gut seems to require an extensive network of regulatory immune cells including Tregs and (tolerogenic) dendritic cells.
Thymus-derived Tregs were discovered by Dr. Leszek Ignatowicz to be a crucial  player involved in "educating" the immune system about the diverse bacterial colonies in the intestinal flora of mice. In response to the diversity of gut bacteria found in the gut, the Tregs express a 'repertoire T cell receptors' (TCR) that recognize the antigens characteristic of individual bacterial colonies in the gut. Upon engagement of these receptors, Tregs suppresses the adaptive immune response, specifically through the release of immune-modulatory cytokines such as interleukin-2. Moreover, it was found that gut bacteria can also be recognized and protected by a distinct innate lymphoid cell population (ILC) in the intestinal lining of mice. These cells behave like antigen presenting cells, and can recognize and present antigens from gut bacteria through the major histocompatibility complex class II (MHCII). But rather than activating CD4+ T lymphocytes through MHCII engagement, these ILC works by suppressing CD4+ T lymphocytes through MHCII engagement. CD4+ T lymphocytes are involved in clearing pathogen/bacteria, and thus the suppression of CD4+ T lymphocytes is involved in the immune-tolerance of normal flora.
http://www.sciencedirect.com/science/article/pii/S2352345X14000083
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4007055/


text:
Why do dogs come in all shapes, but cats are generally all the same?
Minus hair and fur, cats (the domestic kind) seem to be just scaled versions of the same thing.  Dogs on the other hand can have long necks, short necks, long bodies, short legs, long ears, short ears.....

To my knowledge, there are quite a number of cat breeds (domestic) which have the same distinct features as listed by you above, such as longer tails, long ears (Devon Rex), short tail (Japanese Bobtail), different eye colours (Khao Manee), short legs (Munchkin)... what knowledge/source did you base your statement on?

They don't actually come in all shapes. They were bred like that as explained in the answer.

it's artificial selection

Until recently, cats were not extensively selectively bred, but were allowed to roam freely and therefore interbred randomly.  Darwin pointed this out, contrasting cats to species that were routinely "enclosed":

On the other hand, cats, from their nocturnal rambling habits, can not be easily matched, and, although so much valued by women and children, we rarely see a distinct breed long kept up; such breeds as we do sometimes see are almost always imported from some other country.

In contrast, dogs and some other species were selectively bred for certain characteristics "each good for man in different ways":

The key is man's power of accumulative selection: nature gives successive variations; man adds them up in certain directions useful to him. In this sense he may be said to have made for himself useful breeds.

Why were cats not selectively bred, while dogs were? This gets to be somewhat speculative, but it's clear from looking at dog breeds that many of the different breed functions need to have a larger animal than a cat, as well as one with different personality: Herding sheep, hunting foxes or badgers, fighting bulls, etc.  Cats' function for humans has traditionally been to hunt mice and rats, a role for which they're already beautifully adapted.
(There are a number of small dog breeds, of course, but these parallel cat breeds in that many are ornamental, or else originated as rat-hunters.)

Also, if a cat is to be out hunting mice & other vermin, it has many opportunities for random mating.

Indeed, we'd have guard cats, hunting cats, retriever cats, rabbit warren cats, racing cats... let's go to the cat races!

Cats are small size for hunting closer on the ground for small rodents
dog were born with longer legs for travel linger distance because of great stamina
cats dont have stamina like dogs but they are great sprinters to run 30mph for short burst


text:
Are identical twins clones?
Identical twins have the same genetic make up but they differ in development so are they in a way clones?

I don't see the point of your question. Seems like an unnecessary debate on the semantics. Lets say if we clone you, it is not really necessary that your clone will behave like you. There can be developmental differences too. Will that make the clone of you actually "not a clone" of you? In any case, in professional references people hardly use the word "clone" to mean genetically identical. The usage of the term "cloning" in molecular biology and developmental biology is restricted to certain procedures.

I'm voting to close this question as off-topic because OP basically asks what a clone is. Too trivial imo.

Are identical twins clones?
A clone is an individual that is genetically identical to another (see wikipedia > cloning). As you said, identical twins (better called monozygotic twins) are genetically identical to one another and therefore an identical twin is a clone indeed.
The role of the environment
Be careful, to not think of clone (incl. monozygotic twin) as individuals that look exactly alike or behave exactly alike. Even for traits that are highly heritable, environmental variation is causing a lot of phenotypic variation and two monozygotic twins do not encounter the exact same environment and can eventually grow up to be very different people. Note that the two blastulas will differ a little bit in concentration of proteins, fats, developmental factors and other things. Such small differences can have important impact on the development of the fetus.
See this post on heritability to have a better understanding of the underlying environmental variation explaining phenotypic variation in populations.
But they are clone for life, right?
Well, it depends on the exact definition of clone but it is important to understand that the expression of genes varies a lot in response to the environment. See for example wikipedia > epigenetics. Also genes may change slightly as we age (see Can genes change as we age?).

The same wikipedia article you quote clearly states that twins are not clones (see my edited answer)

The article says Human cloning is the creation of a genetically identical copy of a human [..]  It does not refer to the natural conception and delivery of identical twins This claim is about the expression human cloning and not about what a clone is.

What is wrong with using the definition for human cloning? The question clearly refers to humans. However, even if you would like to be picky: I think to such a general question, the more generally used and clear definition given by merriam webster applies much better than stretching the technical definition normally used for bacteria and apply it to humans.

As I understand it, the term human cloning refers to a set of processes to create clones. Generally, this set of processes does not include monozygotic twins. This does not mean that identical twins are not clones of each other. A clone is generally defined as an organism that is genetically identical to another one. In this regard, two monozygotic twins are clones. Does it make sense?

What you seem to say is that we define a clone not only based on its genetics but also by the process by which it has been created. Note however, that such definitions yield to possible issues such as the definition of a parent cell.

It would be great IMO, if one of us could offer an answer who draws to the issue behind the definition of clone (and eventually cloning) and how this relate to monozygotic twin. It will be important to make clear that, monozygotic twins, just like clones, are genetically identical.

I picked up on your suggestion and tried to expand my answer to encompass the different definitions of cloning.

Simple answer: No.
Merriam webster defines a clone as follows:

a plant or animal that is grown from one cell of its parent and that has exactly the same genes as its parent.

Identical twins have identical genes to their sibling not their parent. The reason behind this is that this definition of cloning refers to the artificial biotechnical method of creating genetically identical offspring. While identical twins are a naturally occurring phenomenon caused by a splitting of the embryo during early development.
Edit:
Long answer: It depends entirely on how you define a clone.
On one hand there is the original (biological science) definition (used in Remi's answer) which is mostly applied to bacteria: In that definition, clones are distinct organisms with identical DNA information. In that definition, identical twins are indeed clones, since they share the same DNA information.
On the other hand there is the definition from Merriam Webser (quoted above) which is the nowadays more commonly used definition outside the scientific community (also depicted in popular movies like Star Wars). That definition refers to the technical process of "human cloning" which is defined in the The wikipedia article that Remi quoted:

Human cloning is the creation of a genetically identical copy of a human. The term is generally used to refer to artificial human cloning, which is the reproduction of human cells and tissues. It does not refer to the natural conception and delivery of identical twins.

