text:
Can the spinal cord contain an "epileptic focus"?
I was wondering, is there a possibility of an something similar to an epileptic focus to exist within the spinal cord?
Note I am using the terminology "epileptic" loosely here, principally for the lack of a better name for it. When I say epileptic focus I mean an excitable area capable of sustaining a pathological rhythmic electrical activity which may or may not extend to other areas of the central nervous system.
I believe it is due to the connection types that occur within the spinal chord (closed loops that exist there are resistant to this) and as such this might be true for other CNS areas (epileptogenic susceptible tissue might be specific of cortex areas). But I did some research on the topic and couldn't find any data on this.
If it isn't possible to have this problem on the spinal chord then, why is that?

What I did find is that some types of damage (http://www.ncbi.nlm.nih.gov/pubmed/1775364) may trigger something like an epileptic focus - couldn't find if it is becomes a permanent inductor of seizures, probably not.

Another possibility is that electrical activity within the spinal chord is hard to measure (http://jn.physiology.org/content/73/1/399.short mentions briefly this difficulty)

Short answer
Epilepsy is a disorder confined to the brain.
Background
Terminology is crucial in this question. The International League Against Epilepsy (ILAE) defines epilepsy as a disorder of the brain characterized by an enduring predisposition to generate epileptic seizures and by the neurobiologic, cognitive, psychological, and social consequences of this condition. ILAE defines an epileptic seizure as a transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain (Fisher et al., 2005).
Hence, by definition, epilepsy is a disorder of the brain. Note that the ILAE is an authorative organ and their definition overrides whatever your medical textbook on internal medicine says.
An epileptic focus is a commonly used term, but as far as I know not well-defined. It's often used in relation to EEG and other methods such as MRI and PET that attempt to define the hot spot of seizure activity. More strictly defined terms in this regard are eloquent cortex and epileptogenic zone. The eloquent cortex refers to any cortical area in which injury produces symptomatic cognitive or motor deficit. The epileptogenic zone refers to the region of cerebral cortex that is both necessary and sufficient to generate epileptic seizures. Its entire removal can be used as a treatment for intractable epilepsy (Richardson, 2003).
With regard to your question, I expect you are referring to the epileptogenic zone. By definition, this refers to a region in the brain.
References
- Fisher et al, Epilepsia (2005); 46(4): 470-2
- Richardson, Brit Med Bull (2003); 65: 179–92
Note
I expect this answer may not be entirely satisfactory. If you are looking to the  physiological basis of the occurrence of seizures and why they occur in the brain and not in the spinal cord, it may be wise to formulate a more specific separate question. Preferably do not grossly edit this question given it received three answers. vervet's answer on focal epilepsy clearly shows the confusing terminology in epilepsy world. Focal epilepsy is not the same as an epileptic focus. However, epileptic focus is a term often used for focal epilepsy. Long story short, specific answers need specific questions, preferably with the definitions embedded to prevent deleted answers and under-appreciated answers like vervet's.

Thanks for the well-round well composed answer, but you are right, I this is not the answer for which I was looking.

I've made (hopefully) suitable edits to made clearer what I meant.

Why the downvote?

Because you knew you were not answering my question but answered it anyway.

Also, because you defined epilepsy as a brain disease (ok, according to some reliable sources) but my question is intrinsically related to why is this a brain disease and not a CNS disease. Some older sources would treat is as more generally as a CNS disease, such as http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1675106/ and this is what I want to clarify.

I would remove the downvote, since you seem to have done it in good nature, but stackexchange does not let me.

Epilepsy is a brain disorder caused by abnormal electrical activity in the brain, which is what often produces seizures. Focal epilepsy just involves part of the brain, while generalized epilepsy cannot be localized to a specific part.
A focal epilepsy could therefore not be caused by a spinal cord lesion.
Some conditions also affecting the spinal cord may predispose patients to epilepsy. For example, multiple sclerosis patients are known to have higher rates of epilepsy. However, the epileptic focus is still in the brain.

You didn't answer what I asked and you didn't put in any pertinent references. Also I was not asking about spinal lesions, nor multiple sclerosis. Epilepsy is usually described as CNS disease and the spinal cord is a part of the CNS

Also I was not talking about lesions or diseases of the spinal cord, since I know that if you put something there you can cause a seizure http://www.ncbi.nlm.nih.gov/pubmed/21992196, what I meant was a spontaneous focus or a spontaneous activity without generalization.

@user27221 What I am saying is epileptic seizures always originate in the brain. Spinal cord seizures are much less common. If your question is about seizures in general you should remove the word epileptic.

As defined by Harrison's Textbook of medicine: "Epilepsy describes a condition in which a person has recurrent seizures due to a chronic, underlying process.", whereas "A seizure (from the Latin sacire, “to take possession of”) is a paroxysmal event due to abnormal, excessive, hypersynchronous discharges from an aggregate of central nervous system (CNS) neurons." The names are not related to any spacial aspect whatsoever.

+1 for the distinction between focal and generalized epilepsy.


text:
Is it possible to still grow taller after growth plates have been closed?
In addition, when do we know we stop growing taller? Or we keep growing taller?
To the first question:
Recently, I went to a doctor to have a check up, he said that my growth plates are closed and cannot grow taller anymore. True or false? Is it possible to have a second growth spurt. I am about 16.

No, because growth only occurs at the epiphyseal plate or growth plate. In the picture here, the epiphyseal plates are the two horizontal lines in the tibia and fibula, and bone growth occurs in the upward direction, or toward the middle (shaft) of the bone. Once the epiphyseal plates close, the bones can no longer elongate.
It's possible to have a second "growth spurt," but it's only because the epiphyseal plates haven't closed. David Robinson, the basketball player, was 6'7" as a senior in high school, but ended up being 7'1". The "growth spurt" is caused by the sex hormones, which is why a significant amount of growth occurs during puberty.

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text:
What are the advantages and disadvantages of using beta-galactosidase compared to luciferase as a reporter gene?
In the University labs, we have used Beta-galactosidase as a reporter gene to quantify the expression initiated by the stress-response promoter in yeast. This was done by exposing one of the two groups to osmotic stress (high salt concentration) whilst the other was unstressed. Then the levels of beta-galactosidase were compared.
A question given to us afterwards asked to give advantages & disadvantages of using Beta-galactosidase compared to Luciferase as a reporter gene in this experiment. And which one would be, overall, more suitable?

I think that @leonardo has this backwards. β-galactosidase can be assayed accurately and cheaply using ONPG as a colorimetric substrate with no solubility problems. All that is needed is a spectrophotometer: my guess is that this is the assay the OP used in their experiment. So my answer is - use β-galactosidase for inexpensive quantitative analysis - no need to add luciferin and ATP or to worry about oxygen availability. I'm struggling to think of a disadvantage for β-galacosidase - maybe there are higher background levels from other cellular glycosidases, whereas there will be no background luciferase activity?

I realize this question is about yeast, but I'm afraid that people may try to expand the answer to all systems, and beta galactosidase is not good for all systems, particularly for animal studies. I've seen too many gene therapy papers try to get away with using it.
Beta galactosidase is not a good reporter gene for in vivo gene delivery studies. There is too much endogenous activity in most tissues to distinguish the exogenous activity. When doing non viral gene delivery, the amount of DNA expressed is often so low that you cannot overwhelm the endogenous activity and therefore cannot conclusively say the enzyme activity you detected is from your new DNA.
Luciferase is far superior for in vivo work. First, there is no endogenous luciferase activity in most animals ( you're out of luck if you're doing work on fireflies ) so you can be sure that any luciferase activity you detect is real. Luciferase activity can be determined noninvasively though bioluminescent imaging, allowing for repeated measurements on the same animal. Beta glucosidase can require killing the animal, dissecting the tissues, preparing microscope slides, and then analysis, so doing a time course study will require using many more animals.
The only advantage I can see beta glucosidase having over luciferase is if you want to see what percentage or precisely what type of cells are expressing the reporter gene. However, I think GFP or another fluorescent protein would be more appropriate because of the endogenous activity issue I described earlier.
Again, my answer applies for animal use. If you're just growing yeast on a plate, the beta galactosidase is probably the cheaper way to go. We did some 384 and 1536 well plate assays on primary hepatocytes with luciferase, and the luciferase reagent was about $250 for 10mL. You might also consider fluorescent proteins for screening. I've made bactieral colonies with RFP that were visibly red, so no need for UV, but even if you need UV light to see the fluorescence, a standard UV transluminator for viewing gels will be good enough, and no extra reagents to add.

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Eyelids interconnected?
I've seen a patient who had a Vitrectomy (eye surgery) done on a single eye manifest massive swelling on both eyelids.
That seems like having my left hand swell after punching a wall with my right one.
Is this example in the eyes rare? How and why does it happen in the eyes? Does it happen anywhere else?

I cannot obviously speak for the specific case you mention (and, anyway, I am not a medical doctor so I would not make a diagnosis in any case), but one thing that comes to mind is that eyes are part of the immunologically privileged sites of the body. This means that an inflammatory response is not elicited in case of the introduction of an antigen.
I quote from Immunobiology by Charles Janeway

Some body sites are immunologically privileged. Tissue grafts placed in these sites often last indefinitely, and antigens placed in these sites do not elicit destructive immune responses.
  Paradoxically, the antigens sequestered in immunologically privileged sites are often the targets of autoimmune attack; for example, brain autoantigens such as myelin basic protein are targeted in multiple sclerosis. It is therefore clear that this antigen does not induce tolerance due to clonal deletion of the self-reactive T cells. Mice only become diseased when they are deliberately immunized with myelin basic protein, in which case they become acutely sick, show severe infiltration of the brain with specific TH1 cells, and often die.
  Thus, at least some antigens expressed in immunologically privileged sites induce neither tolerance nor activation, but if activation is induced elsewhere they can become targets for autoimmune attack (see Section 13-25). It seems plausible that T cells specific for antigens sequestered in immunologically privileged sites are more likely to remain in a state of immunological ignorance. Further evidence for this comes from the eye disease sympathetic ophthalmia (Fig. 13.36). If one eye is ruptured by a blow or other trauma, an autoimmune response to eye proteins can occur, although this happens only rarely. Once the response is induced, it often attacks both eyes. Immuno-suppression and removal of the damaged eye, the source of antigen, is frequently required to preserve vision in the undamaged eye.


