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If my sunglasses provide "100% UVA/UVB Protection" why can't look directly at the sun?
Is it simply the amount of visible light entering the eye? I'm simply confused as to why experts say that sunglasses do not provide adequate protection when they are advertised as blocking 100% of the sun's harmful rays.

Sunglasses primarily restrict specific wavelengths of the electromagnetic spectrum (ultra violet, as mentioned), but neglect to fully restrict visible light. If (every day) sunglasses were designed to restrict enough visible light so that we could safely stare at the sun, then we wouldn't be able to see anything else!

The damage to your eye does not only come from UV exposure, but also from infrared (IR) radiation. Your eye contains a lens that focuses the incoming rays to a narrow point. This point would get very hot if you looked directly into the sun. This is comparable to focussing the sun on a piece of paper with a magnifying glass, it would start to burn. Also, the rods and cones in your retina are only tolerant to a certain exposure of visible light.
Source: https://eclipse.gsfc.nasa.gov/SEhelp/safety2.html

The page you provided as a source is quite extensive. Would it be possible for you to quote the portion pertaining to infrared? Thanks.

Thanks so much for the source you provided, I had a really hard time finding the information I wanted that gave specifics as to the different dangers of looking at the sun besides "Don't do it." It seems like the main problem is the visible light which is what I suspected, although even in the source it is unclear whether hen they are talking about IR whether it is truly the IR radiation or the near IR radiation (or essentially more visible light) that contributes to the issue. Regardless, thanks for your help!

Visible light too is dangerous to have concentrated into your retina.
When you shine a flashlight at yourself, where does all that  visible light go as it seemingly disappears into your body?
Heat!
It makes your molecules more ever so slightly more.
Also, a lot (but not all) of the uv light is absorbed by your cornea.
Visible light will enter your retina, and focused to a point that is REALLY DANGEROUS. The heat from the light hitting your retina will immediately denature all the proteins inside your retina cells, killing them.
This will happen no matter how much IR or UV you block.


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What's the name of this tree?
I photographed this flower on the street in Los Angeles.
It looks like a lilac, but I am not sure.

It is not lilac. which part of earth do you see this? Crepe Mrtyle perhaps - I passed by some.

This is probably a crape myrtle, a plant from the Genus Lagerstroemia.
Here is another photo for comparison:

And here another photo, showing the whole tree:

I doublechecked on the internet. You are right!

source: Stack Exchange

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

sort: votes


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Ejaculation without orgasm: is this possible to do it at will without external stimulation?
I know that ejaculation without orgasm is possible for human males with external stimulations, e.g. prostate massage.
My question is, can a human male perform full ejaculation without reaching orgasm without such external stimulation, i.e. with "ordinary" masturbation? Is this technically possible for the body?

Yes, it is possible. It is all in the brain. One can be sufficiently aroused to ejaculate without any contact.
The most obvious example of this is the case of nocturnal emission

A nocturnal emission, informally known as a wet dream, is a spontaneous orgasm during sleep that includes ejaculation for a male, or vaginal wetness or an orgasm (or both) for a female. Nocturnal emissions are most common during adolescence and early young adult years, but they may happen any time after puberty. It is possible for men to wake up during a wet dream or simply to sleep through it, but for women, some researchers have added the requirement that she should also awaken during the orgasm and perceive that the orgasm happened before it counts as a wet dream. Vaginal lubrication alone does not mean that the female had an orgasm.

Depending by what you mean by "without such external stimulation", you might want to read about premature ejaculation

Premature ejaculation (PE) occurs when a man experiences orgasm and expels semen soon after sexual activity and with minimal penile stimulation. It has also been called early ejaculation, rapid ejaculation, rapid climax, premature climax, and (historically) ejaculatio praecox. There is no uniform cut-off defining "premature", but a consensus of experts at the International Society for Sexual Medicine endorsed a definition including "ejaculation which always or nearly always occurs prior to or within about one minute".

Nocturnal emission is not what I meant actually, as it involves an orgasm. Same for premature ejaculation, which involves orgasm, that just arrives too early. I ask about full ejaculation process without orgasm at all. In slang it's called "milking" but everything I've seen (and tried) involve action done by someone else, to which I refer as "external stimulation". Hope my question is now more clear? Thanks! :)

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


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If people can survive being frozen some, why not indefinitely?
I've heard of cases and also personally met someone who survived with a full recovery after they were taken to the hospital after being found unconscious in the snow for (presumably) more than 45 minutes, and claimed their temperature dropped below 0 degrees (Celsius) after they recovered in the hospital, though obviously I can't go into their medical records and verify that temperature. What mechanism allows someone to survive being so cold for so long, particularly if there is a lack of oxygen to the brain, and if someone can survive it for that long, why not indefinitely like for cryogenics?
I'm no medical expert by any means, so it's possible it's a combination of things of course, but for references the first being that a doctor telling me first hand that it's possible, but rare for someone's pulse to stop in frigid temperatures and still recover after more than 10 minutes with a lack of oxygen referencing something about the decomposition of tissue slowing down, and then also news articles like these that I don't have any particular reason to doubt given the consistency of such a story across different venues, which also suggest something about frigid temperatures allowing people to survive injuries, oxygen deficiency, or tissue damage for a longer than normal time.
I'm not completely sure about the lack of oxygen part of the question because it kind of seems like they evaded that part of the question, but they definitely said frigid temperatures delay the decomposition of tissues in someone's body and suggested someone could survive longer due to that, and I don't know why tissue decomposition would be a problem unless someone had already lacked oxygen for a long time to make them susceptible to it.
https://news.google.com/newspapers?nid=1876&dat=19810109&id=CkosAAAAIBAJ&sjid=uc0EAAAAIBAJ&pg=6891,1583308&hl=en
https://en.wikipedia.org/wiki/Jean_Hilliard
http://www.nytimes.com/1981/01/03/us/dakota-teen-ager-recovers-after-being-frozen-stiff.html
http://abcnews.go.com/Health/hypothermia-save-boy-trapped-ice-30-minutes-heartbeat/story?id=9506900
http://www.dailymail.co.uk/news/article-3406926/Man-presumed-dead-frozen-solid-road-recovers-living-medical-miracle.html
https://en.wikipedia.org/wiki/Anna_B%C3%A5genholm
I remember the old saying "better cold and dead than warm and dead," I guess this makes sense for when you find someone unconscious.

Can you please provide a reference for the claim that people can survive with full recovery after their body temperature went below freezing point?  The record of the coldest body temperature recorded for a surviving human is held by Anna Bågenholm with a body temperature of 13.7ºC. I am voting to close as opinion-based (unless you can provide a trustful reference for your claim).

"heard of cases" - citation needed. I suspect, as @Remi.b suggests, that these are cases of people dropping to hypothermic temperatures, not dropping literally below freezing.

It's possible it's a combination of things of course, the first being that a doctor telling me first hand that it's possible for someone to drop unconscious due to frigid temperatures and still recover, and then also news articles like these https://en.wikipedia.org/wiki/Jean_Hilliard http://abcnews.go.com/Health/hypothermia-save-boy-trapped-ice-30-minutes-heartbeat/story?id=9506900 http://www.dailymail.co.uk/news/article-3406926/Man-presumed-dead-frozen-solid-road-recovers-living-medical-miracle.html

@DaneJoe Two of the articles you link actually report body temperatures at 13.7ºC (which seems to be the world record) and 32.22ºC. Some of the newspaper articles use the misleading expression "frozen solid" but do not actually report a body temperature (that I could find at least). I very much doubt any of them actually had a body temperature below 0ºC

@Remi.b Fair enough. Still, something about these reports suggests there's a possible correlation between frigid temperatures and surviving critical conditions that would otherwise be deemed impossible in warmer temperatures. In terms of chemistry you could say that frigid temperatures can also slow down the negative chemical processes that occur that would normally lead up to death or ensure death after unconsciousness, though could it also be random mutations?

For your curiosity... freezing tolerance ask for very specific adaptations. You can have a look at 1. How tolerant are ants to cold?, 2. How do insects survive the winter?, 3. wiki > Freezing tolerance in plants and 4. wiki > Insect winter ecology

@Remi.b Thanks but I'm not interested in etymology at the moment.

@DaneJoe I think your answer is kind of obvious then and not worth a question here: Cryogenics is about freezing people actually to (and below) 0C. All of the sources you have show people not frozen nearly to that extent. At those milder temperatures you have no ice crystal formation and no real freezing and a much less extreme recovery. It has nothing to do with cryogenics. You might as well ask "Why does food cook in my oven at 150 degrees C but it doesn't cook outside at 35C"

@BryanKrause I think scientists who get paid a salary to research it would disagree that it's a waste of time. This is about the specific mechanisms that allow people to survive frigid temperatures which could also easily be any pattern that might show itself as a precursor to such technology, especially the points about that frigid temperatures seem to allow people to survive longer with lower oxygen and reduce tissue decomposition. If the temperature is cold enough, then no bacteria is active either, which means no decomposition whatsoever.

The issue is that your question (People can survive for little time at freezing temperature. Why not indefinitely?) is based on a false prior that humans can survive at freezing temperature. The question is therefore opinion-based and must be closed as such. Asking What are the known mechanisms to tolerate below zero body temperature? would be an acceptable question (although arguably too broad but I am not sure).

You might be interested in protective hypothermia.

@DaneJoe The problem is that you made your question based on a premise that people survive frozen but can't survive cryogenics...except they do not survive frozen. They survive slightly colder than normal.

@Remi.b If it was opinion based I wouldn't be asking a question. I'm not an expert so I'm not going to rule out the possibility of someone surviving freezing given the evidence I presented, which is the opposite of opinion as it is the extrapolation of data to lower temperatures. These are temperatures much lower than "slightly" normal without doubt.