According to that definition, identical twins clearly are not clones and they would probably be offended to be called such.


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Which species of Agave are known to have inedible flowers?
It is well documented that many species of Agave have edible flowers, however I keep coming across statements to the effect that "most species" of Agave have edible flowers. This implies that it is known that some do not, but I have been unable to find any specific references to species known to be inedible. I'm particularly curious about Octopus Agave (agave vilmoriniana), which I could find no confirmation either way, but would like to know any information & sources regarding the inedibility of any Agave species.

According to Wikipedia each agave plant produces several pounds of edible flowers during its final season.

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


text:
What keeps organs suspended in the body?
I'm a bit confused what prevents our organs from not collapsing into a heap or putting pressure on each other. I have a 3D anatomy app and have been studying the relationship between the organs. According to the models, the organs are remarkably complementary in geometry and compact, but this still doesn't explain what prevents gravity from distorting them or squishing them.
My Question
What keeps organs suspended in the body?

Organs have internal structure to support them, and are attached to other organs and the various linings of the compartments in which they reside. They have many blood and lymph vessels going in and out of them as well. They do move somewhat with gravity, as the simple (for most people) experiment of standing on your head or laying backwards off an elevated surface will tell you. The body has evolved to contain them in a certain, not terribly flexible volume, so there's not much room for them to move around.

Most of the organs are attached to the abdominal wall by a fold of peritonium called mesentary.
Mesentary is a membranous tissue arising from the posterior wall of the peritoneal cavity and is responsible for keeping the organs at their designated places.Mesentary wiki


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Function of human kidneys
Why are the kidneys called metanephric? What does the term metanephric actually mean? I tried to search that on Google but couldn't find the exact meaning.

Start with mammalian kidney development: http://www.els.net/WileyCDA/ElsArticle/refId-a0001152.html

There are metanephric diseases, which refer to the location of pathologic tissue relative to the main kidney mass, but unless someone with more expertise wants to weigh in, I don't think that kidneys themselves are called metanephric.
There is also a developmental stage of the kidneys, in which they are referred to as metanephros. Perhaps you're thinking of that?


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When sperm and egg mix, are the genes rearranged?
I remember once my high school teacher said when the sperm fertilizes the egg the genes are mixed very randomly, is that true?

It is rather wrong! Segregation and recombination both occur at the moment of the formation of the gametes (meiosis) and not at the moment of the fertilization. You might want to have a look at the wiki articles for meiosis, recombination and segregation.

Your question is unclear. Perhaps you should clarify with your teacher about what exactly they wanted to say. Or otherwise you should clarify what you really mean by "mixing"? Sure, because of diffusion, the paternal and maternal chromosomes would be uniformly distributed in the nuclear space.

No.  When sperm and ova are forming, the chromosomes you inherited from your mother lines up with the chromosome you inherited from your father, and "crossing over" happens.  It would be like taking a Merriam-Webster dictionary, and another brand of dictionary, and picking a random point (like say, the middles of the "C" section), cutting both books at that point, and joining the portion of one with the portion of the other, making new books that are part Merriam Webster, and part the other kind of dictionary.  That happens in every chromosome, and the gamete is made up of those franken-chromosomes.


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What does a diamond symbol actually mean in pedigree?
Does it mean a person who is neither a male or a female, a homosexual or an individual whose sex is unspecified?

I find myself voting to close a lot of your questions as unclear or homework - could you start making effort to make questions answerable and effort to answer for yourself

A simple google search gives tons of answers. Try not to ask too trivial questions just for the sake of posing a question.

I'm sorry. I'll keep it in mind.

The figures in this article show symbols commonly used in pedigrees. Squares represent males, circles represent females, and diamonds depict individuals of unknown or, for reasons of confidentiality, disguised gender. A double line between parents indicates consanguineous marriages (between blood relatives) (see Figure 3). Filled symbols represent individuals who display a certain trait, such as an inherited disease. Bars next to the symbols represent genetic loci, and different alleles are color-coded. Diseasecausing mutations are shown as stars or crosses. Symbols that are half filled indicate heterozygous individuals, but often this information isn't known.

From Wikipedia:

If the sex of the person is unknown a diamond is used

Sources:

http://www.biologyreference.com/Oc-Ph/Pedigrees-and-Modes-of-Inheritance.html#ixzz43btGJSuv
https://en.wikipedia.org/wiki/Pedigree_chart


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Why do Arctic predators accumulate vitamin A?
Top predators in the Arctic are known to accumulate vitamin A, often to levels that are toxic for human consumption.  A 2012 study by Senoo, Imai, et al. found that the livers of several predator species in the Arctic showed much higher levels of vitamin A than other Arctic species or closely related continental species, with no symptoms of hypervitaminosis A.
Why is it that these species accumulate vitamin A?  Does this have something to do with the food sources available in the Arctic as opposed to the mainland?  Or are there physiological reasons why Arctic predators would tend to accumulate vitamin A rather than breaking it down or otherwise eliminating it?
References:

Senoo, Haruki; Imai, Katsuyuki; Mezaki, Yoshihiro; Miura, Mitsutaka; Morii, Mayako; Fujiwara, Mutsunori; Blomhoff, Rune (2012). "Accumulation of vitamin A in the hepatic stellate cell of arctic top predators". Anatomical Record 295 (10): 1660–8. doi:10.1002/ar.22555. PMID 22907891.

This study seems to be the only research on this particular topic, so no one will be able to provide you a definite answer. The authors suggest the following explanation: "Without huge capacity of storage ofvitamin A in HSCs in the arctic top predators, these ani-mals may suffer from hypervitaminosis A after intake ofthe large amount of vitamin A through the food chain,and cannot stay in the top of the food web there."

@Hav0k That "explanation" fails to account for why non-Arctic predators do not store vitamin A at such levels.

It doesn't explicitly state it but the implication is that non-Arctic predators don't have high vitamin A content in their food chain.  Many saltwater fish carry high levels of vitamin A.  So if this is the primary food source, e.g. seals eat fish, bears eat seals, then you need high tolerance for it.  Land animals have less vitamin A, so their predators don't need the tolerance.  I can't find any evidence of it but I thought vitamin A helped animals survived the cold, but there are also high concentrations in tuna liver, which are typically temperate or tropical.