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Why temporal lobe is called temporal?
http://en.wikipedia.org/wiki/Temporal_lobe
Does this have something to do with tempo (time?)
Temporal lobe is behind (posterior) to frontal lobe, inferior to parietal lobe and is in front of occipital lobe.
Why it's called temporal?

The temporal lobe is in the temporal region of the head, near the temples of the skull, hence the name. It's name does not relate to it's biological function, it is mainly involved in processing language, visual memories, and emotions. The medulla oblongata is one region of the brain that deals with a lot of the "tempo" type functions (tempo as in keeping rhythm) such as controlling the heart beat and breathing rate.

Temple indicates the side of the head behind the eyes.

The different etymologies of temporal can be found on this wiki article

yes, temporal in this sense has a different etymological root to tempo.

is temporal means sideways?

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text:
How can pasteurized milk last 7 days?
In Estonia, the product bought from the shop lasts about 2-3 days, in Finland 3-5 days and In Oslo Norway 7 days.
The better infrastructure of transportation explains some for Finland and Norway.
But how on earth so big difference between Norway and Finland?
I heard today that some countries are fluoridating milk.
Ii is not in Finland and Norway.
However, it may be the case that some minerals are existing naturally more in Norway than in Finland. Also, more rain dissolves more minerals in Norway than in Finland.
How can pasteurized milk last 7 days?

Is it not more likely to be a difference in food safety regulations/company policy than a biological difference?

In the UK pasteurized milk lasts around  7 days. I'd assume 7 days was pretty typical.

I'd go with @RoryM there but I can't find any regulations on-line to suggest so - can't think of any other reason... perhaps processing techniques, have you looked at different brands within nations which might have different processing techniques?

I would rather think about regulatory differences instead of biological ones. (Edit, as also Rory M highlighted in a comment)
Extended shelf life can be obtained through microbial ultrafiltration. However in Europe, ultrafiltration labelling is not mandatory, so it is difficult to distinguish if a milk product was simply pasteurized or also ultrafiltrated. The converse case, biologically speaking, two milk products could be generally the same but one country could be more stricter than the other on shelf-life legislation. (The shelf-life relates more to the unsuitability for sale rather than for consumption).

Evidently the shelf-life of pasteurised milk is very dependent upon post-pasteurisation temperature of storage. Here is a paper in which the effect of temperature on shelf-life has been analysed. A sentence from the abstract says:

The microbiological stability for pasteurized milk packaged in HDPE bottle and stored at 2, 4, 9, 14, and 16 degrees C was estimated at 43, 36, 8, 5, and 3 d, respectively.

I think that you would need to know exactly how the milk had been handled from pasteurisation plant to retail outlet before you could make any valid comparisons. Any period out of cold storage could clearly have a big impact.


text:
Is epilepsy more heritable from maternal side?
I am thinking if paternal or maternal genetic line is the risk factor.
Mitochondrial DNA is coming from maternal line.
I do not know the pathogenesis of epilepsy so well that I could answer my question.
Is epilepsy more heritable from the maternal side?

Epilepsy is a neurological disorder characterized by hypersynchronous discharge of neurons .i.e abnormal electrical activity in the brain. Epileptic seizures caused primarily due to i) inhibition of inhibitory neurotransmitter systems such GABA neurotransmitters or ii) Enhancement of excitatory neurotransmitter systems such as nAchR. These conditions arise due to head injury, trauma and genetic factors. But there is no evidence as of now regarding Mitochondrial DNA taking part in inhibitory and excitatory systems. so, epileptic seizures are not specific in inheriting from any side (Maternal or paternal side) as far as pathophysiology of epilepsy is concerned.

I am thinking about the genetic factors, since more genetic factors are inherited from the maternal side because of mitochondrial DNA. If mitochondria play any role in the disease, then maternal side has more role in the pathology of the disease. I have seen one case where the disease spread only through maternal genetics - and do not understand this.


text:
Effect of Aging on SA node's sympathetic fibers
I am trying to understand the effect of aging on the sympathetic fibers of SA node.
I know that aging shifts the vagal curve to left in frequency due to aging.
However, I am interested if aging has similar effect on sympathetic fibers.
In young heart, heart's intrinsic functions can work with simultaneous parasympathetic and sympathetic processes.
If there is no change in the sympathetic function, then those processes have to happen at different times.
I am having this kind of schematic picture in my mind:

where intrinsic functions occur in 100-110 BPM normally.
However, aging shifts V1 to V2, no intersection anymore between V2 and S1.
What is the effect of aging on the sympathetic fibers of SA node?

A bit late to ask, but where does South Africa come into this?


text:
What is a common body composition in mammals?
The Physiology Of The Racing Greyhound states that most species have about a 40% muscle mass to body mass ratio. Understanding Body Composition puts "optimal fitness" in humans at 16-25% body fat for women and 12-18% in men. These add up to pretty much anywhere from 50% to 65%, leaving 35-50% as more or less unaccounted for. In looking, I have been unable to readily locate any further breakdown, let alone any source that provides a full breakdown. At least Wikipedia is lacking in specifics in this regard.
In adult, healthy mammals, what is a common body mass breakdown into muscle tissue, fat, bone, and internal organs, by percentage of total body mass?
I am particularly interested in wild carnivores, but almost any mammalian species will do in a pinch. Specific examples and citations are appreciated.

If this question is a better fit on some other site, please feel free to migrate.

Think about the variety of body compositions in different mammals, even within a single species, heck across the life span of an individual; a bear coming out of hibernation will have a dramatically different composition compared to a bear going into hibernation.

@KevinCarolan That's why I wrote "adult, healthy mammals" and did my best to allow for answers discussing only specific species. However, if you feel that the answer is "there is no data available", then even though it pretty obviously isn't what I was hoping for when I wrote the question, that could certainly still be a valid answer to the question. (However, I still suspect that the figures quoted at the linked pages must come from somewhere.)


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Would some dinosaur egg be the most massive cell that ever existed? Are dinosaur egg relatively small compared to eggs of modern birds?
The egg of a large modern bird is a very large cell, not the largest possible biological cell since there are very long nerves in squid, but it's likely the most massive modern cell.
But, what about the cells of prehistory? Many dinosaurs were far larger than modern birds, but I had trouble finding information on just how large their eggs could be. I was also surprised that the eggs were not bigger than those of modern birds. It seems the ratio of egg size to dinosaur size was much smaller... or has that even been studied?
Maybe the large eggs were all destroyed?

I was also surprised that the eggs were not bigger than those of modern birds. It seems the ratio of egg size to dinosaur size was much smaller. - where have you read this?

I suppose that you define "large" in terms of volume. Note that there will have some issue of definition about what a cell is when you consider cases where cells of an entire tissue vanished to end up with more or less a big single cell with many nucleus.

I didn't read it. It's an observation I'm having a hard time confirming or invalidating.
Let's just use mass for largest. Volume is confusing.

The largest known dinosaur eggs were the size of a basketball. The egg of an ostrich is also very large, comparable in size to dinosaur eggs.
The reason why even the very large dinosaur laid relatively small eggs is diffusive ventilation of oxygen and "breathing" through the eggshell.
The rate of ventilation is proportional to the eggshell surface area while the required amount of fresh oxygen is proportional to the volume of the egg. The surface area is proportional to the square of its radius while the volume to the cube of the radius. As the size (=radius) of the egg increases the ratio between the incoming oxygen through the shell to the amount of oxygen needed is decreasing, making too large eggs unsustainable.
Another consideration, also related to oxygen diffusing through the eggshell is that a very large egg requires a thick shell, and too thick shell prevent oxygen diffuse through it to the embryo.
References:

USRA.edu: how big can eggs be?


text:
What is the armpit hair for?
Modern human beings, especially women, cut their armpit hair. It seems to me the armpit hair is trivial/useless. Shortly speaking, what is the armpit hair for?

While I won't answer fully at this time: Insulation is always one purpose. Bare pits = cold! Also, for men at least, we have glands that emit scents that correspond to our MHC allele makeup (immune system variation) - and women tend to prefer scents that differ from their family which results in more MHC diversity in the bloodline. A mat of hair can act as a scent-sponge, increasing the effect. It can also be a sign of cleanliness; bad smells are often bacteria in origin - having hair but no bad smell = clean. Hope this helps!

There are three theories on Wikipedia: http://en.wikipedia.org/wiki/Underarm_hair

Hair has been used for defense, think of lions, horses and roman centurion helmets. It's hard to cut or bite through. I'm not an expert, but it may be that beards, pubic and underarm hair cover exposed parts of the body that have vital arteries under the skin(neck, armpit and groin).

I don't think trivial is the word you wanted to use... possibly redundant, or useless?