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how can a recessive allele become represented in a significant number of individuals in a population
Darwin believed that individuals that are poorly adapted to their environment are less likely to survive and reproduce. This means that their genes are less likely to be passed to the next generation. Given enough time, a species will gradually evolve.
-individuals in a species show a wide range of variation
this variation is because of differences in their genes
-individuals with characteristics most suited to the environment are more likely to survive and reproduce. The genes that allow these individuals to be successful are passed to their offspring.
In genetic terms, evolution is any change in the allele frequency of a population.
A recessive allele can become represented in a significant number of individuals in a population, how?

A recessive allele is one whose phenotype can be masked by a dominant allele. A recessive allele is not necessarily deleterious, and the dominant allele does not necessarily have higher fitness than the recessive allele. Fitness and dominance are often confused, but they are not the same thing.
In some scenarios, the recessive allele indeed confers a fitness benefit, and when it does, it is predicted to increase in frequency rapidly because homozygous recessive individuals have higher fitness than both homozygous dominant genotypes and heterozygotes.
A recessive allele can also persist in a population if it is deleterious in homozygotes but confers a heterozygote advantage. The most famous example of this phenomenon is in Africa, where individuals heterozygous at the sickle cell locus have a fitness advantage because they are resistant to malaria. A higher prevalence of sickle cell phenotypes occur because selection for heterozygotes maintains a high frequency of recessive alleles in the population. For more, see Templeton (1982, http://www.indiana.edu/~curtweb/L567/readings/Templeton.pdf) and Allison (1954, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2093356/).

There is also effectively no selection pressure against recessive alleles that are deleterious when they are at a low frequency: selection pressure will only occur when mating two individuals that have the recessive allele. It isn't necessary to invoke heterozygote advantage to explain that part (though in some situations, like you point out, it does contribute).

@BryanKrause Perhaps you should put that in an answer since, well, it is the answer. The fitness of a homozygous dominant individual and a heterozygote is identical by definition.

@Nathan When it comes to fitness as the phenotypic trait of interest, then the sickle cell locus does not show a simple pattern of dominance. There is overdominance (aka heterozygote advantage).

@canadianer  The fitness of a homozygous dominant individual and a heterozygote is identical by definition. Yes, if you are talking about dominance for fitness. It is not uncommon to consider some other phenotypic trait though (coat color for example)

Dominance
Dominance explains the relationship between alleles in determining the phenotype. Consider two alleles A and a. If A is dominant, then individuals AA and individuals Aa present the same dominant phenotype while individual aa present the recessive phenotype.
Selection and dominance
When you ask

A recessive allele can become represented in a significant number of individuals in a population, how?

I am not sure why it seems unlikely to you. No one said that the recessive phenotype was less fit than the dominant genotype.
If the alleles a and A are present at the same frequency in the population, then most individuals will carry the dominant phenotype. But the alleles A and a may well not be at the same frequency. Selection (as well as other evolutionary processes that I won't talk about here) will affect the frequencies of these alleles. If the dominant phenotype has a higher fitness than the recessive phenotype, then the allele A will increase in frequency. If, on the other hand, the recessive phenotype has higher fitness than the dominant phenotype, then the allele a will increase in frequency.
From allele frequency to genotype frequency
Let $p$ and $q$ be equal to the frequencies of the allele a and A, respectively, such that $p = 1-q$ is necessarily true. Under a few assumptions (see here), the frequencies of the genotypes AA, Aaand aa are $p^2$, $2pq$ and $q^2$, respectively. For more information on why this is true, you can have a look at Solving Hardy Weinberg problems.
Let's imagine a scenario where, the recessive phenotype has a higher fitness. The allele a will increase in frequency in the population until eventually reaching a frequency of $p=0.95$. At such allele frequency, $0.95^2 = 0.902$ (or 90.2%) of the population will carry the recessive phenotype.
Note that at very low frequency of the recessive allele, the recessive phenotype is very rare (as it's frequency is the square of the frequency of the allele) and there is almost no selection acting on the locus of interest. But all of that is a story for another time.

My answer below demonstrates how recessive alleles can fixate and persist in potentially large numbers of the population.
 https://biology.stackexchange.com/a/61176/9771

If a question is a duplicate it should be closed as such. If it is not but the answer can be entirely found in an other answer, it is better IMO to partially copy-paste and re-adapt the answer to the current post than just providing a link. A link only is at best a comment, not an answer.

Ordinarily I'd have partially copied as you say, but as the other thread is figure heavy, I wasnt on my computer at the time, and there are other answers which will probably be accepted, I figured an answer was valid.

Ok. Note, that figures are included as links on each post and are stored independently of the post. So, if you just copy paste the whole thing (incl. the links) you don't have to bother about figures more than about any other piece of text. There is no need to download, re-upload the figures which would indeed be a pain without a computer.

Ah yeah good point! I did think SE would reformat the link to the title of the question though. I thought it usually happened automatically but i must be missing something.

Recessive diseases are insidious because most of the time the dominant (healthy) allele masks them. Then every once in a while, someone in the village gets a wide range of chronic, unexplainable symptoms that the local shaman explains as a random curse.
While these are a no-brainer in the developed world, they are a daunting problem for primitive cultures and third-world nations where superstition is much more commonly practiced than science and no one knows what a "genome" is.
With even distribution, a quarter of the population has the disease and half of the population have 1 allele for the disease.

I only read the first sentence. 1. Dominant does not necessarily mean healthy 2. By definition the heterozygote shows the dominant phenotype. It is always true when you have a pure dominance relationship. It is not only true "most of the time".


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How to selectively filter BLAST results for an endogenous retroviral LTR to retrieve members of the same ERV family?
I'm running a local BLAST search on a HERV-K(HML2) LTR sequence in the human genome. I get thousands of hits.
I want to retrieve the hits that correspond to other HERV-K(HML2) LTR sequences only.
What alignment length/identity filters should I use on the hits to select LTRs of the same family? Insertions and deletions could easily alter the alignment lengths meaning the cutoff length for the filter I want isn't clear. I can work out what alignment length cutoffs remove what percentage of the results to identify big drops at specific cutoffs, but it hasn't been very helpful.

I don't think there is a definite answer to this problem, but here are a few things that might help you, apart from a simple length filter for the hits:

Filter for regions: since LTRs are repeats you might get multiple BLAST results from the same repeat region/locus (especially if your input sequence is smaller than said region). You probably want to keep only one hit per region
Check for a conserved (sub)sequence: hopefully your specific LTR sequence has a 'core' that needs to be present, so that it can be considered part of your familiy. You only want to keep BLAST hits that have an absolute match for this 'core'.

I don't know what your application is, but RepBase has a curated set of ERV loci in a BED file that you can use to retrieve sequence/define regions of interest et cetera.
Of course, generally speaking repetitive regions may be harder to map in terms of genomic location, and in my lab, where we regularly study ERVs in cancer, we usually map RNAseq data to Repbase sequences in a fasta file to derive total expression estimates on a per-family basis.


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Rationale behind different classification of nerve fibres
Two main types of classification of nerve fibres are numerical and Erlanger-Gasser classification, based on diameter and conduction properties.
In numerical classification group Ia and Ib both have same conduction velocity and diameter, then on what basis are they different ,is it just because they are innervating different structures, then why this criteria is not followed further?
Also in Erlanger and Gasser classification both A and B types are myelinated and C is unmyelinated, then why is B not clubbed as subgroup of A? How is B different from A(delta) even though both are myelinated and have same conduction speed?

Source :https://en.wikipedia.org/wiki/Axon

Why downvote??? Where I am going wrong?

There are a bunch of different questions here, for one thing.

If I ask them separately then the main question can't be asked.


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Do ants really find the shortest path to a food source?
There exist many computational intelligence algorithms based on the observation that ants deposit pheromones in such a way that they find the shortest path to food sources. This logic is used to optimize computer networks.
I cant really relate to that. I have seen ants take an extremely long path to food. This is not always for safety reasons either. What do biologists have to say about this?

Look on Wikipedia for "ant mill", or YouTube for "ant death spiral" and you will find they make paths that are not only sub-optimal, but are in fact invalid paths altogether.

Short answer

Do ants really find the shortest path to a food source?

No! But they can find a decent path
Longer answer
Optimization algorithms are used to search through a possibility space that is too large to explore every single possibility. Such algorithms attempt to find a good enough solution, often without necessarily knowing how 'good' the found solution is to the best possible solution. So optimization algorithms don't always find the best solution. Actually, most of the time, they do not find the best path but a good enough one in a reasonable amount of time.
Same holds true for ants. In the analogy, an ant colony is an agent based algorithm where agents leave pheromone trails. The concentration of the pheromone depends upon the length of the trail. By following the trails that smells the strongest and by regularly making small errors (so that they can keep exploring other paths), they end up with a decent solution. For more info, just google How do ants find their path?.

If we don't know how good the found solution compares to the best, then how do we know it is good enough?

@Ooker How do you judge what path to take to places? I think you'll find that you don't relate it to the "best" path (which you might not know) but to the situation instead, such as "is it okay to spend this amount of time".

Similarly, when you take your car to go to some place, the path you take is generally "good enough" and not the best. It is good enough because it  takes a reasonable time to go to destination...

@Remi.b "Such algorithms attempt to find a good enough solution usually without ever knowing how 'good' the found solution is to the best possible solution." - Optimization problems do in fact (generally) know what the true solution is, however, can't always acheive this through calculation. When implementing an optimization function, there is generally some epsilon that is defined, to where if the error of the computed solution is less than epsilon, then the optimization algorithm's solution will be accepted as "close enough".

@Remi.b If an optimization algorithm isn't aware of the true solution that it's trying to acheive, then it has no way of validating a potential solution. I will admit, there definitely are many cases where no true solution is known, however, this is much more prevalent in theoretical work, as apposed to the much more practiced, applied computational approaches.

@Charles Thanks, I brought a small modification to avoid stating that an optimization algorithm never know what the best solution is.