The phytoplankton at the bottom of the food chain have high levels of vitamin A and precursors like beta-carotene.  At each step up the chain, vitamin A bioaccumulates.  Top predators in the Arctic deal with this by storing the vitamin A in the liver (bears, cetaceans) or blubber (pinnipeds).
This is the same mechanism that causes accumulation of pesticides like DDT in animals.  https://en.wikipedia.org/wiki/Bioaccumulation
Carotenoids are part of the photosynthetic system, and also protect the organism from sunlight.  Phytoplankton are unicellular, so each cell needs protection.  Therefore land plants contain much less carotenoids, since most of the cells are interior and protected from the sun.  For example, grains, roots, and wood have very low levels of carotenoids.
This occurs in polar regions due to up-welling nutrient-rich waters supporting high productivity.  Temperate and tropical deep ocean regions are typically deserts due to low nutrient levels, particularly iron and fixed nitrogen.

This answer does not answer the question on the difference between top predators of the arctic area and those of the mainland (or the oceans) closer to the equator, and the question why they do not suffer symptoms of hypervitaminosis A. Regarding the first question, does the phytoplankton in the Arctic area have higher concentration of vitamin A and precursors like beta-carotene?


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qPCR: do both primers have to contain a GC-clamp in order to be effective?
I'm developing software which, among other things, designs primers pairs (forward and reverse) for qPCR. In my research on various properties, I read about GC-clamps and I understand the basics of it I think. There is still something unclear to me.
Do both primers in a pair need to have a GC-clamp in order for it to be effective? Or does one GC-clamp in, let's say the forward primer, just increases specificity, and both primers containing a clam increasing it even more?

The new question is too Health'y for me to answer. Very nice edits for Health though. Likely others can answer it.

If we are adding gc clamp in both primers, the sequence should be different or same?

You can have GC-clamps (3' terminal G/C) in both primers; this may overall improve the PCR efficiency. However you should take care not to put too many G/Cs. This may lead to stabilization of primer pairs, leading to formation of primer-dimers. Also see this post: When designing primers how important is the GC clamp?
GC-clamps are not always essential and you should look at other parameters too.

So, in summary: A clamp in one primer is good for efficiency and clamps in both are better (with the right amount of G/C ofcourse). So I don't need a GC-clamp in both of them. Is this right?

@TomKral Not strictly necessary but good if you have it in both.


text:
Is NADH found in all type of cell in human body?
Is NADH found in all kinds of cell in the human body? I am curious about microglia specifically.

Can you add some background; especially about microglia. Why do you suspect that microglia would be any different?

As NAD+/NADH is involved in both glycolysis and in the tricarboxylic acid cycle it is difficult to imagine any cell capable of generating energy not having some NADH. (Are there any cells that are not capable of this? Calcified cells such as bone?)
A quick internet search for ‘microglia’ and ‘metabolism’ indicates that microglia have energy metabolism and so I would expect them to have NADH. How much (compared to NAD+) would depend on their metabolic state.


text:
Does caffeine actually enhance cognition?
I have heard, respectively:

Caffeine measurably enhances cognitive function.
Caffeine does not measurably enhance cognitive function in any significant way.
Caffeine enhances cognitive function, but only indirectly, in that it counteracts the effects of fatigue.
Caffeine enhances cognitive function, but only indirectly, in that it counteracts the effects of caffeine withdrawal.
Caffeine has no physical effect on cognitive function, but has a psychological effect.

What is the actual behavior of caffeine in relation to cognition?  (I'm particularly interested to know if any research addresses the claim that it only counteracts the effects of caffeine withdrawal)

Welcome to Biology.SE. If you can link to your sources, then that question would be a great fit on SkepticsSE.

Hi!  To be honest, I posted here rather than on Skeptics because a) I don't really have sources per se; these are just things that I have been informally told about caffeine over the years - I tried to do some research but I don't know enough about biology to be able to read papers in the field and b) I'm more concerned about learning the actual behavior of caffeine re:cognition than on fact-checking and figured that it would be better to just ask people who know (i.e, here).  But if you think I'd have better luck on Skeptics I can ask there instead.

Edited to make my actual query more clear.

Caffeine response is dependant on the individual. Caffeine has a very similar chemical make-up to adenosine which your body uses to transfer the energy you eat into energy your body can actually use (chemical energy). When your body has enough adenosine, it begins what is called a negative feedback cycle that stops adenosine production and sustains homeostasis. The feedback loops works by delivering a signal to put the body in a regenerative phase upon further adenosine binding. However, caffeine, being the wonderful individual that it is, disrupts that negative feedback loop and continues the conversion of excess (eaten) energy to chemical energy. But where in your body its dispersed is dependant on the individual.
The conversion to chemical energy is indirect though. Since adenosine is a principal neuromodulator, it actually tricks your body into behaving as it would at your most natural wakeful state. For example: Glutamate, GABA, norephinephrine, serotonin and acetylcholine are all inhibited by adenosine build-up at A1 receptors (a type of adenosine receptor) but caffeine stops adenosine from inhibiting these neurotransmitters. These five neurotransmitters all assist in metabolism (Glutamate is an essential compound in cellular metabolism).
Caffeine will never give you energy, it just uses your energy faster, in fact it probably causes energy debt from the work your body does to flush out the toxin.
In short: Yes it can enhance cognition, if the extra ATP (energy molecule made from adenosine) is carried to the brain. As it is not a homeostatic process it's difficult predict.
When the body is constantly put out of it's homeostasis, it adapts the toxin into its homeostatic balance (kind of like a beat em' or join em'). In this way, an individual's body begins to need the caffeine to function normally. Caffeine dependance is very low however, since it has been around for centuries, we've evolved to know it as a toxin but to not depend on it.
References:
J Alzheimers Dis. 2010;20 Suppl 1:S3-15. doi: 10.3233/JAD-2010-1379.
http://thebrain.mcgill.ca/flash/a/a_11/a_11_m/a_11_m_cyc/a_11_m_cyc.html
http://pharmrev.aspetjournals.org/content/51/1/83.short

Are you sure this is how caffeine works? It actually acts on the adenosine receptors as far as I know and does not affect cellular metabolism of adenosine. Can you add some references to support this?

The adenosine receptors caffeine acts on directly is different from those involved in ATP production. Looking at my answer now, I can see how it could be confusing. It would have been best had I specified the ATP (and other chemical energy) synthesis is indirect. Thanks for pointing that out, I'll adjust my answer.

In a study by Wight et al. (2013) [1] it was shown that bees feeding on nectar containing caffeine seem to enhance the bees' memory of those flowers. They hypothesized this based on the fact that:

Two caffeine-producing plant genera, Citrus and Coffea, have large
  floral displays with strong scents and produce more fruits and seeds
  when pollinated by bees (8, 9)

They tested this hypothesis by feeding bees sucrose solutions with different concentrations of caffeine and measured their behavioural response.