I have been trying to read up a bit on this. I started out looking on wikipedia and it seems there are three hypotheses which are not necessarily mutually exclusive.
1.Aid the wicking of sweat away from the skin
2.Reduce friction between the thorax and upper arm
3.Facilitate the release of sex pheromones
The first would seem possible because it would help to prevent over-heating of the lymph nodes under the armpits and that also fits with the fact there are a lot of sweat glands there.
The second, I can't find any citations which support this but I understand that people who shave their armpits tend to suffer from dry underarms. This could be a result of increased friction.
The third is apparently controversial although it seems perfectly reasonable and highly likely to me. There is a famous experiment by Claus Wedekind who got men to wear a t-shirt for a few days. He then got women to choose a most preferred male purely by the scent of the t-shirt and found interesting results relating to the MHC profiles. The armpit hair could help to trap the odour produced by the sweat and help with mate attraction, like some kind of scent sponge. I don't understand why this is so controversial, loads of animals influence mate choice with scent - perhaps people don't like to think we are genetically attracted to each other by sweat because it seems animalistic and less romantic.
In summary, there is no sure answer and it could well be all of the above, or something entirely different.

The third is controversial because modern men are more likely to (sexually) select women with less armpit hair. I can't say if it is purely due to media, though, or if there is genetic component.

Realistically that is too recent of a trend to have any noticeable effect on the natural presence of armpit hair.

It's not proper to think of evolution in teleological (purpose-driven) terms--armpit hair is probably a trait that was never eliminated because it is not harmful to the species, rather than a useful trait that was specifically "selected for".

Good point about avoiding thinking in teleological terms. I think what is difficult to explain is why most body hair has been lost yet some retained. I would have thought that the loss of body hair would have affected the armpits just as it has the rest of the body (I know we have hair all over our bodies but it is only so dense in a few places). It suggests that there is a reason the armpit hair (and other areas) has been retained and that the genes affecting hair growth are up-regulated in these localities. This would suggest to me that there is some purpose of having armpit hair. Any ideas?

ps, production/growth of the hair is an energetic and nutritional cost - though it is probably minor.

@rg255 Hair was probably retained in the most sensitive areas: the pubic area, the armpits, and outside various openings and membranes such as the eyes, ears, and mouth.

@rg255 To speculate further, it is possible that men on average have more body hair because they on average have a lower body fat percentage, leaving them more exposed. This could also explain the high prevalence of limb hair in both sexes: limbs and their appendages (fingers, toes) are farther away from the heart, and therefore more vulnerable to the cold.

I think that has a lot to do with testosterone (and other hormone) levels: give a woman testosterone pills and she will likely get rather hairy!

@rg255 Well, of course, but that is only the mechanism by which the exhibition of the trait is controlled--and while more efficient control mechanisms  for the "fittest" traits are certainly "weeded out", they do not dictate which traits are the "fittest".

sorry that wasn't meant to come across as a criticism if it did, the increased testosterone may well be, in part, selected for as an advantage in that way.

@rg255 I wish there were a more direct way of speaking on SE, I wanted to tell you I was intrigued by your profile. Where on here could we address science policy, psych. of interdisciplinary science, etc.?

my email is in there isn't it?

@QuietThud have you tried chat?

Yep! Is there a way to invite specific users, though?

Microbiome manipulation is a common theme in these answers/comments, and there are experimental methodologies for investigating such things. For example: "Topographical and Temporal Diversity of the Human Skin Microbiome" at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2805064.
One selection pressure that hasn't been mentioned is the reduction of harmful bacteria that occurs when providing a growth advantage to more benign bacteria. Many hairy areas are those where bacteria in general can live and prosper. Various ways hair could impact the microbioime are are easily imagined, for example greatly increased surface area should favor aerobic vs anaerobic bacteria. More specific host-bacteria interaction, e.g. specific bacteria being selected for due to the presence of certain hair surface proteins or the microstructure of the hairs surface might be harder to investigate. How hair surface varies in different location might be informative.

The explanation I heard from the documentary called "Curiosity: World's Dirtiest Man" is that armpit hairs allows for the growth of microbes which allow for the production of smell. This smell is useful for the attraction of mates in primates (although this function is probably lost in humans as our society became more hygienic).


text:
How to explain Genome, Genes, RNA and protein in one figure to non-biologist?
I have a presentation to do where non-biologist are attending. In order to introduce a little bit my work I have to do a quick summary on genomes. So what is a genome, a gene, an mRNA and a protein. And the best would be to have that in one figure, an easy to understand. I found this : http://dnamismatch.com/Test/wp-content/uploads/2013/07/Genes-and-genomes.png
Anyone knows other resources ?
Thanks

I'd go with using an analogy - e.g. The genome is a cookbook, each recipe is a gene, the cook is the mRNA and the product is a protein (perhaps not entirely analogous but you get the picture) - you have to find something that can adequately explain all of the four parts in one coherent and correct example. Personally I think the figure you've shown is poor (aesthetically and only roughly illustrates what genomes and genes are, not proteins or mrna)

Some info about the topic of the talk might be helpful in guiding answers here

the topic : retrovirus and cancer . So I have to introduce genomes and genes in the case of retroviral integration

There can be different ways and giving analogies would work. What is the educational background of the audience and how much time do you have for your presentation?

the audience consists of both biologists and no scientist at all.


text:
Why is it called "Ebola virus disease", not just "Ebola" or "Ebola disease"?
Why do scientists (pretty consistently) call it Ebola virus disease, rather than just Ebola, or Ebola disease?
Many other diseases are caused by viruses, but they don't seem to have this detail of terminology.  Nor do you hear the analogous terminology for bacteria.
For example:

Rubella is caused by the rubella virus.
Influenza is caused by various influenza viruses (genus names Influenzavirus A/B/C).
Some strains of E. coli (pathogenic E. coli) cause disease, but you never hear E. coli bacteria disease.

I think there is no specific reason. It is probably simply a naming which got widely adopted.

This is now how new viral diseases are being named, possibly because one can have/carry a virus without having a disease (e.g. HIV, herpes simplex, etc.). It is not as uncommon as you think.
A bit of googling will turn up reputable sites which discuss the epidemiology of Hantavirus disease, Hendra Virus Disease, Powassan Virus Disease, Lake Victoria Marburgvirus disease, Lujo virus disease, Ross River virus disease, Nipah virus disease, respiratory syncytial virus disease, Kunjin virus disease, Chikungunya Virus Disease, Heartland virus disease, St. Louis encephalitis virus disease, West Nile virus disease, Eastern equine encephalitis virus disease, Western equine encephalitis virus disease, and California serogroup virus disease (includes infections with the following viruses: La Crosse, Jamestown Canyon, snowshoe hare, trivittatus, Keystone, and California encephalitis viruses) and others, but I'm stopping here.
Bacteria cause diseases, but many already had/have names: Typhus (Rickettsia typhi or Rickettsia prowazekii), Rocky Mountain Spotted Fever (Rickettsia rickettsii), Diptheria (Corynebacterium diphtheriae), Lyme disease (at least three species of bacteria belonging to the genus Borrelia), Pertussis/Whooping Cough (Bordetella pertussis), Tetanus (Clostridium tetani), etc.
Interestingly, I have started to see scholarly articles for Clostridium Difficile Disease, which was an entirely new name for what we used to call Antibiotic-Associated Diarrhea. So maybe there will be a shift in that direction as well; time will tell.
How diseases are named is another whole thing.

"Viral diseases" is also the term used in WHO reports on "International Nomenclature of Diseases", see e.g. "Viral Diseases: Infectious Diseases (International Nomenclature of Diseases)".

I notice that a lot of the examples you provide are geographical names. Maybe the convention is to use the name of the disease if there is one (encephalitis, chikungunya) and to use "[geographical place] virus disease" where it's a geographical term to avoid confusing it with the place name (St. Louis, Ross River, Ebola River, the town of Marburg, and so on).


text:
Can female Drosophila melanogaster lay eggs without males?
Can female Drosophila melanogaster lay egg without males?
I maintain our lab stock but find a line that seems to have all females (or all males). The flies have been in the vial for two weeks, but I don't see any eggs hatching or become larva.

wow - so just like chickens... i wonder how this is an evolutionary avantage for the females?

Yes, I regularly have to collect female virgins (12500 of them in the last week). They will lay eggs especially when there is extra yeast available. It is actually a good way to check virginity (in case a fly hatched early and was already mature, or a male made it through sorting etc.) - put some extra yeast grains in the vial when you collect them, leave them for a few days and then check for larvae, if they are not virgins there will be eggs and larvae, if they are virgins there will only be eggs!

Very old females (such as those in vials that have not been flipped for a long time) will often lay unfertilized eggs in the absence of males.
This happens to me occasionally when I am collecting virgins and then forget about them for a while.

I find even young females do this, but do you add extra yeast to the vial? perhaps this stimulates mine to produce more eggs (see Ashburner, Sullivan and Hawley) more rapidly.

Usually this happens to me when I'm collecting virgins, so there's often no yeast; this probably explains our discrepancy.

cool, there is definitely research suggesting yeast increases egg production. and as useful way to check virginity whilst getting them really fired up ready to mate!


text:
What is the frequency of double-hets between parent and child?
Say both parent and child are genotyped for all SNPs. In this setup we are only looking at variant positions between one parent and child - so neither parent nor child are homozygous reference (no AA/AA) in the millions of positions we are studying.
Assume all variants are biallelic and there is no de novo mutation (no AA/BB or BB/AA)
P    C
AA   AB
AB   AA
AB   AB
AB   BB
BB   AB
BB   BB

What is the fraction of AB/AB among these possibilites?
We are looking at all positions in the genome so the minor allele frequency (MAF) of B allele varies. You can choose whatever B frequency you like.

I'm a little confused: are the genotypes in the rows representing different loci or just different potential, non AA/AA scenarios of one locus?

Potentials. I am going to go with 1/6, regardless of B's MAF.

I don't understand the question. You say so neither parent nor child are homozygous while in your example you have examples where one of the two or even the two are homozygous. Then it is unclear what you mean by no AA/BB or BB/AA. I suppose the / notation separate one parent genotype from the child genotype. I don't know if you're assuming sexual reproduction and talk only about one parent or not. I think you want to assume that all A alleles are at the same frequency. In the same time you seem to say the MAF varies, however you say the "MAF of  B" varies which makes little sense.