@Charles I don't agree. You can test the strength of a solution against other possible solutions. You don't need to know the distance of the best route possible to a location, if you work out 1,000 potential routes and then take the shortest of those

@Tom.Bowen89 If you have a collection of solutions, and you are just testing one solution against others, how can you be sure that any of those solutions are anywhere close to the output that's needed? A type of "most desired output" must be defined, otherwise you "cannot see the forest from within the trees". Which is to say, an ideal solution, or minimum error tolerance, must be defined. If not, there can be no confidence as to how accurate your algorithm is and the outputs it's producing.

@Tom.Bowen89 I will also add that in many optimization problems, they take a probabilistic approach, so multiple instances (collections of solutions that stem from different initial conditions) of the algorithm must be had. Which is to say that, each instance of the algorithm running will produce completely different solution sets. That being said, again, some kind of desired result must be defined in order to assess the accuracy of these solutions.

@Tom.Bowen89 So, to go off of your example of the shortest path.. what if the true shortest path is 10 miles, however, the best solution your algorithm produces is 50 miles? How would you be able to assess the accuracy if you don't have an idea about the true shortest path? This is important because, as stated in my most previous comment, if the best solution is still very far off from the true solution, the algorithm will need to be ran again in order to obtain different potential solutions. There must be some kind of "outside" assessment as to your algorithm's performance and accuracy.

@Tom.Bowen89 I recommend you looking into simulated annealing algorithms, as it's a common platform in computer science for introducing the dynamics of optimization and approximation algorithms. https://en.wikipedia.org/wiki/Simulated_annealing

@Charles is there a way to calculate the confidence of the accuracy of the calculated path? Correct me if I'm wrong, but isn't that in statistics the confidence of a guess can be calculated independently with the correct value?

@ooker You cannot calculate the confidence in whether you have the best path from just sampling (trying solutions and seeing which ones work) unless you can brute force the entire state space.  However, if you know something about your state space, then you can use that problem-specific information to determine how good your solution is.  For example, if you know the space is differentiable, you can use any information you might know about the maximum derivatives to create an upper/lower bound.

@Charles: "If an optimization algorithm isn't aware of the true solution that it's trying to acheive, then it has no way of validating a potential solution." - That's not true - very often in real life the criterion is "Solution must cost less than X". If a solution is found that has a cost less than X, it is "good enough", and hence valid. If it is a lot less than X, so much the better. There's no need to know the absolute best achievable value. The value of X depends on the (external) constraints of the project, not on the parameters of the optimisation problem itself.

That's exactly what I said in a previous comment, lol. Please read all comments before trying to correct someone. "When implementing an optimization function, there is generally some epsilon that is defined, to where if the error of the computed solution is less than epsilon, then the optimization algorithm's solution will be accepted as "close enough"."

@Charles: I did read that comment, and it is different from what I'm saying. I'm not saying that you define an epsilon that gives an acceptable (proportional or absolute) difference between the true optimal value and the best found - that still requires a priori knowledge of the optimal value. I'm saying instead that you define a threshold X that's independent of the optimal value - i.e. you don't actually care at all how close you are to the true optimum, just whether you find a solution that "works" in whatever context you're operating in.

@psmears How you define the heuristic isn't always consistent, and is too difficult to generalize, which is why your statements aren't valid. It's different from algorithm to algorithm, which is ultimately based on information you've already obtained going into the development of the algorithm.

Comments are not for extended discussions. Please follow this up in the chat (and eventually on some CS SE site).

@Charles: You're confusing the algorithm with the problem domain, and specifically the problem's acceptability criterion (for the ants, perhaps: does the energy in the food at the end of this path exceed the energy expended taking the path by enough to ensure survival?) with the stopping criterion/heuristic of a particular algorithm ("OK we've spent enough time & energy checking out paths, now let's get on and eat."). The former will likely influence the choice of the latter, but it's important to be aware of the distinction. Good luck with your studies, your protein project sounds cool :)

@Pimgd https://xkcd.com/85/


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Is it safe to publish a person's genome?
I recently went through the process of having my genome analyzed by 23andme, and received my raw data.
Its very interesting to me, and I want to share it with the world.
Is it safe to publish the raw genome to a public site, or are there reasons I should keep this information private?
What could someone do with the raw genome of another person? Outside of privacy concerns, is there any potential for malicious concerns from someone with this information?

This is how the clone wars begin.

Welcome to Biology.SE. Here, we only deal with Biology question, not with questions of personal safety, information security, future political decision or justice. Your question touches all these fields and it is hard to imagine what SE site would be welcoming your question. Maybe informationSecurity.SE.

I would assume that this question is off-topic on Biology.SE, but I am unsure. 2. It's not a 'raw genome'. It's information based on an extremely limited number of ascertained variable sites, referred to as SNP genotypes. 3. The fact that you ask this very question should make you not give away the data. If I were you, I would - if I wanted to tell people about it - give away the major findings (e.g. ancestry estimates) without giving away actual variant data.

@Kritner I am not willing to go into a star wars argument, but I don't think the clone wars have anything to do with making genetic data public or not :)

I believe this topic is on-topic for Biology.SE due to the specific knowledge required to understand the implications of my question. Other sites not filled with experts in the topic may mis-inform me

@AndrewDiamond The fact that it takes some knowledge in science and economy to discuss whether a country should build a new nuclear reactor does not make the discussion of the decision purely scientific or economic. It remains within the field of politics. You can ask us specific question that are purely scientific that will eventually help you take your decision though.

There is some debate, about which I'm not very familiar, over whether or not health insurance companies should have access to such information. If the data reveals a genetic disease, it could be the basis to reject coverage.

It is as safe as to publish your fingerprints. Right now, there is little that anyone can do with your genetic information but in the future, this will change.
One of the feared consequences it concerns what companies may do with that information. Can it be used against you? In some cases, it may.
For example, if you have a predisposition for a genetic disease, then an insurance company may find a way to refuse to insure you. As far I know, right now this is illegal, but you never know.


text:
In this poisson distribution in olfactory receptor (OR) pseudogenes neutral mutation rate, how is the mean used?
The 2005 paper A comparison of the human and chimpanzee olfactory receptor gene repertoires describes a poisson distribution, with a mean of 0.701
From that mean, how is the gene disruption rate of 1kb per year calculated? And, how is the age 3.86 Ma for relaxation of selective constraint calculated from (0.451/0.701)·6 Mya = 3.86 Mya?
The parts of the paper,

TL;DR How is mean = 0.701 used to calculate stuff in that paper?

Do they have a typo/miscalculation? λ=0.701 is the mean number of disruptions per shared pseudogene since the last common ancestor (6 Mya). Therefore, the neutral gene disruption rate is 0.701 / 6 Ma = 1.17·10$^{-7}$ disruptions/gene/year. This value differs from the paper by a factor of 10.

They also report the mean number of CDS disruptions per human specific pseudogenes was 0.480, but then used 0.451 in the subsequent calculation. As far as I can tell (which is not very far), this is also a typo. However, this is not my field and so it is more likely that I am wrong.

Does 1.17*10^−7 disruptions/gene/year mean roughly 1 disruption per gene over 8.547 million years?

I am having a bit of trouble understanding what 1 disruption/gene/8.547Ma would mean. Is a disruption defined as anything from a single base-pair mutation, to a whole codon or similar being replaced/lost in transcription? If so, then with around 400 shared pseudogenes, and 1 base pair mutation per gene, that sounds like a lot less then 0.1kb per year since every base pair is 2 bits. Sounds more like 800 bits per 8.5 million years, which is 0.1 kb


text:
Bird Identification
I found this bird when I came back home. I have never seen a bird like this. Also, she is not moving even if I touch her slightly.

Welcome to Biology Stack Exchange. For species ID questions, it is often helpful to include some information on where and when the animal was found: for birds, information on the location (i.e., country / state / province) and local environment (coastal, forested, urban, etc) would be especially helpful.

Also some indication of size.

It looks like a Bulbul to me.

Thid bird looks a young one to me, based on the type of feathers it has around the neck.

It's a scaly breasted munia or spotted munia (Lonchura punctulata).
A relatevely common bird in captivity, probably escaped from someone cage? (check for rings)
Here a picture from the web:

Here you find more facts about it:
http://www.hbw.com/ibc/species/scaly-breasted-munia-lonchura-punctulata


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What can a human do in a short time (10-20 years) to improve their genome?
I'm wondering what can I do to make my children receive better genes?
For example, can fitness, cold showering, studying etc. change my hereditary material and affect my children?

Reproduce with someone whom you think has "better" genes than you. There is nothing you can do for your own genes.

You could also reproduce a whole lot, and cull the children who end up with worse genes, preserving only those with the best genes. Some species, like certain birds, do this by allowing their offspring to fight for food, only feeding their stronger offspring. Of course this is easier if you have multiple offspring at once. IANAL but you might want to check whether this is legal in your jurisdiction before proceeding.

@BryanKrause: despite the ethics debate over designer humans, well-intentioned genetic engineering sounds much more humane and efficient than your solution.

@kmm Couldn't epigenetics be affected within one's life?

There is evidence that epigenetic marks can be inherited, though last I checked it was still somewhat controversial.
I recall a paper where obese parents were (epi)genetically more likely to have obese children. Therefore, if you spend your life taking care of your health, it's likely that your children may benefit from this.

No amount of lifestyle practice will change your germline (heritable) genome.
However there were 2 recent articles where researchers experimentally fixed dangerous genetic defects in embryos using CRISPR-Cas9 which could form the basis of future tech that corrects all known dangerous genetic diseases.
Bear in mind that the idea of "designer humans" (using gene-editing to make more perfect humans rather than just fixing serious hereditary problems) remains incredibly controversial and bitterly contested/debated (and illegal in most Western nations). Expect it to remain that way over the next 10 years.
If you want perfect offspring and aren't up to waiting, you might consider diving into robotics and AI instead and build a robot. That way, if it has any problems, you can always order new parts or provide tech support.