We hypothesized that caffeine could affect the learning and memory of
  foraging pollinators. To test this, we trained individual honeybees to
  associate floral scent with 0.7 M sucrose and 7 different
  concentrations of caffeine and tested their olfactory memory. Using a
  method for classical conditioning of feeding responses (proboscis
  extension reflex, 11), bees were trained for 6 trials with 30 s
  between each pairing of odour with reward. This inter-trial interval
  approximated the rate of floral visitation exhibited by honeybees
  foraging from multiple flowers on a single Citrus tree (see methods).
  The presence of low doses of caffeine in reward had a weak effect on
  the rate of learning (Fig. 2A), but it had a profound effect on
  long-term memory. When rewarded with solutions containing
  nectar-levels of caffeine, three times as many bees remembered the
  conditioned scent 24 h later and to responded as if it predicted
  reward (Fig. 2B, logistic regression, χ72 = 41.9, P < 0.001). Twice as
  many bees remembered it 72 h later (Fig. 2C). This improvement in
  memory performance was not due to a general increase in olfactory
  sensitivity resulting from caffeine consumption (Fig. S2A). In fact,
  the effect of caffeine on long-term olfactory memory in bees was
  greater than that produced by high concentrations of sucrose when the
  same experimental methods were used (e.g. 2.0 M, Fig. S2B).

However, bees would not prefer nectar (or sugar solutions, as  at higher concentrations (>1mM) as they would find it distasteful.
I am not sure if this hypothesis is extensible to higher organisms. It may have some effects on alertness and attention but there are no stringent studies to assess its effects on learning.
This review [2] on the possible cognitive effects of caffeine concludes that:

Thus,  caffeine  apparently  cannot  be  considered  a 'pure'
  cognitive enhancer. Its indirect action on arousal, mood and
  concentration contributes in large part to its cognitive enhancing
  properties.

[1] Wright, G. A., et al. "Caffeine in floral nectar enhances a pollinator's memory of reward." Science 339.6124 (2013): 1202-1204.
[2] Nehlig, Astrid. "Is caffeine a cognitive enhancer?." Journal of Alzheimer's Disease 20.S1 (2010): 85-94.


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Do plants have distinctive DNA genomes from each other like humans do?
Can exact same species of plant have a distinct genome from others of same exact species growing nearby or in a different place/country etc. ?
Can a leaf be traced to the the exact plant based on DNA if we were to be given DNA of the "parent" plant of the leaf, and two test plants' DNA of exactly the same species?

It's kind of an interesting question. The answer is yes for sexually reproducing species of plants, but plants that reproduce clonally can form massive genetically identical colonies

probably yes for both sexually and asesually reproducing plants as well as i am taking a wild guess on cloned species also, because of natural and artificial mutations.

Short answer: Yes!
Now for the longer answer. Yes, they do have distinct genes in general, but what you may see as different plants can also sometimes be clones. For example Quaking Aspen Trees which commonly grow in clonal colonies.
If you had a massive database of genetic material from plants you would be able to trace it. You may be able to, by doing sampling, work out where a sample was located geographically.

We need to distinguish plants which replicate by sexual reproduction from those who reproduce asexual.
Due to the higher recombination rate in sexual reproduction it should be easy to find your plant to which the leaf corresponds to. Because you can see lot of single nucleotide polymorphisms and maybe other changes in the DNA unique to the plant whose leaf you found.
If your plant species reproduce by vegetative reproduction it could be more difficult because you can not find a lot of DNA changes making your plant unique. But since there are some mutations in DNA from vegetative reproducing plants (see here and here) you probably should try to find them.


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Grouping OMIM disease codes
I have ~100 sets of genes, and each set includes between 2 and 70 genes. I'd like to perform an enrichment analysis on each of these sets to test if they're enriched for OMIM disease labels. However, I'm encountering a problem where the OMIM codes are too "sparse", such that each OMIM code only occurs maximum once in all gene sets. As far as I can tell, this makes the codes unsuitable for enrichment analysis in this case.
I believe that grouping the OMIM codes could solve this, as long as each group-label occurs multiple times in my lists. Grouping OMIM codes seems doable: for example, OMIM codes 601495, 613500, 613502, and 613506 all refer to types of agammaglobulinemia. I could imagine grouping codes based on something like gene ontology labels.
My question: is there a standard way to group OMIM codes?
I see some papers doing something like this, e.g. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4458913/, but I'm new to the field and don't know how "standard" approaches like these are.

Hi and welcome to Biology.SE. Without a clear scientific question to answer there isn't enough information here to answer the question.

Thanks for letting me know. I edited my question to include more information. Let me know if I can add more.

It's still hard to tell exactly how you want to group them and to what end, so I've provided a general answer below. I hope it helps!

Based on OMIM ID codes
In a broad sense NIH have already divided the IDs. If all you are checking is OMIM code enrichment, this might be an okay resolution since it can tell you the chromosomal locus (autosomal, sex linked, or mitochondrial).

Each OMIM entry is given a unique six-digit number as summarized below:
1----- (100000- ) 2----- (200000- ) Autosomal loci or phenotypes
(entries created before May 15, 1994)
3----- (300000- ) X-linked loci or phenotypes
4----- (400000- ) Y-linked loci or phenotypes
5----- (500000- ) Mitochondrial loci or phenotypes
6----- (600000- ) Autosomal loci or phenotypes (entries created after
May 15, 1994)

Other databases as an alternative method.
If you are interested in specific phenotypes, you may need to get more involved.
OMIM doesn't really attempt to group diseases together beyond their ID nomenclature as far as I'm aware. There have been several projects that set out to do this, like the one the question points out, and the examples below. They mostly use phenotypic data in combination with OMIM information.
Two databases that aim to solve this are:

HPO
LDDB
Enricher web-server see @MaximKuleshovs answer below!

These are tools with controlled vocabulary for phenotypes and associations from OMIM codes. They could help you check for disease/phenotype specific enrichment. This would certainly allow programmatic grouping, although I have not worked with either before and I presume it would be very involved!
It's up to you!
Wikipedia has a list of OMIM codes listed in alphabetical order if you wanted to try to group them manually by whichever criteria you desire.

Without your source code it's hard to tell, but maybe the maximum of one occurrence rate could be a code problem rather than a scientific problem.

Thanks very much! That's exactly what I was looking for. I tried grouping by different arrangements of the numerical OMIM code (include using the first digit) but I don't think it makes much sense for my application. I'll look at other databases and/or try a custom solution.

There's an approach from "Enrichr: interactive and collaborative HTML5 gene list enrichment analysis tool" paper:

The OMIM gene-set library was created directly from the NCBI’s OMIM
  Morbid Map. We removed diseases with only a few genes and merged
  diseases with similar names because these are likely made of few
  subtypes of the same disease. In addition, since most diseases have
  only few genes, we used our tool, Genes2Networks, to create the
  OMIM expanded gene-set library. We entered the disease genes as the
  seed list and expanded the list by identifying proteins that directly
  interact with at least two of the disease gene products; in other
  words, we searched for paths that connect two disease gene products
  with one intermediate protein, resulting in a sub- network that
  connects the disease genes with additional proteins/genes. Each
  sub-network for each disease was converted to a gene set.