For the above reasons, I am voting to close as unclear (four years after the question has been posted :) )

by no AA/BB or BB/AA I mean if the one parent we know about is AA we never BB in the child.

"I don't know if you're assuming sexual reproduction and talk only about one parent or not."
because often we only have access to one parent


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Identify bee in photo (found in Utah, USA)
A friend took this photo of a bee in his back yard in central Utah (© Jon Mott, CC-BY 3.0). I have no formal training in systematics or entomology, so to me everything looks like the bees' poster child Apis mellifera. Can someone with a bit more experience confirm or refute this?

Maybe You should contact a local apiary and ask them about common bees in your are.

Yes, this looks like Apis mellifera, which is also one of the most common bees you'll run into. If you have other pictures, you could check the identification tips at the bugguide page for the species.
As a side note, in general to really confirm an identification a specialist would need to see a collected specimen (that is, a live or pinned bee) as the distinctive characters (things like size, wing veins, or in this case, long hairs on the eye) may not be visible in photographs.


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Which kind of tick is this and what is that thing around its back?
I was recently bitten by a tick. After having removed it from my body, I put it in a glass. By now, it has stopped moving, so I put it under a microscope and looked at it. I was surprised about being unable to get a sharp image of its body (upper part in the images) – what could that be? And can someone help me identify it?
I found a picture of a tick with a somewhat transparent thing around its back here – maybe that's what made it hard for me to get a clear focus on the back? And maybe it's related to this one?

It was found in Oldenburg, Lower Saxony, Germany. Its length is between 1.2mm and 1.4mm (I don't have anything that's very usable for precise measurement of such small lengths).
If clearer focus on a particular part of that thing is needed for identification, please tell me.

Where geographically was it found, and how large is it?

@kmm: edited to address your questions

As your link suggests, it looks like a female tick of the genus Ixodus. It is likely female because the scutum or shield only covers part of the dorsal surface. E.g.,

which comes from Bristol University Tick ID. The translucent posterior portion may just be from light passing through.
If you are able to zoom in closer on different parts, you can key out what species it is.


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What's the Efficacy of Ampakines in the Treatment for ADHD?
What's the Efficacy of Ampakines in the Treatment for ADHD? Ampakines are a class of drugs that serve as potentiators of the AMPA glutamate receptor. By so doing they serve as nootropic, anxiolytics and antidepressants.

Health stackexchange?


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Can TGF beta family induce all somatic stem cells?
I think this is not possible.
Conclusion about this preview article TGF-$\beta$ family signaling in stem cells:

While TGF-$\beta$ family signaling regulates stemness of normal and cancer stem cells, its effects are diverse and depend on the cell types and physiological state of the cells.

Can TGF-$\beta$  induce all somatic stem cells?

What do you mean by induce?

@Chris Induction. You can think it as sending a positive signal. I think it does not need growth value. Only that some process is induced to start or made stronger - not inhibited here.

But what do you want to induce? Differentiation? Migration? Proliferation? Retreat into a nice? This is a pretty broad topic at the moment.

TO be induced by a TGF-$\beta$ ligand, a cell has to express one of its cognate receptors

Signalling in the TGFβ pathway normally puts a brake on the progress of cells through the cell cycle - it counteracts the action of myc for example, partly by regulating the expression of myc. In Burkitt's lymphoma myc escapes this regulation because of a chromosomal translocation, tipping the regulatory balance over to uncontrolled cell growth.
This anti-proliferative action of TGFβ signalling is so critical that you might expect it to be ubiquitous in cells, and the expression atlas entry for the TGFβ receptor is consistent with this.

So in naturally occurring somatic cells, the answer is yes because this antiproliferation action. Think now about induced somatic cells (those artificially derived from somatic stem cells). Can this same behaviour occur in all induced stem cells? I do not understand if this behaviour can proceed into processed cases and when we do not have such a behaviour on stem cells derived from somatic stem cells.


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Can Squirrels Eat Every Mushroom?
Squirrels have the ability to eat toxic mushrooms as described below. Are there any mushrooms that they can't eat without dying?

According to Dr. John Rippon, an IMA member and world expert on fungal diseases, squirrels have an interesting adaptation that allows them to eat mushrooms containing deadly amanita-toxins without being affected. There are three important chemicals in the amanitas. Two will knock you right off, but are destroyed in cooking. The third one is the interesting one: it consists of the second amanitin, bound tightly to a glycoprotein molecule. When we digest the mushroom, the enzymes in our gut break the bond between the toxin and the glycoprotein, leaving the toxin free to enter our bloodstream, while the glycoprotein is excreted (a glycoprotein is a [protein containing sugar molecules and accounts for the viscous properties of mucus], in case you don't know). What the squirrels have done is line their gut with a toxin-compatible glycoprotein, so that as soon as it gets split from its original glycoprotein molecule, it gets rebound to the squirrel glycoprotein, and excreted along with it. Obviously, the squirrels don't cook their food to destroy the first two molecules, but presumably those get bound in exactly the same way. Thus, squirrels and a few other animals (guinea pigs also, I believe) can eat mushrooms that are highly toxic to other animals with no ill effects.  Source

from doing a bit of research, I think I can say that as of now there is no proof for the same.


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How do plant galls form?
I am curious how Gall Wasps, bacteria and other organisms induce galls to form.
Specifically, what chemicals induce gall formation?

http://gardening.stackexchange.com/questions/2052/what-is-this-anomalous-growth-on-my-oak-leaf

One type of gall: cedar-apple rust http://en.wikipedia.org/wiki/Gymnosporangium_juniperi-virginianae

I'd like to add to Amy's excellent answer.
Generally, galls are induced by the forced accumulation of plant hormones at different levels to those naturally maintained by the plant, in a localised area. Usually the hormones targeted are auxins and cytokinins which are both involved in the regulation of normal growth patterns; disrupting these patterns leads to disorganised growth, or in some cases a differently organised growth. There are several methods that I know of:

The gall inducer directly synthesising the hormone.
The inducer chemically inducing the host to synthesise more hormone.
The inducer chemically inducing the host to transport more hormone to the site.
The inducer genetically modifying the host to cause synthesis of the hormone in the host cell.

Some examples of the different methods:
Direct production: The bacterium Pseudomonas savastanoi directly produces indole-3-acetic acid (IAA, a type of auxin). This direct accumulation has been shown to be responsible for gall formation in oleander knot disease. Some key papers: Palm et al. 1989, link 1; Glickman et al. 1998, link 2.
Chemical induction of transport: Root-knot nematode worms induce root gall formation in clover. They probably do so by producing flavonoids which up-regulate transportation of auxin into cells (see link 3).
Genetic induction: As already mentioned by Amy, Agrobacterium tumefaciens is a very well characterised example of induction by genetic modification, however, A. tumefaciens is also known to directly produce auxins in large quantities. Another interesting example of genetic modification is in viral gall-inducers. They are not so well studied as their bacterial counterparts, but in some cases (e.g. white clover mosaic potexvirus) it has been shown that virus infection initially leads to a complex change in the types of cytokinins produced by the plant (e.g. Clarke, 1999; see link 4). It has also been shown that if cytokinins are applied exogenously (i.e. injected into the plant) after viral infection, that the virus cannot replicate well. This suggests that the virus is manipulating the host's hormone production in a complex way.
There is also the interesting case of Rhodococcus fascians, which seems to produce a chemical which is not structurally similar to any known cytokinin, and yet has similar effects (Goethals et al., 2001; link 5).
You specifically asked about gall wasps, but unfortunately this mechanism is, as far as I can tell, not completely known. It is speculated (e.g. in Shorthouse & Rohrfritsch, 1992; link 6) that this involves direct injection of phytohormones. The evidence to support this is simply that other insects, particularly aphids, excrete phytohormones in their salivary sheaths when they inject them into a plant.
Finally, I'll just say that the fact that gall induction is carried out by bacteria, viruses, nematodes, fungi and wasps, and that some mechanisms are shared across all those associations,  demonstrates the ability of evolution to converge on the most elegant solution to a problem. It also shows that plants are so great, everyone wants a piece (but I would say that, because I'm a plant biologist).
References:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC209694/
http://apsjournals.apsnet.org/doi/abs/10.1094/MPMI.1998.11.2.156
http://www.publish.csiro.au/?paper=PP98157
http://www.plantphysiol.org/content/120/2/547.full
http://www.annualreviews.org/doi/full/10.1146/annurev.phyto.39.1.27
http://www.nhbs.com/biology_of_insect_induced_galls_tefno_3838.html

I don't think you're disagreeing with me, all I said is that we don't know much about gall producing insects !

You're right Amy, sorry! Answer updated with some grovelling.

ha ha ha (don't worry, you already had my upvote)

I recently aquired, "“Britain’s Plant Galls, a Photographic Guide.” It expanded upon what you said about insects injecting growth hormones: Sawflies belong with the gall wasps in the order Hymenoptera. The female has a tiny saw-like ovipositor with which she cuts slits in plants prior to laying her eggs. She injects a stimulant when laying her eggs and the galls start to grow before the eggs hatch. Most sawfly galls are solid at first and usually contain a single larva that gradually hollows them out. Mature larvae of most species leave their galls before pupating – often in the soil.

It seems not much is known about how insects induce gall formation (perhaps someone with more of an entomology can jump in).
But we do know quite a bit about Agrobacterium tumefaciens, which causes crown gall in roses, grapes, and other plants. Agrobacterium invades cell tissue and inserts a piece of it's own DNA into the plant cell. The plant cells incorporates the DNA into its genome and begins expressing a number of new genes, including genes that lead to an over production of the plant hormones auxin and cytokinin.  These hormones cause the undifferentiation of the plant cell and uncontrolled cell division, leading to the formation of a tumor-like gall.
More on Agrobacterium at Wikipedia. I can recommend some journal articles if you're interested.