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How should you choose from the various methods of constrained ordination?
I have a bacterial OTU matrix from various sample points and times. So for each sample I have the sequence counts across the various OTUs that they were assigned to.
I also have a corresponding matrix of abiotic variables including temperature, pH and the concentrations of a range of nutrient compounds. This data was collected at the same time as the bacterial OTUs.
This is a tutorial written by the people behind the R package 'vegan', it offers three separate types of constrained ordination. I just don't understand what the differences are between these and what would suit my data-set best. There is not much advice out there at all for this sort of thing so any help would be appreciated.

You might want to check out Mike Palmer's webpage on ordination, specifically the constrained ordination section: http://ordination.okstate.edu/
The main difference between constrained ordination techniques is the distances that are preserved. Redundancy analysis (RDA) preserves Euclidean distances, so in order to use it, you need to transform your OTU table with an appropriate transformation (e.g., Hellinger), after which a Euclidean distance calculation is appropriate. It also works best identifying linear relationships between environmental variables and species responses. Canonical correspondence analysis (CCA) preserves the chi-squared distance, which tends to emphasize common taxa, and looks for unimodal responses to environmental gradients. Distance-based redundancy analysis (dbRDA) accepts any distance matrix, allowing you to use non-metric distances, and then looks for linear relationships with distances and environmental variables.
Before applying these metrics, you'll need to understand their advantages and limitations, and then you'll need to make a decision about which combination of constrained ordination techniques and distance metrics are best for answering your questions. This is something you'll need to justify yourself, based on your own question, because different approaches are better at emphasizing different aspects of your data. I strongly suggest you study a copy of Legendre and Legendre (2012) for more information about these methods.

There is also a good chapter about ordination in this book


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Can we have the action potential an AC current?
As well known brain are connected to our body by neuronal cells. it transmits and receives its data by action potential during neuronal cells. i wonder if any one can explain to me the properties of this current. can we consider this current as an AC current?

No. This question is too broad - there are many resources for you to read up on the basics of action potentials.

Indeed, an action potential really isn't a current at all, at least as an electrical engineer would understand current.  Rather, it's a wave of cell membrane depolarization.

@jamesqf an action potential is indeed no current, it is a voltage difference that changes over time. The action current is definitely a current, namely a net flow of charged ions through the cell membrane.

@AliceD: Yes, but that ion flow current is perpendicular to the axon, whereas the action potential propagates along its length.  It's also pretty fundamental to the nerve's (normal) operation that an AP propagates one way.  Changing it to an A/C current would mean redesigning everything from scratch :-)

You know those analogies of the brain being a computer and nerves being wires leading to and from it?
Those analogies are LIES.
There are no wires in the nervous system. Each neuron is a capacitor, the sodium potassium pumps create an electric charge in each neuron, and the neuron keeps that charge until the neighboring neuron (let's pretend it's not a sensory neuron) gives it a signal, in the form of an electric jolt or neurotransmitters.
That causes the neuron to equal out the charges on the inside and outside, called depolarization.
Watch this video: action potential crash course
A nerve could contain a bunch of neurons in a line next to each other, with one depolarizing the other.
This functions like a wire, in the way that it can transmit signals, but should be though of more like a domino effect, where the dominoes can stand themselves back up after the depolarization.
Electrons do not move from one end of the nerve to the other, only the "wave" of neural depolarization.
And since each neuron operates like a capacitor, it would be DC not AC current.
When I first learned about neurons, I was flabbergasted that it worked this way. I thought it was like wires, with a positive and negative end...
It couldn't be more different...

There are a few inaccuracies here. "Those analogies are LIES." - No, they are analogies. "Each neuron is a capacitor" - neurons have capacitive elements, but that doesn't make them 'capacitors.' "the sodium potassium pumps create an electric charge in each neuron" - only sort of. The Na/K pump establishes ion concentration gradients. The resting potential comes from differential permeabilities in the presence of those gradients. "Electrons do not move from one end of the nerve to the other, only the "wave" of neural depolarization." - Electrons don't move to the end of a wire either.

"A nerve could contain a bunch of neurons in a line next to each other, with one depolarizing the other." - Nerves are bundles of axons. You don't have sequences of cells in a line in nerves, just a parallel bundle of fibers. "And since each neuron operates like a capacitor, it would be DC not AC current." - Besides the problem that neurons aren't really capacitors, capacitors can be present in both AC and DC circuits, they just behave differently.

@BryanKrause electrons DO move to the end of the wire

Not really. On net they do, but you won't find an electron from one end ending up on the other end. The same is true of ions in a neuron.

dc, not ac current.

No, the same is true for DC current. The electrons do not flow down the length. On average they do, but individual electrons do not travel down the length.


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Where do birds and squirrels go to die?
This may sound like a silly question, but I have been wondering about this for a while. I live in a suburban neighborhood with a lot of trees. A lot of trees means birds and squirrels. You can hear them all day and cant leave the house without seeing them.
So why don't we see dead birds and squirrels more often? I only really see them after they have been hit by a car.
My first thought was that nature was just really efficient at cleaning them up. Flies, foxes, and maybe birds of prey get to them before I notice. But that would have to be awfully efficient. When I see a dead squirrel in the road it can take weeks for the sun and the flies to remove it entirely. A fox would have trouble getting in to my backyard (lots of trees but it is fenced in), and I rarely ever see a hawk or a falcon in my area.
My second thought was that there may not be as many birds and squirrels as I think. Yes, there are a lot of them, but maybe I am seeing them same ones over and over again? Squirrels don't really travel THAT far from their homes so maybe I just see the same 10 squirrels all of the time, which makes me overestimate their numbers.
There is a store near my house that always has hundreds of pigeons hanging out in the parking lot. They fly up to the power lines and occasionally fly down for what I assume is left over food or trash. I'm guessing they aren't there at night, but during the day you can always see them. Why wouldn't you see more dead pigeons in an area with so many pigeons? I know they have relatively long lifespans but still, some of them must die of unnatural causes.
Does anyone have any idea where they go?

A major cause of squirrel death is predation:

Survival and mortality of the Arizona gray squirrel (Sciurus arizonensis)
Causes of red squirrel (Sciurus vulgaris) mortality in England

You won't see those bodies, for obvious reasons.
Disease, starvation, and harsh weather are other major causes of death. Squirrels dying in these ways are probably likely to die in their nests or otherwise hidden places. Again, no visible bodies.
So that leaves being hit by cars as the major cause of mortality where you'd have a chance of seeing bodies. You've already noted that you do in fact see these bodies, so there's no contradiction there. I'll add that depending on where you live, roadkill can be cleaned up by scavengers more or less quickly -- in areas where buzzards, coyotes, crows, etc are common, they can be cleaned up quickly, but in more urban and/or colder areas they may last longer.

I live in Georgia about 15 miles outside of Atlanta. While it is kind of close to the city, my neighborhood is surrounded by trees. Im not sure what would prey on squirrels in my area aside from foxes and birds. Thanks for the answer, but partial credit because I still dont know where the birds go!

@bsayegh: Well, humans (at least those raised in Appalachia and suchlike places) do prey on squirrels.  Squirrel stew is quite tasty :-)  Dogs and cats probably get a number, too.

@bsayegh - birds (hawks, owls, etc) are major, major predators of squirrels.  Foxes are important but cats are probably much more so. Coyotes, opossums, weasels, snakes - all common around Atlanta. So there is no shortage of squirrel predators. As for birds -- this is why Stack Exchange recommends asking one question per post. But the general answer is the same, except that pigeons being about half the mass of squirrels scavengers are even more important.

When a squirrel dies in a nest, the other squirrels who use the nest leave the remains there. The deceased body adds insulation and structure to the nest. I read where when a drey (squirrel nest) is removed it is not uncommon to find the skeletal remains of more than one squirrel.
As for the birds, I had a bird hit my window (female cowbird) and she died instantly of a broken neck. I have a big back yard and I walked half way out into the yard and laid her to rest on the grass in the sun. Less than an hour later, she was gone. I do see hawks and other raptors over my yard and I'm sure that's what took her...either way someone enjoyed a good meal that day...

Hi Joanne. Interesting info about dead squirrels in dreys. However, we're looking for answers here that not only comment on info they've heard/read/learned about, but we actually want and require that you support your answer with something more tangible. Please find a journal article, online article, encyclopedia article, etc that supports the claims you make, and explicitly mention/link your source in your answer. In doing so, visitors will know that they can better trust the information you provide or look up your source to make the judgment about how factual claims are themselves.Thanks

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


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Identifying the Pheasants
I took a few photos at the Aviary of Hong Kong Park. The photos included some pheasants, and the below shows 4 of them. What species are they? I am not sure if 1, 2, 4 are actually the same species or not. Unfortunately on the official website http://www.lcsd.gov.hk/en/parks/hkp/birds_collection.php they are not included in the bird list, perhaps they are newly introduced.


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Is it correct to use the terms multinucleate and syncitia interchangeably?
If you see the skeletal muscle,it is having several nuclei and is said to be "multinucleate".Similarly the cardiac muscle is also having several nuclei yet it is specifically termed"syncitial".So my question is: Is there any reason behind this or are the terms interchangeable?
I am listing the sources from which the question came up in my mind:
[Source1]

Individual muscle fibers are formed during development from the fusion of several undifferentiated immature cells known as myoblasts into long, cylindrical, multi-nucleated cells. Differentiation into this state is primarily completed before birth.[Source2]
The cardiac syncytium is a network of cardiomyocytes connected to each other by intercalated discs that enable the rapid transmission of electrical impulses through the network, enabling the syncytium to act in a coordinated contraction of the myocardium.[Source3]

No, the terms multinucleate and syncytium are not synonymous in this context.  Most cardiomyocytes are not multinuclear. To be clear, syncytium is used to refer to multinuclear cells that originate from fusion of uninuclear cells, including the skeletal muscle, but that isn't what is referred to in the context of cardiac muscle.
The Wikipedia page on syncytium summarizes this nicely:

Cardiac tissue is therefore described as a functional syncytium, as opposed to the true syncytium of skeletal muscle.