Enrichr itself has two OMIM libraries in Drugs/Disease categories. Moreover it has Human Phenotype Ontology library and MGI Mammalian Phenotype libraries.


text:
Does alpha-amylase from different species have different *optimal* conditions?
Do the optimal conditions for the enzyme isoforms differ between species? Specifically, do the optimal pH and temperature for alpha-amylase differ for that enzyme produced by B. lichiniformis and A. orzyae.

They may differ as different organisms have evolved to live in different environments.


text:
Does copper exacerbate wounds?
There is a three edged stiletto (weapon, not shoe) with a triangular cross-section that is often touted as being "extra dangerous" because of the triangular puncture it makes, and its copper construction. The claim is that the copper inclusion causes something colloquially referred to as "blood poisoning."
Is there any basis to the idea that a copper blade would cause some kind of secondary toxic effect?

Can you post a link either to the weapon itself or to some other source discussing its "extra dangerousness"? I've found some triple-edged stilettos, but nothing made of copper.

That's the trouble, it's all been anecdotal. I've seen these copper stilettos sold at fairs and whatnot, some of which even by otherwise reputable vendors, but I can't find any info online.

Copper is a micronutrient and is essential for human body. See here

Meaning it is toxic only at levels the body can't handle and its deficiency can cause some health issues

Ironically, copper and copper-containing alloys are also known to have antimicrobial properties (https://en.wikipedia.org/wiki/Antimicrobial_properties_of_copper), meaning that it's conceivable that you'd be less likely to get blood poisoning from a copper blade.

Excess copper in the body can be toxic but I'm not sure a copper blade would be especially toxic unless it was coated with something else or it remained in the wound. Copper can be acutely toxic when ingested, or chronically over a long period of exposure (like lead), but is more often associated with a failure in copper excretion. Since the body has ways of dealing with excess copper, I just don't see much merit in the super-toxic copper blade, unless it is designed to break off in the target.

I also think, that the copper is much less of a problem than a deep wound by such a weapon.


text:
Why are skin moles (pigmented spots) circular in shape?
I have never seen a rectangular or triangular shaped mole.
Is there any reason for why moles are roughly circular in shape?

Totally unscientific personal remembrance: I knew a guy who had a big mole which did have one nearly rectangular "edge". So it seems they can be "edgy", but just usually aren't?

Dude! Gorbachev is your best shot!

Note: I am not stating that moles are in general circular in shape because there are no statistical studies to conclusively state so. This answer is mostly about default circular shape of cell colonies.

Moles (melanocytic naevi) are not strictly circular but generally have  have a rough circular shape. Moles can have irregular shapes too and you can easily check that by a simple google image search.
The exact causes and mechanisms of mole formation are not known but the somewhat circular shape can be explained by a simple spatiotemporal model of growth.
Moles are formed because of pigmented cells called melanocytes (which contain the dark pigment melanin). A mole would grow when a very small population of these pigmented cells divide and expand. In a 2D surface, cells would continue to divide and expand along both the axis at an equal rate, if there are no specific constraints. Since the expansion is same along both the axes, you get a roughly circular shape. For similar reasons, bacterial colonies (on petri plates) are also more or less circular. Note that there are stochastic factors that would contribute to irregularity.
Triangles and rectangles are very specific geometries. There need to be some constraints that would limit the cell growth to adopt these geometries. So the default shape would be mostly circular.

Short answer
Naevi do not have to be circular in shape. In fact, they come in a wide variety of shapes and colors.
Background
A beauty spot, or mole is called a naevus. Naevi (plural) are formed by the growth of the pigment cells in the skin, the melanocytes .
There are various types of naevi:

Congenital naevi are present from birth and occur in about one in 100 people. They may be more likely to develop into melanoma (cancer) than nevi appearing after birth (WebMD).
Acquired naevi develop later in life (Dermatology Net NZ);
Dysplastic naevi are typically larger than average and more irregular in shape. They tend to have uneven color with dark brown centers and lighter, uneven edges. These nevi are more likely to become melanomas (malignant skin cancer) (WebMD).
Dysplastic naevi may turn into melanomas (NIH), but melanomas are outside the scope of this question.

Now let's turn to your question - not all naevi are circular. Below I have illustrated just a mere tiny handful of the wide gamut of shapes found among different types of naevi. In fact, naevi come in a wide variety of shapes and colors (source: Dermatology Net NZ):

Small congenital naevus ; medium congenital naevus ; and hairy congenital naevus

Café au lait macule ; Speckled lentiginous naevus ; and Naevus of Ota

Reticular naevus ; Junctional naevus ; and Starburst naevus
In fact, naevi occur in more extreme forms too:

source: No Hands but Ours
Reference
- Cichorek, Postepy Dermatol Alergol (2013); 30(1): 30–41


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What are the most common mechanisms motivating mammals to mate?
I read somewhere that dolphins and humans are some of the only species known to have sex for fun. I was just curious

What motivates mammals to mate? (Like what compels them to do it, not what the purpose of doing it is)
Are those motives solely aligned for reproduction or are there other benefits to mating?

There are pheromones and other hormonal signals. I don't think sex was ever about fun. IMO, fun (or the ecstatic feeling/dopamine release) is probably just a response that would increase the chance of mating (in the sense of the organism wanting to try again).

What determines when pheromones and hormones are released? Are there mating seasons where environmental factors trigger them?

There are environmental factors. It can be periodic like in the case of estrus. I have to read a bit to answer your question in detail.

Different animals are compelled by different things. If you have a specific animal in mind I'd suggest focussing the question on that. As it stands the question would require too broad an answer.

I enjoy questions on animals mating


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Article or answer to whether "blood volume pressure" and "electrodermal activity" have any correlation to stress and or feelings overall
As the title suggests, I would like some help finding if there is any correlation between between blood volume pressure and electrodermal activity?
The paper I'm writing is about measuring stress and engagement levels of the subject by comparing the levels of electrodermal activity and blood volume pressure during media consuming. This can be anything from music, movies, tvshows etc.
But the papers im looking for can be about the correlation only. Not by measuring the same type of things as I do.
If you know any good articles, I don't really care much about the publication date.
I have full access to ieee articles through university.
Thanks.

Questions should be specific and not lead to discussions. Also, please minimize the use of acronyms. I'm very interested in skin conductance and stress, so I would be happy to look into your issue, but as it stands this question does not meet this site's standards. Please edit and refine the question if you would like to receive input. The help center contains info on what a proper question format is. Have a look!

Okey, updated the answer now.

@SimonNilssonGuldstrand What Christiaan pointed out still stands. What correlation are you looking for? Do you want background on how the two are linked, or interpretation of stats from a certain paper?