Perhapse the wasp carries the bacteria =)


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Interlocus Contest Evolution means suicide?
I was reading Matt Ridley's "Genome" book. I am trying to understand the Interlocus Contest Evolution in his X-Y chapter. I do not understand why the X and Y chromosome would want to kill each other. Wouldn't that cause the death of the species (actually, have any species died that way?).
Can someone shed light on the issue?

X and Y chromosomes don't "want" anything-they are not conscious. I know that sounds obnoxious, but it's very important in evolutionary biology to understand that there is no agency and no intended final product for natural selection. I think the best way to think about it is like this: let's say there's a mutation on the X chromosome that happens to make females more fit at the expense of making males less fit. It seems possible that the evolutionary arms race that this establishes (i.e., males bearing a mutation that compensates or overcompensates for the new expense of the mutation that, say, their successful mom gave them, would then start to sweep to fixation in the population, and so on and so on) could result in population collapse. Apparently, there's theory out there that confirms this: http://www.els.net/WileyCDA/ElsArticle/refId-a0003669.html. Also, I vaguely remember a paper about toxic sperm (vs. female mating behavior) in Drosophila melanogaster suggesting that populations could collapse. As Bonduriansky mentions in the link, though, one resolution to the arms race would be the evolution of genes that get expressed very differently between the sexes (i.e., a gene that is good for a female but terrible for a male would evolve to only be turned on when it's found in a female). I hope that helps?

Did this answer your question?


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How long does a signal from the brain take to reach the limbs?
If the brain sends a signal to move what's the time it takes the signal to travel via neurons to motor neurons in hands, arms and legs?
How fast do those signals travel?

Speed of transmission is going to vary depending on the neuron fiber subtype.
Specifically, the biggest gains will be seen with cross-sectional area (feel free to ask why on physics.stackexchange.com) and neurons with myelin sheathes (fat wrappings which affect saltatory conduction rates).
You're specifically asking about Efferent neuron transmission rates, but here's a general idea:

Keep in mind that the entire circuit (from pre-motor cortex to muscle spindles) will involve several different types. In-general, your central nervous system (brain, brain-stem, spinal chord) are A-alpha, and if I recall correctly - the somatic nervous system (the voluntarily-activated neurons throughout the rest of your body in the PNS [peripheral nervous system]) are A-delta. If I'm wrong, somebody please correct me.
On average non-voluntary reflexes (which is actually information going to the CNS, being processed, and then going out to the motor neurons) take about 0.3 seconds. However, the average human can blink in about 0.1 seconds, which is probably a better measure.

how well are these functions really dedicated to the specific fiber types?

@shigeta - They're some overlap (the Vagus is a good example), but the function maps to the fiber type fairly well since space is the primary limiting factor for the peripheral system. However, I'll admit I haven't refreshed myself of the topic for a while, so it's possible the ratios are less strict than I believe.

How much about that 0.3 is transmission of the signal to the limb? Is there a reason to believe that the difference between the normal reflex of 0.3 and the blink of 0.1 is do to time it takes to transmit the signal?

@Christian - Roughly half, I'd assume. A full reflex arc is from a sensory neuron to the spinal column and back out to the muscles. The difference is probably due to length and the added junctions.

It is generally not a one-way process. The lag also depends on which frequencies you look at (the brain and limbs kind of speak using several channels at the same time). Near 10 Hz the lag is few dozen milliseconds.
Look for articles about EMG and EEG (or MEG) coupling for more precise info.
Use the paper http://homes.mpimf-heidelberg.mpg.de/~mhelmsta/pdf/2002%2520MEG%2520muscle%2520Review.pdf as a starting point.
PS. There is no neurons in limbs

Can you add some references?


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How and why do skin tags develop?
WebMD writes:

Skin tags are small, soft pieces of skin that stick out on a thin stem. They most often appear on the neck, armpits, upper trunk, and body folds. The cause of skin tags is not known.

Do we really know nothing about why they appear? Is there research that suggest hypotheses of the causes of skin tags?
It seems to me a pretty well established phenomena for it to be without good research.

Given that skin tags are considered benign, it doesn't surprise me to find very little published research focusing on them. It's unlikely that much grant money exists to answer questions about them.
That said, though, I found a handful of groups that have done some work on them. It seems that they all noticed a statistical relationship between the occurrence of skin tags, obesity and metabolic syndrome. These are the papers describing their research efforts so far:
http://onlinelibrary.wiley.com/doi/10.1111/j.1468-3083.2011.04401.x/epdf
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4740583/
http://www.ncbi.nlm.nih.gov/pubmed/21860156
None of the groups suggest a mechanistic explanation for the occurrence of skin tags, which makes me think that this remains a very open question. However, they all notice a correlation between skin tags and elevated leptin levels.
Leptin is best known as a hunger/satiety regulating hormone. However, it functions through the activation of the JAK/STAT pathway, which in turn activates a number of genes involved in cell survival and in turning off apoptosis, or programmed cell death.

This image comes from this paper in Nature, which, unfortunately, is behind a paywall.
So, my guess based on these data is that increased levels of leptin activate proliferative pathways in cells, leading to the occurrence of skin tags. That this proliferation results in benign cell growth probably has to do with competing tumor-suppressor and related pathways, which I can reasonably assume to be active and functioning, where outright cancer is not present.
What I wonder now, but can't find any information on, is whether skin tags are the only visible evidence of differential cell proliferation, or whether there are other instances within the body. That is, if the leptin-to-skin-tag hypothesis holds, is there something special about skin cells in that response, or are they just the only visible signs of it?

Are there any cases of skin tags forming into cancerous tumors?


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What causes a 'stuffy' or 'runny' nose when you have a cold?
When humans get the common cold, a common symptom is a stuffy or runny nose. Is that the body's immune response or is that the virus's doing?

Interesting. I haven't heard that before. A similar but unrelated question is: http://biology.stackexchange.com/q/445/238

There are different causes and mechanisms behind runny and stuffy nose.
I cover them separately below.
Runny nose
My professor of pathoanatomy and pathophysiology says that the correct answer here is serous inflammation to the runny nose.
Serous inflammation

Marked exudation by relatively thin fluid
Cold is caused by Acute respiratory viral infections

Acute viral respiratory infection

Exudate is very watery and clear - serous inflammation.
At 3rd day, whitish mucose excretion - catarrhal inflammation.
At 5th day, greenish colour - a lot of neutrophils and mucose.

The other answers mostly discusses about the mechanisms (secondary), but not the cause itself.
The most upvoted answer describes factors affecting the inflammation but not explicitly mention serous inflammation and its factors.
Stuffy nose
Congestion in nose is a passive and local process resulting from reduced outflow of blood from a nasal tissue.
The nasal epithelium is very thin which makes it vulnerable to flu and cold.
The viral particle passes through the membrane (often because of scarring) and causes the change in the vascular permeability of the surrounding big vein.
Mechanisms of stuffy nose are covered partially by Ram and Aleadam:

local edema
because of changed vascular permeability of large veins surrounding the nose
bradykinin
histamine (cetiritzin)
counteracted by epinephrine

which respond against viral particles and cause

atrophy
dryness of nose.

Stuffy nose is about the reduced outflow of blood from a nasal tissue i.e. isolated venous obstruction.
Even small obstruction (scarring) can lead to it.
I know no safe systemic medication that can prevent the change of vascular permeability of the nasal big vein.
Local steroids like Nasonex improve the recovery time by reducing the congestion when taken during long term - however, it cannot prevent the vascular permeability change of the large vein.
I have an intuition that the the nasal venous congestion can be relieved by the systemic lymphatic drainage massage by special movements involving

abdomen (attention to deep breathing with abdomen and exhale too)
supraclaviculus
under medial occipitalis
under auricles

which help to drain the accumulated fluid from the nasal tissues.
I know no substitute or medication to replace the stimulation of lymphatic drainage.
Prophylactics for the symptoms
You can oil your membranes but to oil them all even at the back side is difficult - even more difficult if have to have them oiled continuously.
So there remains some membranes unoiled.
I think it takes rather much time for the venous side to recover.
Therefore, you feel stuffy nose long time after the runny nose has ended.
Local oiling is not enough during cold and allergic times for many patients.
Some medicines for Prophylactics

Xylometazoline (Olynth) - cause atrophy and dryness, but good for stuffy nose
Quixx - sea water
Eucalyptus and vitamin E (Coldises spray for instance)

It's mainly caused by swelling of large veins and by an increase in vascular permeability that leads to an accumulation of fluids in the nasal mucosa. These effects are mediated, at least in part, by bradykinin and histamine, and can be counteracted by epinephrine. These mediators are part of the immune response to the viral particles.
You can read more about it here:

http://www.cardiff.ac.uk/biosi/subsites/cold/commoncold.html
Chernick-Mellins basic mechanisms of pediatric respiratory disease
By Gabriel G. Haddad, Steven H. Abman, Victor Chernick (page 520)

The stuffiness is due to edema or swelling of the mucous membrane covering the nasal cavity. The swelling is caused by vasodialatation or dialatation of the capillaries and leaky vessels which accumulate fluid within the mucous membrane.
The runny nose is mainly due to hyperactivity of the mucous cells of the lining which causes vastly more secretion than normal, triggered by the inflammatory reaction to the infection.


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Are humans evolving since their first appearance?
Is the evolution a very prolonged progress, or are we going to witness further evolution of the human species?
If so, in which direction? Are there any widely predicted changes for humans?