The "intercalated disks" of cardiac muscle are filled with gap junctions and desmosomes. The desmosomes hold the cells together physically, while gap junctions allow ions (and small molecules) to pass directly between cells, forming "electrical synapses". This allows electrical signals to propagate between the myocytes to coordinate contraction.
Gap junctions are formed by proteins, rather than fusions of the plasma membrane, so they are relatively small. This means that not everything in the cytoplasm can pass through them, mostly just ions and some small molecules. Proteins, for example, would not pass through gap junctions. Therefore, cells that are connected via gap junctions, like cardiomyocytes, are still somewhat independent, unlike fully multinuclear cells.
There are also types of neurons, including some in the CNS, that also form gap junctions and act at least somewhat in concert in this way.

Just to add some information related to the biological terminology as a whole, not only to the cardiac muscle (which was already correctly addressed in the accepted answer):
Multinucleate and syncytium are not synonyms and cannot be used interchangeably.
As the name clearly shows, multinucleate refers to a (single) cell containing several nuclei.
However, according to the mechanism of formation of such cell, it can be classified as:

Coenocyte: when a single cell with a single nucleus performs several cell divisions without dividing the cytoplasm (cytokinesis);
Syncytium: when several uninucleate cells aggregate, forming a single multinucleate cell.

Therefore, every syncytium is a multinucleate cell, but not every multinucleate cell is a syncytium.


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Why do we perceive colour? (i.e., distinct values?)
This is a question I often asked myself, but never really found a satisfactory answer to. It may be that I always went about it from a wrong starting point because the question is induced by physics. But I think an evolutionary perspective may be the most satisfactory one to explain this.
Humans and other animals had much to gain from differentiating not only dark and light but also colors to identify edible things, or threats etc. For this purpose we developed multiple types of cone cells. But what reason is there to not perceive light as we perceive sound, in a spectrum? We could easily distinguish said things by just knowing how high or low the light frequency is (or for that matter, what the spectral 'fingerprint' of specific objects is). Why differentiate between an - albeit big - array of colors?
Or, to go one step further, why did we need an extra type of cone in the middle, the yellow-green wavelength? Is there an evolutionary reason? I'd settle for using the three more or less distinct cone sensitivities as explanation that the brain just has enough information to arbitrarily differentiate these into very discrete cognitive signals.
But evolutionarily, there has to be a purpose, so that one of the questions is the right one. The colors must bring something to the table. Or not?
Thanks in advance. I am also grateful for anyone nitpicking my arguments, because it always helps.

"But what reason is there to not perceive light as we perceive sound, in a spectrum?"

We do perceive light in a spectrum. Not just in a spectrum, but in a combination of spectral components (because we rarely in nature observe true single-wavelength light). If you are thinking about names of colors, those are just words we made up to describe colors to other people, and the range and spacing of those colors differs across language groups. We do the same for sound in the context of music: B-flat versus an E, for example.

Or, to go one step further, why did we need an extra type of cone in the middle, the yellow-green wavelength?

Colors are perceived in vision by the ratio of activity of different cones, and intensity and spectrum can be confused. If you have no "green" cones, there are big stretches of wavelengths that only activate one of the other two cones. In that situation, there is no way to discriminate between intensity and color.
If, on the other hand, you are wondering about transduction, it's because sound and light have different physical properties. The cochlea effectively "maps" sounds onto a physical arrangements of hair cells. You could do something similar with a prism, but you would lose spatial acuity (effectively, you would need a whole spectrum analyzer for the receptive field of each photoreceptor: your retina would have to be absolutely massive). Instead, color vision works by differential chemical sensitivity to different light wavelengths.
Your question doesn't seem to be much about evolution, besides the title, so I left off that part.

Thank you, the prism idea makes perfect sense! Eyes are very much made for spatial resolution and then there is a trade-off there. But I don't buy what you said about intensity vs. frequency perception: If the brain had no way to differentiate, wouldn't that be the case for three cones too? Mathematically, I can extrapolate from two received signals and 'map' an intensity curve over color values 'given' by my reception, to adjust for the 'blind' spot. The blue and red cone even overlap in their spectral range, if I'm not mistaken, so in principle there is no problem there, right?


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Found this bug in my apartment in New York. Does anyone know what it is?

It was around 2-4 mm in length.

It's probably just the second instar (nymph) of a cockroach (Periplaneta americana).
Compare with this image of the instars:

Source: http://entnemdept.ufl.edu/creatures/urban/roaches/american_cockroach.htm

Yikes! Thanks for the picture though, it looks like what I found.


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What biotechnology can be used to treat lazy eye, and possibly cure lazy eye?
I tried very hard researching and finding the root cause of amblyopia. It is mainly because of imbalance in eye muscle. But, there are a lot more complicated causes of this disease. Thus, I need some help in finding a biotechnology for treating lazy eye.

I wish anyone could provide me a little clue.

Is it Graves disease cause by a thyroid problem ?

That's an extremely well documented subject on the net. there are even pages by doctors about it.

In order to treat amblyopia you first have to treat the initial problem with the eyes that caused it, which is a medical issue and probably not what you are asking anyway. However, as wikipedia states, "after the underlying cause is fixed, vision is not restored right away, as the mechanism also involves the brain."
As a rule of thumb anything related to brain functions (in humans) is so complex that we don't really have the (bio)technology to just cure it. Sure, their are some advancements in a few areas, but especially if you want biotechnology to do this, you'll probably have to wait at least 10+ years for a medically save and readily usable method.


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Is it possible to have life that feeds on thermal energy
On earth, as far a we know, there are two main ways that bacteria gain energy.
First, there is Photosynthesis, the transition of light into chemical based energies such as ATP.
Second, there are chemical processes in which the cell breaks down a variety of molecules down to gain energy from the reactions. A example of this is Chemosynthesis.
Is it possible for their to be a bacteria or type of organism that gains energy from thermal energy?
For example, there could be a bacteria that lives in a volcanic area, somewhere hot enough that there is a excess of thermal energy. Would there be a way for such a cell to use this thermal energy in much the same way that some cells use Sunlight in Photosynthesis?

It's a good question! You might take a look at how systems like heat pumps, thermoelectric generators, coal/gas/nuclear power plants or even cars get energy out of high temperature. They all have a hot end and a cold end, and extract work from the movement of heat from one end to the other. If you are in a uniform temperature, it's hard (impossible) to use it effectively.

It is theoretically possible but no known organisms does it. The problem is you need a pretty strong and persistent temprature gradient to generate usable work out of it, and those are not that common in nature.

Heat is probably the most inconvenient pain-in-the-behind energy source to use (as bacteria). Main reason is that you have to harvest it as it moves across a membrane/gate, and then the cell or whatever has to be built to handle the temperature on the other side.
Even worse: as the bacteria harvest heat, they will end up the same internal temperature as their food source, requiring them to move somewhere and cool off (infeasible for bacteria).
A somewhat viable theoretical example: highly mobile partially amphibious reptile that lives in a beach-type environment in tropical climates. It would harvest heat while basking on the sand and jump in the water to cool off. Energy harvesting occurs as heat moves across the lizard's hide outside to inside. The harvesting is 1-way: cooling off doesn't cost energy.


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why do chaperones bring protein into mitochondria? why would mitochondria need protein?
Sounds trivial? Please help to sort out. I saw this picture while looking at dehydration reactions and cell revision.

And proceeded to the reference web page.

Protein Folding and Processing in the ER: Various changes occur to proteins in the ER.
  Chaperones and Folding: Polypeptides must assume the correct folding pattern in order to function properly. The correct folding of a protein is mediated by chaperones (they also are proteins--chaperones are abundant in the ER lumen). A completed polypeptide will assume the correct folding pattern spontaneously, however before translation is complete, it could assume an incorrect formation or it could aggregate with other partially made polypeptides. To prevent this, chaperones in the ER (and cytosol) bind to the nascent polypeptide and keep it from interacting with anything until the polypeptide is completely synthesized. (Chaperones bind to polypeptides destined for mitochondria then release them as they pass through the mitochondrial membranes. Chaperones on the inside of mitochondria bind until these polypeptides have completely entered.)

With regards to protein synthesis and folding, this kind of info is not in my textbook. Not in couple of the online open textbooks either. I even search for where do protein fold? to find out if there was a relationship. It doesn't say protein fold in mitochondria and turns out it's a question most scientist are looking for answers.
For whatever protein synthesis I have learnt so far, there was no mentioning of protein strands going into mitochondria but mitochondria as a power houses. What's going on here?
Why would a protein go into a mitochondria? How does it exit and where to?

Almost everything the cell does and every organelle involved proteins, often in the form of enzymes. Mitochondria are no exception.The list of everything proteins do in mitochondria would be absurdly long or incredibly vague.

As you probably know, mitochondria (together with chloroplasts) are a very interesting organelle: they are a result of an endosymbiotc relationship that took place more than 1 billion years ago.
And, because of that, mitochondria have their own (circular, as a prokaryote) DNA. And here comes the common misconception: a lot of students think that mitochondria (and chloroplasts as well), because they have their own DNA, can synthesise all proteins they have (the most famous ones are the enzymes of Krebs cycle and Respiratory chain). But that's not correct.
What happened is that, generation after generation, along a very big period of time, mitochondrial genes were, little by little, transferred to the host's nucleus. According to Nature (2017):

During the course of mitochondrial genesis, many genes were transferred from the genome of the mitochondrial endosymbiont to the genome of the host.

Thus, today, a human mitochondria has only 37 genes:

From those 37 genes, only 13 code for respiratory proteins. Therefore, those mitochondrial genes are responsible for only a minor fraction of the proteins present in a human mitochondrion. So, where do the other proteins come from?
They come from the nucleus, encoded in the nuclear DNA. Those proteins are synthesised in the cytosol and, using peptide signals, are transferred to the mitochondria. According to Dudek, Rehling and van der Laan (2013):

Most mitochondrial proteins are encoded in the nucleus. They are synthesized as precursor forms in the cytosol and must be imported into mitochondria with the help of different protein translocases.