@James i would prefer both, but one of them is enough. I'm writing a paper myself that include these points of measure and need to have facts that back up how they are linked. So a graph or short text describing it would be superb.

@SimonNilssonGuldstrand If you could incorporate that into your question and explain specifically the information you are looking for and add the reference request tag. If you don't make it clear, the question is likely to get closed.

Please see the tag wiki for reference-requests and provide the necessary information as mentioned there.

I have updated this question as much as I can. Are you guys still interested in helping me find an answer? @Christiaan


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How long does it take for a person to lose all offsprings due to inheritance?
From this I know we will only inherit some genetic informations from parents, which is about 50 percent. But the problem is, gene has finite size, after some generations a person leaves only $0.5 \times 0.5 \times 0.5$ parts of genes to the offsprings, and it will be casted into zero. My question is, how long does it required for a person to lose all genetic information in the world?

Why would someone (a lineage) lose all genetic information in the world? Definitely the person will mate with someone else from the same world and not from another galaxy.

I think your question conveys some misunderstanding.
A child is related to each parent by a factor of ½. Humans have a diploid genome, meaning they have two copies of each chromosome (see: autosome). When two humans reproduce, they each contribute one copy of each chromosome to the offspring, in other words, they contribute a haploid genome to make a diploid child. Genetic information is not "lost" - the genome is not shrinking by a factor of ½ every generation.
However, relatedness does decrease from generation to generation. You are related to each of your parents by a factor of ½, each of your grandparents by a factor of ½ $\times$ ½, your great-grandparents by a factor of ½ $\times$ ½ $\times$ ½... You are also related to your children by a factor of ½, you are related to your grandchildren by a factor of ½ $\times$ ½... You get the picture, right?
For example, imagine the genome carries just one gene. Your father carries alleles $AA$ at that locus, and your mother $aa$. You would then be $Aa$ and, because half of your alleles came from your father and the other half from your mother, be related to each by a factor of ½, but all three of you have the same number of genes (1) and that gene is the same length (in nucleotides, barring mutations) in all three.

But at some point, your offspring will have increased in number to the point that they're a significant fraction of the population, and will start mating with each other.  So if two of your great-great-grandchildren marry (each 1/16 of your genes, if I counted right), their offspring have 1/16 + 1/16 = 1/8 of your genes, not 1/32, no?

@jamesqf Right idea, but the fractions add up a little differently. Two of your great-great-grandkids marrying would each provide 1/2 of the 1/16 of your DNA they have, giving their progeny 1/16 of your DNA still. If two of your children, each with 1/2 of your DNA, were to have kids (gross, I know), the child would have 1/2 of your DNA, and not be your genetic clone (100% of your DNA).

I feel rg255 answered your question very well, however my mind snapped to an exponential relationship, which is part of what I feel your asking and what rg255 has said (but I have a pretty picture to add).
An exponential graph illustrates the relationship you are speaking of where a substance is infinitely divided by itself.

In this way it will never reach zero. It will inevitably and exponentially shrink but not disappear.


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How to read this DNA inversion diagram?
In the following diagram about chromosome inversion, I don't understand:

Why do we need to take the reverse complement from step 1 to 2? Isn't inversion just reversing the bases in the region?
How is the bottom diagram derived? For example, where does the ACCCCACTC come from? I thought it should be: GACTGCCGT for 5'→3' and CTGACGGCA for 3'→5' (inversion of the sequences in the second step).

http://web2.mendelu.cz/af_291_projekty2/vseo/print.php?page=315&typ=html

Your misunderstanding probably stems from the differences of definition of inverse in bioinformatics (reverse) and cell biology/genetics.
What is shown in the picture is chromosomal inversion, in which the segment of DNA gets cut, flipped and ligated. Note that in the DNA, 5' would be ligated to 3' and vice-versa. So the 5' of the bottom strand i.e. T is ligated to the 3' of the top strand i.e. C. Similarly for the other ends. Therefore, you see a reverse complementation.
The sequence of the top strand however should have been 5'-TTAC-TGCCGTCAG-TAG-3' which has been incorrectly shown as 5'-TTAC-TGGGGTGAG-TAG-3'. That is a mistake in the picture.
Have a look at this picture [1]:

[1] Okamura, Kohji, John Wei, and Stephen W. Scherer. "Evolutionary implications of inversions that have caused intra-strand parity in DNA." BMC Genomics 8.1 (2007): 160.

That’s what I thought as well at first but if you actually look at the sequence of the red (flipped) bit, you’ll notice that it differs between the middle and the bottom picture: the red bit reads 5′→3′ TGCCGTCAG in the middle picture, but TGGGGTGAG in the bottom picture.

@KonradRudolph Oh! That seems like a mistake in the picture.


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Need to solve a "pseudo-metabolic" network for rates
following problem:
I have data on a certain complex association network (from monomers 1 ... 8 to complexes of all combinations, such as, 12 ... 13 ... 18 and so on until 12345678, so that I know

the structure of the network (255 vertices)
the edges of the network
the concentrations of the vertices

From this data I now wish to infer the preferred route(s) of assembly for those complexes - which should be the rate constants for the edges, such as 1 --> 12 or 145 --> 1458. Does that make sense?
I have now tried various standalone applications for network creation/analysis as well as R packages. Metabolic flux analysis seemed promising for me, but it turned out that it only works with set external concentrations and assumes steady-state for all metabolites within the network. Which is not the case for me. Do you know of any alternative method?
Thanks and best wishes,
Simon

Hi. May be this question would be more suitable for cross validated, for example. But anyway, if i got you right, you are trying to put some marks for edges that is associated with the way they need to be assembled? I'm not biologist at all, just try to get your full task.

Thanks for your recommendation, I will look into posting it over there.
Yes, exactly, I want to find out the relevant routes of assembly (=paths), which should be the ones with the highest "flux" there...

yes, but the best resource for this question, i guess, this https://www.biostars.org/

Flux balance analysis always assumes steady-state, and in this case concentration data is irrelevant.  It sounds like you're after some type of dynamic method that can handle time-varying concentrations. In this case the problem is much more complex, and you really need to describe the problem in more detail. What kinetic assumptions are you willing to make? (Michalis-Menten, or ... ?) Are you going to fit time series data? What are boundary conditions? What type of data do you have, a pulse experiment (unit step input), or ...  ?


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Healing of Skin Superficial Wound
How does the body heal a skin wound without bleeding?
I had a wound in which thick layer of skin was gone and which was too painful to touch. I could see the wound secreting clear liquid rather than forming a scab like in a blood wound. What is this yellowish thick liquid being secreted and does it form new skin?

The clear/transparent fluid you are talking about, is most likely serum, an amber-coloured, protein-rich liquid which separates out when blood coagulates

Jordi Zambrino-Are there 13 proteins? can you name them.

@TheVoid What are you on about?