Sorry - posted the answer link (found it by searching for my answer to it!) http://biology.stackexchange.com/questions/5007/how-is-evolution-possible-in-contemporary-humans

also this one http://biology.stackexchange.com/questions/9739/are-there-any-scientifically-based-predictions-or-theories-of-future-human-evolu

Humans are still evolving.
If you have a proper understanding of evolution you will not doubt this....
What is evolution?

"Evolution means change, change in the form and behaviour of organisms
  between generations. ... When members of a population breed and
  produce the next generation we can imagine a lineage of populations,
  made up of a series of populations through time. Each population is
  ancestral to the descendant population in the next generation: a
  lineage is an ancestor-descendent series of populations. Evolution is
  then change between generations within a population lineage."

Evolution is simply a process of change, which Darwin called descent with modification. It is a change in trait values of populations over time. It results from four mechanisms: mutation, migration, drift, and selection. The first three lead to random change from one generation to the next, which may increase or decrease fitness, while selection will generally lead to adaptation.
How do we know evolution still occurs in modern humans?
Well human traits (characteristics like hair colour, height, eye colour ...) are often determined, to varying degrees, by genetic information. That information is passed from parent to offspring (inheritance) and that information can accumulate new variation (e.g. by mutation), while some variation can be lost from the population (by drift, migration, selection). These are the conditions required for evolution. Therefore, from one generation to the next, population trait values can change.
How will humans evolve in the future?
Difficult to say, evolution is a quite random process and difficult to predict. However, the process of adaptation (the result of genetic variation and selection) is a little more predictable. Following from the above, if there is genetic variation in a trait then there is a good opportunity for it to evolve by selection (Fisher's Fundamental Theorem). For example, we now see more women choosing to have children later in life, this means selection will be stronger against genes which cause early-life mortality in women and selection will favour genes that slow reproductive ageing in women.  Conversely, modern medicine is reducing selection against genetic diseases as we are better able to combat them, so we will probably evolve to show genetic diseases more frequently - selection against genetic diseases is weaker, therefore disease causing mutations can persist more easily in the population, see mutation-selection balance.
If you are able to prove that a trait is subject to selection and that there is genetic variation then you should be able to say that, in the short term at least, evolution in that trait will proceed in a predictable manner. Here are some posts (1, 2) about evolution in modern humans, open ended evolution, and why selection might not produce the predicted response.

Are humans evolving since their first appearance?

The idea of first appearance suggest an important misunderstanding. There is no such as a first appearance of humans (or any other species) that would not be arbitrary. The Homo lineage evolves and keep evolving but don't think of humans as being created at some point and then eventually evolving. Life came to existence 4.6 billions years ago and it is evolving and diversifying ever since but no species has ever been created anew.

Is the evolution a very prolonged progress

The only, non-arbitrary definition of evolution is a change of allele (=gene variant) frequency in a population over time. Such change occurs several times every second in humans. So evolution is constantly occurring. It really does not take much time. However, I realize that when layman ask "How much time does it take for evolution to occur" they mean something of the kind "How much time does it take for a previously absent phenotypic trait to come to existence in a population?". The problem is that the answer very much depend on what phenotypic trait and what are the selection pressures on this trait.

are we going to witness further evolution of the human spieces?

Yes, we had, we are and we will. Humans are still evolving and you might want to have a look at the post Human Evolution in Modern Times.

If so, in which direction?

In plenty of directions in the same time. Each phenotypic trait will evolve (not completely independent of each other though). There is no single direction for a whole species. You should therefore specify the trait of interest for the question to make sense. Again I think that the post Human Evolution in Modern Times will help you.
Want to have a basic understanding of what evolution is?
Understanding Evolution (UC Berkeley) is a free online very introductory course to evolutionary biology. It will help you to very quickly raise you level of knowledge of evolutionary processes.


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How to identify genes in Ralstonia that synthesize PHB and promote granule formation?
The compound polyhydroxybutyrate (PHB) is of considerable industrial interest as a biodegradable substitute for plastic. PHB is synthesized from glycerol by the bacterium Ralstonia eutropha. PHB accumulates to high levels in proteindelimited inclusion bodies called PHB granules that are thought to protect the compound from degradation. PHB stains with the blue dye polyphorin 3Z27, so Ralstonia colonies on polyphorin plates have a blue color when glycerol is present (and PHB is made), but a white color if glycerol is absent (and PHB is not made).
Since bacterium E. coli is not able to synthesize PHB, but it would be useful to engineer an E. coli that does so. What approaches can I use with E. coli to identify the Ralstonia genes that synthesize PHB and promote granule formation?

As far as I can tell the original results for this kind of question were presented back in the late 80s - early 90s: Poly-P-hydroxybutyrate (PHB) Biosynthesis
in Alcaligenes eutrophus H16, Cloning of the Alcaligenes eutrophus genes for synthesis of poly-beta-hydroxybutyric acid (PHB) and synthesis of PHB in Escherichia coli., Molecular basis for biosynthesis and accumulation of polyhydroxyalkanoic acids in bacteria.


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What is projected to go extinct first?
Though a number of animals have been going extinct at alarmingly quicker rates (so called anthropocene extinction), a number of 'star'  threatened animals are still alive.  Which of the following charismatic endangered species is modeled or expected to die off soonest: polar bear, panda, black rhino, african elephant, mountain gorilla,bengal tiger/ tiger.
Where can I find population projection models for each of these species?
Mountain gorillas  have the current smallest population,  but polar bears are clearly in  a lot of (and quickly widening)  trouble due to melting ice. African elephants are seeing species loss due to poaching,  and drying conditions making food/water scarce,  which could also speed their decline, but they have the largest of the populations.
Since WWF and other conservation organizations use these charismatic species to 'sell' conservation and raise interest, awareness and funding,  losing one (or many) of these species could affect conservation considerably. This will either be positively via a reactionary  disappointment by the public or negatively by losing a "poster species".

Welcome to Biology Stack Exchange. Your question needs some clarification in order to be answerable. The 'species' you have listed are in fact groups of species, each with their own extinction risk. For example, there are five extant species of rhino, of which three are listed as Critically Endangered by the IUCN. The IUCN Red List (http://www.iucnredlist.org/search) may help you to clarify your question.

Need to clarify species (what sort of rhino, elephants etc) and show some research effort (otherwise it's "homework") and the question needs to be leading to far more objective answers (will draw primarily opinion based answers).

@rg255 How's that?

Personally I don't think that's enough, you've just put some extremely rough guess. Get population numbers, trends in population decline/resurgence, show what is causing problems for each species... the fact you don't even know that black rhinos are more abundant than three of those species says you've made no effort whatsoever (it took me about three minutes to find numbers for all of your species).

I understand that black rhinos are not the rarest rhino species. My list is not attempting to be a list of the rarest (as indicated by the inclusion of the African elephant and tiger,  which both are only lasted as endangered with 1000s of individuals), but rather a list of commonly recognized so-called charismatic endangered/threatened species.

Further, I'm fully aware that rough population numbers are readily  attainable via wwf,  Wikipedia, iucn, and dozens of other sites. But again my question is not which is the rarest,  but rather where i can find population projections estimating time of extinction of these charismatic species. The rough guess i added was to show you i am aware of their relative threat level,  but again i didn't go into more detail because their absolute pop size is not important to me. I'm interested in their projected extinction rate/time/outcome

"I understand that black rhinos probably have the current smallest population" - they don't (populations of tigers, mountain gorillas, and giant pandas are smaller). If you make that as a claim then clearly you've not done any research.

To get specific projections for each species you will need to search the primary literature for each species. The best current estimate of extinction risk that is comparable between species will probably be the IUCN Red List classification.

@rg255 just looked at the wrong rhino species when i looked at the numbers. I've corrected.

Black Rhino, status: critically endangered
With around 5000+ black rhinos left in existence, and population numbers seemingly recovering (up from ~2400 in 1995), the black rhino is not really under any immediate threat.* The major threats to black rhinos is poaching (for the rhino horn trade), and, with prices for rhino horn increasing, it looks like it will be a problem for a while to come. Furthermore, corruption, war/civil unrest, easy access to guns, poverty, funding cuts (etc.) contribute to make the battle against poaching more difficult.
African Elephants, status: vulnerable
There are around 470,000 African Elephants left in the wild, and 25-30% of these are the Forest Elephant subspecies, so they aren't going anywhere soon.* Numbers are steadily increasing (~4% per year), although some populations are reducing. Poaching for ivory and bushmeat are signficant problems, but habitat loss and fragmentation is a massive issue. Elephants occupy a large number of habitat types and populations cover vast ranges, it is very difficult to protect an entire population range such that elephants could freely and safely move throughout their range (particularly at national borders), but things are getting better in many cases and efforts are ongoing.

An increasing number of transboundary elephant populations are co-managed through the collaboration of relevant neighbouring Range States. Large-scale conservation interventions are also planned through the development of conservation and management strategies at the national and regional level.