According to the Human Protein Atlas, 1070 proteins have been detected in the human mitochondria. Thus, since 13 of them are from mitochondrial origin, we conclude that at least 98.7% of the mitochondrial proteins are imported from the cytosol.
Sources:

Nature.com. (2017). Origin of Mitochondria | Learn Science at Scitable. [online] Available at: https://www.nature.com/scitable/topicpage/the-origin-of-mitochondria-14232356 [Accessed 5 Aug. 2017].
Dudek, J., Rehling, P. and van der Laan, M. (2013). Mitochondrial protein import: Common principles and physiological networks. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 1833(2), pp.274-285.
Proteinatlas.org. (2017). Search: subcell_location:Mitochondria - The Human Protein Atlas. [online] Available at: http://www.proteinatlas.org/search/subcell_location:Mitochondria [Accessed 5 Aug. 2017].


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Kitchen sponge microbiomes; management versus replacement versus "don't use sponges"?
I have unfortunately just skimmed through the recent open access paper Microbiome analysis and confocal microscopy of used kitchen sponges reveal massive colonization by Acinetobacter, Moraxella and Chryseobacterium species (M. Cardinale et al. Scientific Reports 7, Article number: 5791 (2017) doi:10.1038/s41598-017-06055-9)
It reports an extensive analysis of a group of kitchen sponge specimines. From the abstract:

Two of the ten dominant OTUs, closely related to the RG2-species Chryseobacterium hominis and Moraxella osloensis, showed significantly greater proportions in regularly sanitized sponges, thereby questioning such sanitation methods in a long term perspective. FISH–CLSM showed an ubiquitous distribution of bacteria within the sponge tissue, concentrating in internal cavities and on sponge surfaces, where biofilm–like structures occurred. Image analysis showed local densities of up to 5.4 * 1010 cells per cm3, and confirmed the dominance of Gammaproteobacteria. Our study stresses and visualizes the role of kitchen sponges as microbiological hot spots in the BE, with the capability to collect and spread bacteria with a probable pathogenic potential. (emphasis added)

A quick take-home message from the paper is that typical efforts to try to re-sanitize used sponges may only shift the sponges bacterial population toward a more potentially pathogenic population, and that it is probably a better idea to simply dispose of the sponge perhaps weekly and get a fresh one instead of microwaving it.
There's a nice write-up in the NYTimes science section, Cleaning a Dirty Sponge Only Helps Its Worst Bacteria, Study Says:

Stop. Drop the sponge and step away from the microwave.
That squishy cleaning apparatus is a microscopic universe, teeming with countless bacteria. Some people may think that microwaving a sponge kills its tiny residents, but they are only partly right. It may nuke the weak ones, but the strongest, smelliest and potentially pathogenic bacteria will survive.
Then, they will reproduce and occupy the vacant real estate of the dead. And your sponge will just be stinkier and nastier and you may come to regret having not just tossed it, suggests a study published last month in Scientific Reports.

Personally I've always hated the whole concept of kitchen sponges and now feel vindicated. Isn't something that can trap biomatter (bacteria, food particles) and keep it moist for extended periods of time the antithesis of what you would want to clean your dishes with?
Question: Aren't sponges simply a bad idea for washing dishes in the first place?
I'm not looking for opinion, rather I'm asking about policy and practice. Since what we do in the privacy of our own kitchen sink is our own, I'd like to ask if kitchen sponges are generally approved for use in restaurants or institutional food preparation settings? Do they have sterilization protocols? Does this paper speak to those?

Background:

above: "(A) Kitchen sponges, due to their porous nature (evident under the binocular; (B)) and water-soaking capacity, represent ideal incubators for microorganisms. Scale bar (B): 1 mm. (C) Pie charts showing the taxonomic composition of the bacterial kitchen sponge microbiome, as delivered by pyrosequencing of 16S rRNA gene libraries of 28 sponge samples (top and bottom samples of 14 sponges, respectively). For better readability, only the 20 most abundant orders and families are listed." From here.

above: "Neighbor-joining phylogenetic tree of the ten most abundant OTUs in the analyzed kitchen sponges, as retrieved by pyrosequencing of 16S rRNA gene amplicon libraries. The relative abundance (percentage of the total sequence dataset) and the detection frequency (number of sponges where they were detected) are given in parenthesis after the OTU number. The most similar reference sequences retrieved by BLAST and EzTaxon alignment (type strains only) were included in the tree, followed by the corresponding accession numbers. Red circles indicate risk group 2 organisms, according to the German Technical Rule for Biological Agents No. 466 (TRBA 46631). Numbers at the nodes indicate percentage values of 1000 bootstrap re–samplings (only percentages ≥ 50 are shown). Scale bar represents substitution rate per nucleotide position." From here.

I vote to close. This isn't a question but a review.

@David the section at the end with the sentences that end in question marks would be the question, as would the title (also has a question mark). How can you say this is not a question. I will add Question: to the question, in bold, to help you find the sentences that are ending in question marks (besides the title). There is nothing wrong with summarizing a small part of a recent paper as background to a question. It happens all the time. There is a big difference between a summary and a review, and this is not a review in any way. Your stated reasons for closing are not in line with SE.

@David you could also consider making some positive recommendations how to further improve the question, rather than reaching for the "insta-close" button. Public health and sanitary procedures are certainly on-topic here. If you'd like to see some improvement in the question, why not take a moment and explain what you'd recommend?

@uhoh - I don't think most of us can answer what restaurants do or don't do. There are probably not a lot of health inspectors on the site. As such, your major questions are probably as easy for you to google as for us. Norovirus is the most likely agent to cause illness from a restaurant; that's a virus, not a bacteria. Salmonella is high, as is listeria, campylobacter and e. coli. Other fecal-to-oral transmissions are harmful. If those aren't grown in the sponge, then you have a cruddy but not dangerous sponge.

Putting things into perspective (again, not a health inspector), you're less likely to get sick from food if employees wash their hands well after relieving themselves, if the public isn't allowed to touch/serve themselves the food (those tongs!), and the kitchen is kept clean.

@anongoodnurse thanks, but I'm asking about the nature of sponges, and if it's a good idea to use them to wash dishes and I'd like to stay focused on that. Wouldn't a non-porous mesh or scrubber be better than something that provides an ideal medium for growth? The same way that reusable wooden kitchen implements are discouraged or in some cases against code compared to plastic/teflon/metal.

@anongoodnurse I'm not interested in what "most of us" can answer. It would not make sense to hold back on question because "most of us" can't answer them, would it? In fact wouldn't "I don't think most of us can answer..." be equally valid on perhaps half of all the questions in any SE site, and particularly on the good and/or challenging questions? How is saying that helpful in this case?

Your question as stated seems to be about kitchen hygiene and not biology. Good questions in this area may or may not be appropriate on SE Health. 2. However, as posed "Aren't...a bad idea", the negation presupposes the answer "yes" and the word "idea" invites subjective discussion rather than fact. As such this falls into categories described in questions to avoid asking. So if you do post on Health, try to ask a precise question in a neutral way, e.g. "Is there any evidence that kitchen sponges are a source of disease?"

@David OK thanks! That's very helpful! Now that you've initiated the close process, I'm not sure if it makes sense to revise the question now, or wait until the whole thing runs its course. I'm probably a bit unusual in that I try to babysit my question and respond to helpful suggestions in real time to avoid closing, but once it's started it's often like trying to stop a train. Plus it's getting a bit late here for me to do some "inspired" rewriting, so maybe letting it run its course might be the best way to proceed.

I'm voting to close this question as off-topic because it is about healthy policy and not biology.

If your question is, indeed,

I'm asking about the nature of sponges, and if it's a good idea to use them to wash dishes and I'd like to stay focused on that.

I can answer that.
I like the sponge+mesh scrubber for washing dishes (not countertops or other) because the sponge conforms to the shape of things and reaches into crevices (with dishsoap and water) that I normally can't reach without more effort, and the mesh, well, scrubs. I don't care how grungy it gets; I rinse it out till it looks clean, throw it in the dishwasher when I run a load, which isn't often, and reuse until it's falling apart. Is it an ideal home for bacteria? Yep. You may think this is a red herring, but so is your toothbrush. Yet no one tells you to use a new toothbrush every week.
What is important is not what's in the sponge (or the toothbrush), but 1) how much of that bacteria stays deposited on the dishes washed with a sponge and rinsed with clean water, and 2) are any of the said bacteria dangerous to one's health?
Unfortunately, while the microbiome of the sponge was analyzed, the more important questions were not. There isn't a study yet that answers that aspect. So, until there is, I'll keep using my sponge without fear, as I do my toothbrush.
For example, the most common organisms grown from sponges were from the class Gammaproteobacteria. The important question is, is Gammaproteobacteria a pathogen?
What has been shown is that lack of Gammaproteobacteria in one's environment predisposes an individual to asthma and allergies. Also worth mentioning is that the mouth has a very high density microbiome itself,

The oral microbiome is comprised of over 600 prevalent taxa at the species level, with distinct subsets predominating at different habitats.

The oral microbiome is largely still unknown, but includes some of the species found in the kitchen sponge (chicken or egg situation?) Or is it that the prevalence of these organisms in our environment (including our hands) seeds the sponge and the mouth?

While the similarities suggest a kitchen sponge core-microbiome, the more variable fractions might differ from region to region. Clearly, more data from different regions are needed to support this hypothesis, but apparently bacteria affiliated with the Moraxellaceae seem “typical” for kitchen sponges. Interestingly, Moraxellaceae have been consistently detected on sink surfaces, faucets, refrigerator doors and stoves30, i.e. surfaces that might be regularly cleaned with kitchen sponges, suggesting them as source for these surface contaminations. However, Moraxellaceae also represent typical human skin bacteria, suggesting also other sources for the contamination of kitchen surfaces. In turn, human skin (hands) might represent a source for the contamination of the sponges with Moraxellceae during use. Recently it has been shown that in particular Moraxellaceae get significantly enriched on cotton laundry during a domestic washing process.