@Jordi Zambrino- Ill ask a question on it in a bit, It has to do with the 13 protein factors.

@uncia- Was the wound around the knee area?

How is this primarily opinion based? Just curious.

@TheVoid just above the just above achillies tendon, so whenever i walk wound would contract and expand and more clear liquid ooze out

@uncia- Yes the areas of the body where the fatty layer is thin or on a bone or tendon or cartilage this type of reaction will occur. I would suggest liquid skin ointment to seal it up because the healing process is prolonged and will open right back up if disturbed.

Skin is composed of layers, the uppermost being the epidermis. Upper layers of the epidermis (dry, flat cells tightly packed together, and of varying thickness on different parts of the body) can be abraded off, leaving deeper layers of the epidermis (nearer to underlying blood vessels) exposed. Since peripheral nerve endings do exist in this area, the wound is painful. A wound that does not extend into the dermis does not bleed (for example, a second degree burn can lift the upper layers of the epidermis from the deeper layers; no blood will collect in the blister, but the wound is painful. Peel off the top of the blister, and you have an analogous situation.

Because the surface of the skin is no longer present, fluid (as with a blister, not containing red blood cells) leaks from the blood vessels. Initially a transudate, it can also be an exudate. And, no, it does not contain the cells needed to regenerate the upper layers of the skin. It contains many of the proteins found in serum and may contain white blood cells which help to fight off infection.
New cells are generated from the deeper cell layers (the basal cells) which are still intact. They grow from the bottom of the wound up, so to speak. The scab formed by the dried fluid keeps the layer under it moist, providing a good environment for cell growth.
Epidermis and Its Renewal by Stem Cells


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How are ions 'pumped' across a membrane during electron transport?
A number of sites (including this one) that provide descriptions of photosynthesis state that high energy electrons 'pump' ions across a membrane. What is the actual 'pumping' mechanism? I've looked at Wikipedia and at a number of YouTube lectures/tutorials but so far have only found statements as to the where and when but not the how of this important process.

This is a good question, but the answer is likely to be very technical, and I think these mechanisms are still bein debated; see for example http://www.ncbi.nlm.nih.gov/pubmed/21545285  calling this "one of the most challenging research subjects in life science" ...

Thanks for your interest. I've had a further hunt round and found an article in Wikipedia on active transport . A little way down there's a section about secondary active transport that I think could be related to the pumping mechanism in photosynthesis - but I'm not qualified to say!

Short answer:
Electrons flow through membranes by floating through kind of channels made out of iron-sulfur clusters.
Long answer:
Let's take a look at the electron transport chain in the inner mitochodrial membrane. There is a proton gradient across the membrane building up a potential difference by pumping protons across the membrane as electeons flow through the respiratory chain. They (electrons) like to flow throught the respiratory chain because they can go from enzyme to enzyme each with a lower standart free energy. These enymes together form one big complex within the inner membrane with Fe-S clusters enabeling electrons to flow through the membrane by giving them a kind of a power stroke (see here).
This as an simplyfied answer on a example.

Thanks for your answer. I think I'm starting to understand this a little. I think what I was missing was that: "Whenever a molecule is reduced by acquiring an electron, the electron (e -) brings with it a negative charge. In many cases, this charge is rapidly neutralized by the addition of a proton (H+) from water, so that the net effect of the reduction is to transfer an entire hydrogen atom, H+ + e -". The quote is from this site that I found really helpful - though I'll need to study it a good deal more. As a layman I found 'pump' misleading.

Nice!  Still, I think it should be kept in mind that these are very recent findings; the structure of complex I was only recently resolved, and the precise mechanisms are likely to be debated for some time to come.

Moreover there are many other kinds of proton pumps that work differently.

Thanks for the additional comments @WYSIWYG: I trust that the principle  remains the same i.e. a set of redox reactions with the H+ transported across the membrane in association with the electron as it 'neutralises' the negative charge of the electron? I'm new to biology so want to make sure I've understood the basic ideas/processes correctly.


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When should you use a stringent plasmid?
I was wondering if anyone had good examples of when you would want to use a stringent plasmid vs. a relaxed plasmid in a research setting.

The three general advantages are:

Lower expression. If your plasmid is expressing something toxic to cells at high levels, reducing the amount of DNA can reduce expression.
Lower plasmid burden. If you are concerned about the stress imposed by maintaining many copies of the plasmid, low-copy plasmids are helpful.
Population homogeneity. Relaxed plasmids tend to replicate such that there will be a wide distribution of # plasmid copies/cell. Meanwhile, stringent plasmid replication is tightly coupled to the cell cycle itself, so the number varies less. In certain cases it may be desirable to control the number of plasmids per cell.

Stringent plasmids are also good for doing mutant screens, I assume.


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Stable isotope sample preparation: Bone Collagen
I am performing research in which I need to extract bone collagen from the foot bones of American Beaver (Castor canadensis).  I have read through the literature fairly thoroughly on both the archaeological/anthropological side and the wild life side and have been finding a many tweaks to a fairly simple extraction process, but I still have a few questions.

When processing bone I split the bone and removed the center, which was red/ light pink, (I thought it was the marrow and wanted to make sure that I was getting collagen from only 1 part of the bone to not confuse my isotope data with varying tissues)
There is also some variability across papers in the time that people allow bone to demineralize in a strong acid  ranging from 20 mins to upwards of 10 hours.  Does anyone have any experience with this and size to which you ground your samples.
The literature has a variety of temps ranging from 58 C to 95C, it proposes to gellatinize the collagen in a weak acid over a variable number of hours (approx pH of 3), does anyone who has experience offer a temp and time that worked for them.

Any help is much appreciated, Thanks


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How do I retrieve electronic annotation from Uniprot and GO records that relates to molecular function?
I'm interested in the endonuclease activity of the G3BP1 gene, specifically the uniprot record Q13283.
An external link guides me to UniprotKB-KW electronic annotation. How can I retrieve valuable and concrete information (e.g. catalytic sites, motifs) that explain this annotation from that link?

Since it is only one gene then you can simply note down whatever is mentioned in the Uniprot page. You can try BioMart if you have more number of queries but I don't think it will have structural information but it will have GO annotations.

Species please, links to Uniprot entry please. It you want us to help you, you need to help us.

The endonuclease is controlled vocabulary. In this case, it looks like GO actually cites UniProt as the source for the endonuclease keyword.
With the Uniprot url, whenever you want to see where the information comes from for the annotation in Uniprot, type /publications after the ID. For example: http://www.uniprot.org/uniprot/Q13283/publications


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Is H antigen considered as an agglutinogen?
A and B antigens which have the potential to cause agglutination in certain cases are called agglutinogens. But, as far as I know, H antigen cannot give rise to agglutination. So can it be said that H antigen also is an agglutinogen?