Polar Bear, status: vulnerable
Population estimates range between 20 and 25 thousand polar bears in the wild, and populations are on the whole fairly stable at the moment (in population studies, for populations where enough data was available, 1 grew, 6 were stable, 3 declined over a 12 year period). These animals are dependent on sea ice which, with human caused climate change, is rapidly declining. Climate change poses a more serious threat to polar bears. Relative to many things, like poaching and habitat fragmentation, it will take a very long time to reverse the tide; it may even be too late to prevent fatal damage to the polar bear habitat. They are also at risk from hunting, pollution, and habitat disturbance. Realistically, it is hard to predict when (or if) polar bears will go extinct because there is so much variance in the prediction of climate change and loss of habitat (sea ice).
Giant Panda, status: endangered
Less than 2000 pandas are left in the wild. Hunting and habitat loss remain to be enormous problems for wild pandas; masses of deforestation and fragmentation is occurring in their range. The chinese government has established >50 panda reserves, but this covers around ~60% of the population. The population trend is a decreasing one, which is serious cause for concern, and fragmentation of populations could reduce genetic diversity (increasing inbreeding depression and reducing adaptive capacity). Despite popular belief, pandas reproduce fairly well in the wild, it is in captivity that we have struggled, and that causes problems for breeding programs that can boost numbers and restore genetic diversity to sub-populations.
Mountain Gorilla, status: endangered
Fewer than 1000 mountain gorillas are left in the wild and populations are declining. Habitat encroachment, deforestation for the charcoal industry, bushmeat, and poaching are major issues affecting populations, and much has been fuelled by conflict (e.g. the 1990's war in Rwanda) in their range (in the last 20 years, 140 Virunga rangers have been killed trying to protect Gorillas). Also affecting them is human disease including the common cold which is often fatal to gorillas.
Bengal Tiger, status: endangered
Currently with a population of >2500, and with populations stabilising, and even rebounding in many areas (I was in Ranthambore last year, numbers have risen from ~20 to ~60 in the last 10 years), it seems the Bengal tiger is no immediate threat of extinction.* The major threats are poaching, population fragmentation, and habitat encroachment which leads to conflict with (and killing by) humans in the areas. Project Tiger is a major programme in India which has greatly contributed to successful growth in tiger numbers. The range of tigers is under increasing pressure from encroachment.
Summary
In summary, few models will be able to predict when or if any of these species will go extinct. Even if the short-term problems can be overcome, loss of genetic diversity prevents issues for the long-term prosperity of these species. Many of the problems are fixable in a relatively short time but will take a lot of effort and money, (such as poaching, hunting, deforestation) because they are mainly about cultural and social issues.
Climate change is perhaps more concerning because reversing the effects of human caused climate change will be extremely difficult (social and economic pressure), and slow to reverse; by the time we reverse the trend of rapidly declining sea ice it may be too late. Therefore, out of your species I'd say it's a close call between polar bears (despite good numbers they perhaps have the worst prospects of rescue) and mountain gorrilas (because numbers are so low and conservation projects are fighting difficult problems such as poverty and the effects of decades of civil wars and unrest). This article from national geographic suggests mountain gorillas may have as little as ten years left, while polar bears may be able to cope with some amount of warming, but the rate of warming is a major concern.** The WWF has also warned that pandas are not far from extinction.
What happens if we lose these species?
Many of these species are very attractive to the general public. The loss of some species would likely be worse than others; many of these are used to promote ecotourism and this would have varying effects for each. For the cases of black rhinos and african elephants many of these areas have many other species which are of interest to ecotourists (lions, leopards, cheetahs, white rhino, giraffe, crocodiles, buffalo, and many other mammals and birds, even sharks). However, if black rhinos went extinct then there would probably be losses in those species too (they face many of the same problems). Ecotoruism in the relevant areas tigers and pandas on the other hand are hugely important draws, India and China simply don't have the same diversity and abundance of highly sought after species with which to boost ecotourism should either go extinct (there are other nice species in these areas, but few are as highly sought as tigers and pandas). It's much the same for mountain gorillas and polar bears, these areas have less to fall back on should their species go extinct, so in many cases these species are of major economic importance.
That said, losing one or two of these species could cause some good. The outrage at losing some of the most popular animals in the world would be enormous. Funding for conservation and social pressure would likely swing massively more in favour of conservation efforts, making the fight to protect other species easier. Personally I don't hope we will ever have to rely on this strategy.

* Relatively speaking
** Strong selection may not get adaptive responses to occur quickly enough because generation times, standing genetic variation etc. such that while populations may adapt they don't adapt quickly enough.


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Dnase data for GRCh38
This question below turned to be completely faulty. I don't have to do anything with DNase data for GRCh38.
I asked it because of the file count difference between hg38 and hg37, which I thought to be too big.
For hg38 there're 95 files *Peak.txt.gz. For hg37 there're 236 *narrowPeak.gz, but after merging pairs PkRep1 & PkRep2 (probably FASTQ(SE/PE) reps) we get only 123 files. Finally, this difference (123 & 95) no longer seems to be big and we have even cleaner situation without PkRep1 & PkRep2.
One again: there's no problem with DNase data for GRCh38 assembly and only my question was misleading. I'd like to apologise for the confusion I introduced.

I'm interesed in transciptional activity, thus I'm willing to use DNase hypersensitivity sites to detect regions where transcription factors are allowed to bind.
In previous genome assembly GRCh37 / hg19 I used to use narrow peaks files from these two sources (University of Washington and Duke University, respectively) (files with suffixes .narrowPeak.gz):
http://hgdownload.cse.ucsc.edu/goldenPath/hg19/encodeDCC/wgEncodeUwDnase/
http://hgdownload.cse.ucsc.edu/goldenPath/hg19/encodeDCC/wgEncodeOpenChromDnase/
With the most contemporary assembly GRCh38 there're also some annotations attached (files with trailing Peak.txt.gz):
http://hgdownload.soe.ucsc.edu/goldenPath/hg38/database/
And here four complementary question arise:

Consider only datasets, which come from University of Washington.
For GRCh38 / hg19 I counted 236 narrow peak files, whereas for newer
GRCh38 there're only 95 files. How to explain this differene? Do the datasets represent exactly the same coverage, but with much lower granularity / precision (datasets that come for several tissue lines are merged into fewer files)?
With GRCg37 / hg19 we have both narrow peaks as well as broad peaks,
whereas GRCh38 comes with only one type of of file *Peak.txt.gz.
Does it mean that with the newest version we have only narrow peaks? Are the broad peaks hidden somewhere else?
With GRCh37 / hg19 we have two separate sources of DNase data: UofW and Duke. For GRCh38, it seems that only UofW datasets are availabe. Is any other source of DNase data available, maybe stored separately (Duke or other lab)?
Let's suppose that you're in my place and you would like to determine cis-regulatory areas. What type of data can be used to do so? Mabey DNase datasets but from other source or even completly different type of data (NOT DNase)?

Thank you in advance for your answer.

No need to apologize. Your question was very interesting actually and it will aid the future researchers a lot am sure! I would suggest you to revert it to OP

I am unsure that how much does it answer your question, but have a look at the homepage of DeltaSVM - In his work, Lee et al. have used similar datasets (only for GRCH37 I reckon) and I am sure they will address some of your queries.
As you yourself can better determine which dataset(s) are ones you need.


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Is the DNA different in each type of cell? What DNA is passed to offspring?
Our body contains many different types of cells and each of those cells have their own DNA (correct me if wrong) like skin cells their own DNA that makes them skin cells instead of muscle cells.
So my question is what DNA does a human pass down in a sperm or egg cell? Is it a specialised DNA imprint from which our whole body can be created?

Nope, you are incorrect here. Everey cell carries a complete set of genomic information, it is "only" differently expressed (read out). The only exception are egg and sperm cells, which carry only half a set of chromosomes (23 instead of 46) to be able to combine with their counterpart.

Only cells in the germ line are used to produce sperm and eggs, which are passed to offspring. DNA in all other cells (somatic cells) are not passed to offspring.

Most cells in a human body contain a complete set of the genome, which is two sets of 23 chromosomes. Having two of each chromosome is called diploidy.
Within an individual human the DNA is approximately identical in every cell. Different cells are produced by differential use of that DNA: certain genes are more (or less) highly expressed etc. You can read more about that here.

You inherit one copy of each chromosome from each parent. Gametes (eggs and sperm) are a bit different from regular cells because they contain one copy of each chromosome; they are haploid. These gametes fuse to make the complete set of 23 pairs in the offspring. There are some exceptions such as cytoplasmic DNA and sex chromosomes.

Good answer +1. You might want to indicate the following posts that will answer these questions: Why is there protein variation between cells without much genetic variation?, Do both parents really contribute equally? and Do our gene change as we age?.

For clarity (and due to misconceptions in the question), I think you should specifically mention germline cells (in contrast to somatic cells), and how only cells in the germline are used for reproduction.

I think you should also clarify that it's not actually the parent's chromosomes that are being passed on (looks like that in the figure), but rather a mosaic of their chromosomes, due to meiosis / crossing over.

so in a nutshell you can create a full body clone of a person from just about any type of cell's DNA ?

@user1062760  Well, you can't make a clone of a person from any type of cell -- that's not been done, it's not known how, and it isn't allowed, at least in Western countries.  But the concept is correct; mice can be cloned from skin cells, for example (http://www.pnas.org/content/104/8/2738.full).

Genetics is an evolving field : ) Concepts such as Horizontal Gene Transfer are important, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5379729/
Also the boundaries of the “body” may be considered, e.g. Obviously the DNA sequences of gut flora are distinct from the statistically major portion of DNA of human somatic cells, but are gut flora not an integral part of the body?  Sorry to answer a question with a question but such is the nature of philosophy. Another concept worth noting is microchimerism, a striking example of which is seen in the maintenance in females of a small sub population of cells in the brain and other organs that contain the DNA of former sexual partners; pregnancy specifically, often results in horizontal gene transfer with clear effects https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3458919/

Ideally, DNA itself is the same in DNA-containing cell types. Cell type depends on expression, which depends on epigenetics. I.e. histone modification, DNA methylation, and few other mechanisms.
Also, epigenetics is the mechanism for gene expression regulation. For example, it can silence (usually, methylate promoter regions) an expression of genes on one of the chromosomes in female cells. It's called genomic imprinting. In mammals epigenetics tags from gametes are not stripped after zygote formation.

Epigenetics is not only the mechanism to silence one chromosome in cats. It is the mechanism by which genes (and chromosomes) can be regulated by special enzymes. The regulation includes activation and silencing.

And DNA is not the same in each cell type; think gametes vs somatic cells, random mutations and cells without DNA (RBCs). This answer needs to be toned down.