Should we stop laundering out cotton clothing?
As a physician (a shameless appeal to authority here), I'll worry when studies show that dishes washed with a sponge are colonized by harmful bacteria. So I'll continue to use my sponge to wash dishes partly because I like studies to be meaningful to health and disease, partly because I like my dishwashing sponge, and partly because whatever I use to wash my dishes (except my bare hands, which I deem insufficient to the task) will become a breeding ground for all manner of bacteria.
For all other kitchen cleanup, I use a cloth, which is doubtlessly packed with bacteria as well, but I can fool myself into thinking it is cleaner because I launder them every couple of days, or immediately after a relatively dirtier task.

Thank you for the wonderful answer! I appreciate you taking the time to put these results into perspective. There are all kinds of bacteria in all kinds of places, and if one looks, one will find them, so I was wondering if this article which touts the "massive colonization" of kitchen sponges in the title was scaring me more than it should. Indeed it's the rinsed dishes that matter, and I'm only guessing, but a few individuals of any of these bacteria on a plate is just not something to be afraid of in the grand scheme of things.

Why do you think it appropriate to answer a question on washing dishes on this list?

@David - It's about microbiomes. Where should I answer said question when it was asked here? Or are you trying to tell me you don't approve of an answer to a question you think deserves no answer? If so, that's your problem, not mine. I'm just obviously much nicer than you are.

I'm sure you are. But sometimes being nice isn't nice.

@David - I think that would make a good meta question.

I want to ask in Biology SE about the level of soapiness necessary to prevent this from happening... but I keep remembering your answer here and hesitating. I did ask Can some bacteria eat soap molecules in soapy water rather than get killed by it? How do they hang on to their surface lipids? Evolutionary advantage? and feel there is more answering possible there.

Hey, @uhoh! Yeah, I agree that the soapiness question would probably not be well received. I don't think soapiness is helpful for health reasons; soapiness addresses grease, which isn't as big a hit with bacteria as watery food particles. So, I think increased soapiness will help get rid of grease on dishes, but not bacteria. It also means more water wasting (it takes more water to rinse) and is much harder on your skin (breaks down protective skin lipids more.) Does this help?

@uhoh - I just realized I didn't address the effect of soap on bacterial cell walls. Sorry! I'd have to research that a bit to answer authoritatively. Again, sorry.

@anongoodnurse thanks for your help! I've read a little bit about alcohol on some kinds of viruses but soap vs bacteria seems like a much more complicated scenario.

@uhoh - Oh, yes, much more complicated!

Buy a jug of hydrogen peroxide. A nice big one. Rinse the sponge with the peroxide before use and then wait 5 minutes while the bacteria bleach out and die.
THEN stick it in boiling water to kill any that are left, if you REALLY hate germs. (Although the peroxide should do the job on its own).
Science behind this:
Hydrogen peroxide is a free radical/oxidizer. It desperately wants to oxidize something, and anything will do. It will oxidize the cell wall, weakening it, it will oxidize the phospholipid bilayer of the bacteria, which will pop the microbe, and even if the microbe has an unbreakable will to live, and can somehow stay intact up to this point, it will destroy the DNA and RNA inside. Seriously. If you actually want to see this happen, drop a piece of raw chicken into peroxide and see what happens.

Why the crap was this downvoted? It's a good solution. Looks like there's an anti-sanitizer propaganda/fake news/witch-hunt movement going around and downvoting everyone who suggest sanitizers and similar, spinning their own unproven opinion while putting the burden on proof on people who actually posted a constructive solution. Upvoted in opposition against #FakeDownvotes!

Lol that's funny

@user1258361 ps, I think your comment if funny. but... what IS anti-sanitizer propaganda? did you make that word up?

The best solution is to keep the bacteria in an incredibly hostile environment to prevent bacterial growth in the first place rather than letting the sponges rot and re-sanitizing them after the fact. Additionally, keep unused sponges in a container of aqueous fluid - bacteria grow best in moist/slightly damp conditions rather than a pond.
If you're going to use sponges in the kitchen, put an open plastic container next to the sink containing dilute benzalkonium chloride or cetylpyridinium chloride (quaternary ammonium compounds), and perhaps some extra swimming pool grade chlorine. Soak the sponge in the container when it isn't being actively used. That should largely prevent bacteria and mold from growing.

Dilute benzalkonium chloride (.07% to .11%) is used as a suitable alternative to alcohol-based sanitizers and generally considered safe (although you obviously will have problems if you get it in the eyes or accidentally drink large amounts of it - then again the same is true for regular dishwashing soap). Dilute cetylpyridinium chloride is readily available as antibacterial mouthwash. What I posted works, yet I get downvoted despite neither of you proving that it doesn't work. Dishonest and crooked downvotes with a hidden anti-sanitizer agenda. #FakeDownvotes!


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Do micro-organisms survive and live normally in a zero-g environment?
Have there been any experiments in space regarding micro-organism behavior? Are they able to move around in a drop of water like they do on Earth? Are they able to eat and reproduce normally?
Edit: by zero-g, I mean an environment where you feel zero acceleration. Orbiting the Earth would be this since you're constantly in free fall. A rotating environment is not zero-g as the things inside will feel a "centrifugal" force pushing them into the wall (though it's actually a centripetal acceleration coming up against your intertia).

Several experiments with microorganisms have been conducted in the ISS (International Space Station), and the results were published in peer-reviewed journals, like this one for instance:
A Molecular Genetic Basis Explaining Altered Bacterial Behavior in Space
However, two things have to be clarified:
First, the environment at ISS is not really a zero-g environment. Actually, since the ISS is orbiting at only 400 km from the Earth surface, the gravity in the ship is almost the same of what it is here at the planet surface (89%, to be more precise). What happens is that the ISS is constantly falling, and that endless fall simulates a zero-gravity environment.
For this reason, one doesn't need to go to space to conduct micro-gravity experiments: they can be conducted here, on Earth's surface, in rotating containers (Tirumalai et al., 2017). For instance, this is a device to simulate micro gravity on ground, in a common lab:

Second: most of the experiences conducted on ISS focus on bacteria (and not on other groups of microorganisms, like protozoans and algae), and more specifically on their pathogenicity. The way your question was worded ("Are they able to move around in a drop of water like they do on Earth? Are they able to eat and reproduce normally?") make it seems that you are interested in things like locomotion and phagocytosis in unicellular eukaryotes, but that's not their main concern. Their main concern is that bacteria have different selective pressures in space, modifying their gene expression, and such "new" strains could be potentially dangerous for the crew.
According to Tirumalai (2017):

Microorganisms impact spaceflight in a variety of ways. They play a positive role in biological systems, such as waste water treatment but can be problematic through buildups of biofilms that can affect advanced life support. Of special concern is the possibility that during extended missions, the microgravity environment will provide positive selection for undesirable genomic changes. Such changes could affect microbial antibiotic sensitivity and possibly pathogenicity. (emphases mine)

And according to NASA (2017):

scientists have observed that in space, some strains of bacteria appear to exhibit enhanced growth and increased virulence (ability to cause disease).

Therefore, experiments like AES-1 (for "Antibiotic Effectiveness in Space-1") were conducted to compare gene expression from a non-pathogenic strain of bacteria (in that case, Escherichia coli) growing in micro gravity with the same bacteria growing on the ground.

NASA Astronaut Rick Mastracchio using a crank to activate a group activation pack (GAP) onboard the ISS for the AES-1 experiment. (source: NASA,
 2017)
The findings so far show that bacteria growing in micro gravity have less availability of nutrients. Still according to NASA (2017):

On Earth, the movement of bacterial cells through their media is influenced by the physical properties of the medium, including gravity-driven forces like buoyancy and sedimentation, as well as other forces, such as the viscosity of the medium. As the cells move, they interact with fresh media and absorb molecules of nutrients. The cells also excrete waste products that may sediment down, float up, or trail behind the cells if they move, while simultaneously diffusing away. However, in microgravity, these gravity-driven forces are absent, and ALTERED EXTRACELLULAR ENVIRONMENT MODEL the transportation of nutrients to cells and waste products away from cells are limited to diffusion-only transport. The altered extracellular environment model hypothesizes that the resulting reduction in the movement of molecules leads to less interaction of the cells with fresh media and thus reduced availability of nutrient molecules for absorption.

Analysis of those bacteria showed that they changed their gene expression. The genes over-expressed were mainly associated with:

Low glucose environment
Acidic environment

Also, the experiment showed that such bacteria required a higher concentration of antibiotics to be killed, probably because there is a reduced concentration of antibiotics around the cells.
To finish, a curious device is the "test tube" they use in micro gravity. In space you cannot simply manipulate test tubes like we do here, at 1g. It has to be a special device:

For the AES-1 experiment, the research team prepared 128 bacterial culture samples to send to the ISS National Lab. The samples were each contained in a fluid processing apparatus (FPA), a test tube specially designed by BioServe Space Technologies for use in microgravity.

This is it:

Sources:

Zea, L., Prasad, N., Levy, S., Stodieck, L., Jones, A., Shrestha, S. and Klaus, D. (2016). A Molecular Genetic Basis Explaining Altered Bacterial Behavior in Space. PLOS ONE, 11(11), p.e0164359.
Tirumalai, M., Karouia, F., Tran, Q., Stepanov, V., Bruce, R., Ott, C., Pierson, D. and Fox, G. (2017). The adaptation of Escherichia coli cells grown in simulated microgravity for an extended period is both phenotypic and genomic. npj Microgravity, 3(1). [online] Available at: https://www.nature.com/articles/s41526-017-0020-1
NASA, (2017). [online] Available at: https://www.nasa.gov/sites/default/files/atoms/files/upward_magazine_vol2_issue1.pdf [Accessed 5 Aug. 2017].