H antigen is a precursor for A and B antigens, and hh (recessive) individuals do not express this antigen. See Bombay blood group. This is an example of epistasis. Since H antigen is present in all A,B,AB and O blood groups, transfusion from any of these to an hh individual will cause a haemolytic reaction. Anti-H antibodies are agglutinins and have been referred to as agglutinins in the scientific literature.

The fairly strong anti-H agglutinins present in 'Bombay' and
  'para-Bombay' individuals (see 5.5.6) are generally accompanied by anti-A and anti-B, neither of which can be separated from the
  anti-H specific antibodies.

 Schenkel-Brunner, Helmut. Human blood groups: chemical and
  biochemical basis of antigen specificity. Springer Science &
  Business Media, 2000. e-Book ISBN: 978-3-7091-6294-1


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"Next generation" brain scanners, can they detect CTE?
I've just read the news that a "new generation" brain scanner is under development. I wonder whether they can detect chronic traumatic encephalopathy. I haven't been able to find the paper about these new brain scanners.
So is it possible to detect CTE (during life of the patient, i.e. non post mortem) with this new device, and if not, is there any chance it will be possible in the future?

I do not know the details of the innovation, but it's based on MEG. MEG is a complementary technique similar to EEG, sesitive to magnetic fields instead of electrical fields (hence the 'M' in place of the 'E'). It is used to read population brain activity in real time, and is less useful as a tool to assess structural changes. MEG is currently mainly used for research purpose, and I don't see this innovation changing that. CTE could manifest in longer conduction delays or disruption of communication, but given that MEG can only access certain areas of the brain, it is probably not going to be very useful in general. I can imagine it being useful for some very specific CTE cases.


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Are intercellular junctions, synapses and light-capturing photosynthetic complexes mobile?
I was reading Cell Biology by Gerald Karp and came across a section which said-

Membrane fluidity makes it possible for clusters of membrane proteins to assemble at particular sites within the membrane and for specialised structures, such as intercellular junctions, light-capturing photosynthetic complexes and synapses.

I would be obliged to know more about the topic.

Not necessarily. Sometimes the membrane localized proteins/complexes are anchored to the cytoskeleton or clustered together which limits their movements. See this post.

Membrane fluidity allows reversible association of membrane compounds, which can be thought of as diluted in a two dimensional fluid; this also implies a crucial property of membrane dynamics, which is the differential association of components into more or less stable molecular groups. Once formed, the more stable will be able to cruise the membrane surface, unchanged. This tells you that certain complexes will, by their stability and membrane fluidity, be in constant motion, and thereby statistically well distributed on the cell surface, a very important feature for many infrastructures (look up "lipids rafts" as a topic for examples).
Now, the notion of localization in biology may refer to absolute location (e.g. cell pole), or simply the relative positions of certain compounds. Such is the case for cell junctions, which need to co-localize with certain cytoplasmic compounds, belonging to the cytoskeleton. Relative localization therefore, in this case. Do understand though, that both these infrastructures and photoreceptors need to be well distributed on the cell surface, each for its own reasons (mechanical strength, and optimal photo-capture, respectively).
The example of synapses is different, as the exact site of synaptic attachement in between cells plays a role in neural messaging and its regulation. This is, therefore, a different topic, which may involve absolute positioning of infrastructures. However, at these sites, protein movement along membrane surface and ocmplex forming principles remain the same; this is an example of absolute localization.

Welcome to Bio. Can you add sources or references to allow users to background read on your answer?


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Structure of mitochondrial ribosomes
Is the ribosome found in mitochondrion and choloroplast formed of 30S and 50S subunits as in prokaryotes. I couldn't find any information on internet concerning it.
The general wikipedia page has no information about it though it says

The ribosomes found in chloroplasts and mitochondria of eukaryotes also consist of large and small subunits bound together with proteins into one 70S particle.[9] These organelles are believed to be descendants of bacteria (see Endosymbiotic theory) and, as such, their ribosomes are similar to those of bacteria.

The wording of the question suggests that it may be useful to clarify the meaning of the numbers in the designations 70S, 50S, 30S etc. These are sedimentation coefficients in Svedberg units as determined in the analytical ultracentrifuge, and are an indication of size.
All ribosomes have two subunits. The reference eubacterial ribosomes from E.coli are 70S with a large subunit of 50S and a small one of 30S. The reference eukaryotic cytoplasmic ribosomes (rat liver, say) are 80S, with large and small subunits of 60S and 40S respectively. The actually sizes (S-values) of the subunits in other eubacteria (say mycoplasma)  and different eukaryotes (say yeast) may differ, but the eubacterial ribosomes share an antibiotic sensitivity (e.g. to streptomycin, erythromycin) which differs from that of eukaryotic cytoplasmic ribosomes (e.g. to cycloheximide) and so it is often convenient to refer to 70S-type ribosomes or 80S-type ribosomes, despite the size difference.
Mitochondrial and plastid ribosomes share some of the antibiotic susceptibility of eubacterial ribosomes (e.g. sensitive to streptomycin, but not to erythromycin) and their rRNA is more closely related to the latter. So they have 70S-type ribosomes with 50S-type and 30S-type subunits. However they vary greatly in size. For example, pig mitochondrial ribosomes are smaller at 55S, with large and small subunits of 39S and 28S, respectively. In contrast, yeast mitochondrial ribosomes are larger at 74S, with large and small subunits of 54S and 37S, respectively. More important, they differ from eubacteria in their ratio of RNA to protein, unlike chloroplast ribosomes, which workers in the field have classified as bacteria-like. This is shown in the table:
 [Adapted from Supplementary Table S1 in Science (2014) vol 343, 1485–1489]
The striking thing about most mitochondrial ribosomes is, whether or not they have undergone a decrease in their rRNA, they have additional proteins with no analogues in bacterial ribosomes. Structural work on both mammalian and yeast mitochondrial large ribosomal subunits show that these additional proteins are associated with an altered exit tunnel for the growing polypeptides, which appears to be tailored to conduct the latter directly to the mitochondrial membrane.
Answers (depending on intent of question)

Yes, mitochondrial and plastid ribosomes have large and small subunits.
No, their sizes are not 50S and 30S, but vary greatly.
Yes, mitochondria and plastids have 70S-like ribosomes, rather than 80S-like ribosomes, but these have evolved considerably from their eubacterial precursors.

Sources
Some of my assertions are based on recent papers and earlier work referenced in them. Also access to them may not be free outside university libraries. Apologies for that — if I find more accessible sources I will add them later.

Mammalian mitochondrial ribosomes: Nature (2014) vol 505, pp. 515–521.
Yeast mitochondrial ribosomes: Science (2014) vol 343, 1485–1489.
Spinach Chloroplast ribosomes: Proc.Nat.Acad.Sci. (2007) vol 104, pp. 19315–19320.
Antibiotics and ribosomes (review): EMBO Reports (2001) vol 2, pp. 318–323.