So the removal of half the chromosomes from both parent cells happens as the zygote is formed and not before zygote formation right? otherwise you'd have a fixed set of chromosomes that are removed from each parent cell for entire species

@user1062760 a sperm and ovum are haploid cells so they have a single set of chromosomes. However an ovum becomes haploid in an oogenesis process so in the very beginning it was a diploid oogonum.

I agree with Chris. There are examples in which the gene network is capable of showing multiple types of stable responses (for two kinds this is known as bistability). Positive feedbacks, for instance, can show bistability without the involvement of additional epigenetic regulation. However, as you said epigenetic modification are essential for maintaining the differentiated lineage (a sort of memory which can be inherited). So, it would be great if you can improve your answer and also add some references.

Mitochondrial DNA is inherited mostly from the female line and is derived mostly from the ova. Mitochondria are present in all cells but retain genomes that are distinct from the host organism’s DNA, almost as if they are a separate single called organism. Here is an interesting look at mitochondrial DNA https://www.ncbi.nlm.nih.gov/pmc/articles/PMC19448/#!po=0.943396


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Evidence of species transitions
I had a debate with a person who believes in some kind of creativism, let's call it that way.
And in the middle of the "debate", an interesting question popped up.
What are evidences of "transition between species". Is there a fossil record that shows us the "transition".  I googled it and it was pretty obscure subject.
I would like to answer that question and really it "hits" my beliefs.

As it is, this reads like you are asking whether there is any fossil record at all for evolution between species, which I am pretty sure is not what you want to know. Can you clarify what you mean some more? What evidence would you accept? What transition are you looking for?

Speciation is a gradual and continuous process. A new species does not pop up in just one generation. It takes many. This, combined with the highly incomplete fossil record makes that transitions between two species are likely to be difficult to document. As YviDe asks - what are you after?

Also, what search term did you use to conclude that it is an "obscure" subject? The search for "transition fossil" or "transition species" gets a lot of good hits on the subject.

Welcome to Biology.SE. There are millions of evidence in evolutionary biology. You can find a long list of evidences on this post. However, the question is a little unclear for the moment and I don't really know which evidence would answer your question. I am voting to close as unclear.

You might eventually have a look at this post too.

Could you clarify what you mean by transition between species

People who think in creationism or think about species rigidly might have a bit problem with that, so let me describe an example:
When are humans "adult"?
Legally, at 18 (or your national equivalent). However, everyone understand that people are becoming adult gradually. Sometimes, they "age" very quickly after some harsh experience (16 years old student who parties all days because parents pay for it vs 16 years someone whom father died and he has work to help feed his small sisters as family did depend on father's wage).
Now imagine that you don't have all this information, but very incomplete "images" or "screenshots" of this kind of development. There would be quite a mess from it. You have image of one kid at 13 who is still young, another kid at 19 who is partying, single image of this 16 year old adult who has to feed his family and image of 48 year old gentleman.
If you go with this mindset that most of species that ever lived you can't get and you are just guessing something from a few snapshots that are themselves incomplete as well (e.g. we often don't have whole skeleton but just single bone from a lot of species), your idea on what to expect will change. This is a first step. Then you need to realize that most of fossils that shows some transition do not form lineage, but instead branches that are related. Finally, when you understand this (and modify your expectations and "what to look at", you can take any relatively complete and well-studied set of fossils like human ones. On human lineage (with great apes), we can see gradual increase of brain and in the case of human, gradual decrease in size of jaw. Development of hip bone is nice as well as it shows gradual process of adaptation to upright walking.
Another line of examples, but again, you need to redefine your expectations, is to point on dogs. If we had dogs in our fossil records, there would be large amount of species, instead of one "dog" species.
Or you can just point out at plants and say that "species" does not really mean anything.

I appreciate the analogy with adult age to explain why the question makes little sense.

@Remi.b: I don't think it's nonsensical question per se. Rather, you really need to know what you are looking for unless you will miss the elephant in the room. Furthermore, these "transitional states" show nicely how some systems have developed. Currently, I am working on some anthropological/sociological stuff and if you find these "transitional states", you might understand how particular cultural motive or practice did develop and reconstruct the actual process.


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Collecting virgin fruit flies
Suppose that you place P generation wild type males and mutant virgin females in a vial and allow them to mate. You leave this vial undisturbed in the incubator for 12 days. Could you collect F1 flies for your inter se cross out of this vial? Why or why not?

What do you think? If you don't attempt to answer or provide adequate evidence that you have tried researching your question, it will be closed as "homework" (although maybe not technically your homework, it signifies putting in adequate self-effort).

The answer depends which species (melanogaster, simulans, yakuba etc.), strain/population (e.g. Canton S, DGRP), mutant line (e.g. eb, CiD), food substance, larval density, and incubator settings (temperature, humidity etc.).
The rough answer is no, but if you clear the already hatched flies from the vial in the morning (~1 hour before lights on) and collect flies within a few of hours they should be virgin. Day 12 will likely be too late to collect many as most will have hatched at 25 degrees, at 18 degrees this may slow development but you should be certain that it will not affect your experiment, and report it properly in the methods. You could also collect and store them for a few days in single sex vials (all males or all females), then check the food that you store them in for larvae before using them, this helps to ensure virgins are actually virgins. If you find lots of eggs or even a single little larvae then throw the vial away. This also allows the females to mature properly, allowing them to eat some yeast and they will be more willing to mate when needed.
An experienced fly handler should be able to sort consistently enough to have just a few back up vials. If it is a beginner then make many vials with few flies in, this reduces the damage if a male slips through, it's much nicer to throw away a vial of 10 females than a vial of 100!
(Answer based on >7 years practical experience with D. simulans and D. melanogaster, collecting tens to hundreds of thousands of virgin flies in that time).


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What is the name of this berry producing tree?
I live in Middle Tennessee (USA) and came across this tree while I was hiking through the woods. I'm curious as to what type of tree this is and if the berries have any uses or are poisonous.
The tree is rather short, and I was unable to see any more distinctive features given that the tree was surrounded by other brush. I can supply a better picture in a day or two if necessary.

This is some type of Sumac in the genus Rhus. Probably either Rhus glabra (Smooth Sumac) or Rhus typhina (Staghorn Sumac). The berries of those two species are supposedly not poisonous. But they are closely related to other poisonous plants such as poison ivy and poison sumac. Poison ivy and poison sumac are in the genus Toxicodendron, but used to be in the genus Rhus.
A photo of Smooth Sumac


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Can we say the 'goal' of Mullerian mimicry is a 'decrease in the number of sacrificed indivials'?
Can we say that Mullerian mimicry allows two species to decrease their number of sacrifice individuals because:

Originally, one species needs to sacrifice some individuals to allow predators to recognize the warning signals (e.g., 10% of the population);
Another species, with a different set of warning signals, would also need this same population sacrifice (i.e., 10%);
Now, is the benefit of mimicry that, when two species share the same warning signals, each of those two species only loses half of the otherwise sacrificed number of individuals (i.e., 5% in the example)?

What is Müllerian mimicry?
Proposed by Fritz Müller, is when two or more species, which are both unpleasant to eat, poisonous, toxic, harmful etc. have similar colouration and patterns. A key point to note is that they have common (shared) predators. A classic example is the Heliconius genus of butterfly.
Why does it evolve?
The argument you make is kind of along the right lines, but it is a group selection argument, and is worded slightly badly as it insinuates that evolution is a goal driven process. I will use a toy example/thought experiment to explain why it's evolution is adaptive.
In this example there are three species of butterfly are toxic. We will call these species Butterfly-1, Butterfly-2, and Butterfly-3 (yeah, I'm not feeling very creative today). We also have a predator, a bird which likes to eat butterflies. We will call this species Bird.
Butterfly-1 and Butterfly-2 are very different to look at; they have different colours, shapes, and patterns. An individual Bird then eats one of Butterfly-1 and becomes sick. That individual learns to avoid Butterfly-1. Our Bird is then hungry again, and eats Butterfly-2, and again gets sick, and learns to avoid Butterfly-2. Two individuals die before Bird can learn to avoid both species.
Butterfly-1 and Butterfly-3 are very similar in appearance; they have similar colours, shapes, and patterns. An individual Bird then eats one of Butterfly-1 and becomes sick. That individual learns to avoid Butterfly-1, but also to avoid the similar looking species Butterfly-3. Likewise, if it eats a Butterfly-3 then it learns to avoid both Butterfly-1 and Butterfly-3. This is Müllerian mimicry. Survival is higher in one or both species because of more rapid learning by predators, fewer individuals will die compared to the non-mimicry scenario.
The essence of this is captured in the following statement from this paper:

"Müller provided what could well be the first formal mathematical model to support an evolutionary hypothesis. Following Müller’s original argument (1879), let $a_1$ and $a_2$ be the numbers of two approximately equally unpalatable (or otherwise defended) species in some definite district during one summer, and let $n$ be the number of individuals of each distinct unpalatable species that are killed by predators during a season before their distastefulness is generally known. If the species are distinct in appearance, then each species would lose $n$ individuals in the course of educating predators. If, however, the two species were exactly alike in appearance, then the first species would lose only $a_1n/(a_1+a_2)$ and the second would lose only $a_2n/(a_1+a_2)$. Under these conditions, a mimetic mutant of species 1 that perfectly resembled species 2 would tend to spread from extreme rarity"

Note that there may be caveats and complexities which I haven't discussed, this is a simplification to try and explain the general reasoning

I agree the wording issue; in the linked paper they talk populations, not species-level. +1

Is there a model that tries to simulate this? Although it seems obvious as the OP also noted, a mathematical (dynamical) model would provide a better explanation. I can see a mathematical expression. If possible can you add the full model description?