In Tirumalai  et al The adaptation of Escherichia coli cells grown in simulated microgravity... the operative term is simulated microgravity which makes a clear distinction from the microgravity environment on the ISS. They are not the same and the article takes measures to make this clear. "..thus, simulated microgravity offers a cheaper prototype analog of space conditions. Whether the results seen here reflect peculiarities of the HARV as a model system or an actual adaptation to microgravity is uncertain and would be best resolved by extended studies on the International Space Station"

There is no physical analogy between the rotating drum in their experiment which "scrambles" the direction of gravity, and the orbital motion of the ISS above the earth, which creates a non-inertial laboratory frame which accelerates it in such a way as to continuously cancel gravitational acceleration to first order. The non-zero higher order terms are part of the genesis of micro- in microgravity.

@uhoh Yes that's what I thought too. A spinning container makes centrifugal forces, so the things inside feel a force pushing them into the wall. In orbit, you do not feel a force pushing you in any direction. That's what zero-g means, your felt acceleration is zero. But it is a poorly worded term because it could be interpreted as zero gravity, as in no gravity, which is clearly not the case since you are in orbit just like the Moon.

make it seems that you are interested in things like locomotion and phagocytosis in unicellular eukaryotes, but that's not their main concern. That's too bad that they're only interested in gene expression. Actually I'm interested in any one-celled organism whether it has a nucleus or not. Virii, bacteria, amoeba, anything. But it seems if they can at least reproduce for gene expression experiments, they can eat. I wonder if they can move to the food source, though, or have to be luckily near it at the start.

Sometimes they can even survive better in zero gravity than in Earth gravity! See Phys.org's Researchers discover bacteria thrive in zero-gravity low nutrient environment.

A team of researchers at Rensselaer Polytechnic Institute, in New York, working with Lockheed-Martin Ames Research Center has found that one strain of a common type of bacteria thrives aboard space vehicles, even when faced with minimal nutrients. In their paper published in BMC Microbiology, the researchers describe an experiment they conducted aboard NASA Shuttle Atlantis that showed that Pseudomonas aeruginosa, a very common type of bacteria, grows more dense cultures when in space than it does on Earth when available nutrients are restricted.


text:
Can a human increase cold resistance through some practice?

Can cold showers, moderate underdressing in cold weather increase your cold resistance?
What is responsible for cold tolerance? It's physiology/psychology or it's genetic thing?

By increasing cold resistance I mean feeling more comfortable/survive in low temperature environment comparing to state before practice(cold showers, underdressing, etc).

Purely my own experience, but certainly.  Just spend time in a cold (or hot) environment (without the frequent changes induced by central heating or A/C) and your body will adapt.

A tropical person is much worse adapted to cold by habituation. they did measurements of people in cold baths and tropical people fared worse. Some chinese schools send their children to play in shorts in the snow to make them more resistant. people who endure very cold conditions are able to adapt to them very well, some people who live in the extreme north can jog an hour bare foot in cold conditions and not get frostbite. So, yes they can increase by habituation.

comprehensible: See the Canadian temperature scale https://www.backyardchickens.com/threads/official-canadian-temperature-conversion-chart-joke.35915/

The advanced Tibetan Buddhist meditational practice known as g Tum-mo (heat) yoga allows control of aspects of body temperature.
Physiological measurements on practitioners are described in the paper Benson et al. (1982) Body temperature changes during the practice of g Tum-mo yoga. Nature 295: 234-236

Since meditative practices are associated with changes that are consistent with decreased activity of the sympathetic nervous system it is conceivable that measurable body temperature changes accompany advanced meditative states. With the help of H.H. the Dalai Lama, we have investigated such a possibility on three practitioners of the advanced Tibetan Buddhist meditational practice known as g Tum-mo (heat) yoga living in Upper Dharamsala, India. We report here that in a study performed there in February 1981, we found that these subjects exhibited the capacity to increase the temperature of their fingers and toes by as much as 8.3 °C.

In this paper the authors report measurements made on three subjects. The Figure shown below is the data for the third of these. The authors describe these results as follows:

His finger temperature rose 3.15 °C while toe temperature  increased 8.3 °C (Fig. lc). There were no other large changes in skin temperature. Rectal temperature was unchanged…The most likely mechanism to account for the increase in finger and toe temperature is vasodilation.

If you wish to try this for yourself, here is a description of the practice as quoted in the paper:

g Tum-mo yoga is a form of meditation which allegedly allows its practitioners to alter body temperature. Previously, only subjective descriptions of this phenomenon existed: "The neophytes sit on the ground, cross-legged and naked. Sheets are dipped in icy water, each man wraps himself in one of them and must dry it on his body. As soon as the sheet has become dry, it is again dipped in the water and placed on the novice's body to be dried as before. The operation goes on in that way until daybreak. Then he who has dried the largest number of sheets is declared the winner of the competition".


text:
Is there any difference between Tetanus and Tetany?
Both the tetanus and tetany are related to muscle spasms and the latter is due to lack of calcium but is any collaboration between them regarding Clostridium tetani. also?

Did you do any research on this, and can you share what you found?

@anongoodnurse I want to know if this statement is correct if we say the other way: Tetany is rapid spasm in muscles caused by Clostridium tetani?

Again, did you do any research on this, and can you share what you found?

@anongoodnurse I am asking, not saying !


text:
Can a mother somehow positively affect fetus during pregnancy?
My mother keeps telling me that I like to study and have a predisposition to it because she was a student when she was pregnant. I highly doubt it, because I can't find any logic in these words.
I heard that a lot of mothers try to do something to positively affect their fetuses. For example:

Listening to classical music.
Learning something.
Singing or playing musical instruments.

Can these activities somehow affect a child or is it just a myth?

why the downvote??

You should reduce your question to a single clearly defined question like does listening while to classical music in the womb increase the kid's IQ? Your three questions are too broad. The title question is particularly broad and I suppose the fact that the mother give nutrients to the foetus would be enough to answer yes. I am voting to close as too broad (I was not the one down voting but I can understand the down vote).

I don't think the question is about any specific activity; those are just examples. The question is can the behaviour of the mother during pregnancy have an effect on the fetus.

@canadianer Like smoking, drinking alcohol, not feeding yourself correctly, etc.... Shall we make a short list like that and post it as an answer?

@Remi.b "Can a mother somehow positively affect fetus during pregnancy?"

@Remi.b No, you should not list everything. Especially not things that are obviously not in the spirit of the question.

@Artmal Not smoking is a way to positively affect the foetus.

@canadianer It is hard to tell what is in the spirit of the question without a accurate definition. I still think the quesiton is too broad and the OP should narrow down to a specific behaviour of interest. It is of course my personal opinion. If other users feel like it is answerable, they can give it a shot.


text:
What type of Bacteria?
I did some tests to a bacteria colony and I observed the following:
First of all let's start from the shape and after that we move on to the chemical tests that I did to them:

Form: Circular
Colour: Yellow-to-white (something like pale yellow)
Margin: Entire
Elevation: Flat

Chemical results:

Gram: Negative
Catalase: Positive
Oxidase: Positive

After some research to the databases, I figured out that it might be:
If it belongs to the family of Pseudomonas:

Chryseomonas luteola OR Pseudomonas luteola group Ve-1 with a chance of 48.21%
Flavimonas oryzihabitans group Ve-2 with a chance of 48.21%
Xanthomonas maltophilia OR Pseudomonas-like spp, with a extremely low possibility of 1.34%.

So, my question has 3 parts:

Can someone please tell me if my hypothesis is right?
And if it is possible which bacteria from the above is the correct?
If you manage to find the correct type of bacteria can someone tell me the ideal enviroment to study them better? (agar plates, temperature, time needed, etc.) Thank you for all the efforts made!

Important notice: I have used a blood agar plate with a concentration of 5–10%. It contains as far I know, mammalian blood maybe from sheep or horse. I forgot to check the temperature, but I don't think that it is very important.

Sounds a bit like homework/course work to me...
I don't have an answer for you immediately, but if your observation that the cells are circular (coccoid) is correct, it can't be Xantho/Pseudomonas. If the results are to be trusted, that they are G- cocci, there aren't very many options, just Veillionella, Moraxella and Neisseria, pretty much http://rx.osumc.edu/asp2/microbiology/gramNegOrganisms.pdf.
Try Bergey's Manual of Systematic Bacteriology (I can't find an online copy though).
Your use of media and temperature can be very important. How was it incubated? Anaerobically?

@JoeHealey 30 degrees, aerobically. I will check now the Systematic Bacteriology, thanks for that guide!

Aerobically would rule out Veillonella, but I haven't checked whether Moraxella/Neisseria are Catalase/Oxidase positive or capable of growing on blood agar.

Well I will let you do your research.. When done post the results to the answer. Thanks!

Consolidating my comments, and taking all the results at face value (though microbiology can be very tricky), the most likely candidates are Moraxella, or Neisseria spp.
Gram negative cocci (spherical cells) rules out a large number of possibilities, leaving just the above 2 and Veillonella as candidates.

The OP said that the culturing was done under aerobic conditions at 30˚C. Veillonella is an obligate anaerobe, and so wouldn't survive this. Both Moraxella and Neisseria are happiest at 37˚C but would no doubt grow at 30. Both are cultivable on blood agar. Neisseria is best cultured in a 5% CO2 atmosphere, so is probably somewhat less likely. Both appear as pale-whitish colonies on plates. The OP's observation of yellowish colouring could be artifactual of the plate colouring, I'm not 100% sure.
Both are positive for oxidase and catalase.
Neisseria on blood agar:

Moraxella on blood agar:

One final comment: both of these are pathogens, so continue with all due caution.
Moraxella, in particular, is a respiratory pathogen, so I would advise working in a biosafety cabinet. I'll assume you already have the relevant paperwork/permission to be handling > BSL1 organisms...

Lovely answer, covers me 100%. And of course I have permission to work on pathogens... besides thats my future job! Pathologist....(still studing and experimenting but ok)

Great, that's good - thought I'd check. If it was a school experiment or something, they may not have had the relevant safety frameworks, so thought it best!

University experiment in special labs... and tutors-personnel that are always watching us.