text:
Is it normal for corn to have multiple ears in one place?
I have (out of a mistake) one corn plant in my greenhouse and it made 4 cobs in one place. Is that normal?! I never saw something like this before.

Google 'corn bouquet' and ignore floristry e.g. https://u.osu.edu/mastercorn/bouquet-ears/

This is an example of "bouquet ears", or, what Rob Nielsen coined in his 1999 paper2 as "MESS Syndrome" (Multiple Ears on Same Shank).
Although not a regular occurrence, MESS syndrome is not unusual. According to Nielson in an online article in 2014 [my emphasis included]:

The fact that multiple ears sometimes develop from a single ear shank is not, in and of itself, physiologically unusual. Ear shank development essentially replicates the developmental pattern of the main stalk of the plant.

The ear shank is comprised of nodes and internodes just like the main stalk (Fig. 7).
Each node of an ear shank develops a leaf just like the main stalk, although we add the adjective "husk" to describe them.
The ear shank terminates with a reproductive organ (the female ear), akin to the main stalk terminating with a reproductive organ (the male tassel).
Secondary ear shoots can develop from individual nodes of the ear shank just like secondary ear shoots develop from individual nodes of the main stalk.

Normally, hormonal apical dominance exhibited by the primary or apical ear on an ear shank (or simple competition for photosynthates) suppresses the initiation or development of secondary ears at lower shank nodes. However, under certain conditions or with certain genetic backgrounds, one or more secondary ear shoots not only initiate successfully, but also continue to develop to the point that their presence is clearly noticeable. While the appearance of one or more additional ear shoots with silks emerging from lower husk leaves may not be attractive, I do not believe there is any real detriment to the plant by their existence as long as the primary ear is "normal".

Bonnet (1966)1 described this phenomenon in the 1960s and reports of occurrences happen periodically. In 2006, Nielson3 coined the "bouquet" terminology to describe multiple reports of out-of-proportional growth of multiple ears from single shanks in numerous midwestern farms.

According to Nielson:

The common factor in affected fields was some sort of damage to the development of the primary ear prior to or during silking that seemed to "set loose" the continued development of the secondary ears on the same ear shank.

An Ohio State University article suggests that the cause of this phenomenon is unknown, but Nielson is probably the expert:

Some hybrids may be genetically prone to developing multiple ears on a single ear shank. A threshold genetic trait may be triggered by particular stress events that occur during primary ear formation. Dr. Bob Nielsen at Purdue University has proposed that more than one external “trigger” may enable the development of multiple ears to occur on these hybrids. He has observed that the “bouquet” effect is more prevalent and severe in late plantings where silk clipping by rootworm beetles prevented kernel set on the primary ear (i.e., possibly minimizing or negating apical dominance against secondary ears).

You can see an image of a bouquet from one of Nielson's studies below:

 Source: Purdue Dept of Agronomy; Credit: Bob Nielson (2014)

1  Bonnet, O.T. 1966. Inflorescences of Maize, Wheat, Rye, Barley, and Oats: Their Initiation and Development. Univ. of Illinois, College of Ag., Agricultural Expt. Sta. Bulletin 721.
2  Nielsen, R.L. 1999. What A MESS! (aka Multiple Ears on a Single Ear Shank). Corny News Network, Purdue Univ. http://www.kingcorn.org/news/articles.99/990823b.html
3  Nielsen, R.L. 2006. A Problem with “Bouquets”. Corny News Network, Purdue Univ.  http://www.kingcorn.org/news/articles.06/Bouquets-0912.html.


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Why is there no toxic effect on the bulbuls feeding on Cascabella thevetia (oleander) nectar?
I have a huge Cascabella thevetia by my house and I know that its sap and fruits are extremely poisonous.However I have seen red vented bulbuls and wasps feed on its nectar.Also this confirms it but doesnt specify nectar infact it says plant parts...The same source says the poison affects vertebrates and the birds are definitely vertebrates.So why it doesnt affect them?

I realise that you are asking for an explanation, but note that the WP page that you link to specifically mentions that bulbuls aren't affected.

@Alan Boyd yes.they are'nt.why does it happen when it is so toxic to humans?what is that biological phenomenon that brings about this difference?That is exactly what I want to understand.

The toxicity of Cascabela thevetia is due to the presence of cardiac glycosides such as thevetins A and B. Although these compounds are highly toxic for humans and several domestic animals, other vertebrates are much less sensitive to them.
This review article discusses various aspects of oleander toxicity, and the authors draw attention to species-specific differences in toxicity.

In addition to dogs and cats, Szabuniewicz et al., (1972) also examined oleander toxicity in monkeys, goats, mice, rats and chickens. Dogs, cats, goats and monkeys were found to be very sensitive to the cardioactive glycosides extracted from dried oleander leaves. In contrast, the rodent and avian species were observed to be insensitive to oleander cardioactive glycosides.

They go on to suggest that differences in the toxin target molecule, the cardiac Na⁺,K⁺ ATPase, is the most likely explanation for this:

Akera et al., (1979) postulated that the low affinity between cardiac glycosides and rat cardiac Na⁺,K⁺ ATPases could be due to stearic constraints in substrate (glycoside) binding. In this scenario, quaternary conformation of the OL-subunit glycoside binding sites physically precludes the simultaneous binding of all three glycoside structural components. Species-specific quaternary conformation of Na⁺,K⁺ ATPases coupled with subtle differences in glycoside composition (e.g. various sugar moieties attached to the steroid backbone) could, thus, conceivably account for the observed species-specific responses to cardiac glycosides, including those found in oleander.

We have a tendency to assume that susceptibility to the toxic effects of plant materials is universal, but the toxicity of onions and chocolate for domestic animals are clear examples that this is wrong. The variation in sensitivity to the toxins in oleander is a good example coming from the other direction.
Shannon D. Langford & Paul J. Boor (1996). "Oleander toxicity: an examination of human and animal toxic exposures". Toxicology. 109 (1): 1–13. PMID 8619248. doi:10.1016/0300-483X(95)03296-R.

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text:
What is this large brown bug with pincers?
What is this large, brown insect with pincers? Seen in Waltham, Massachusetts.

You probably have a specimen of a stag beetle.
In Europe we have a very big one: Lucanus Cervus
but it seems to be absent in US.
Then I found an interesting web-site referring to the different stag beetle and mentioning the link to the European one.
In this above site, they mention you have to look into the antenna and as they are not very visible on your picture I think it would be difficult to define precisely what is the exact taxon of the one you found.
For specifically Massachussets region, I found this interesting link.
and they refers to Lucanus Cepreolus, but I would not be 100% sure it is this one as the antennas are not present on your picture.
References

http://beneficialbugs.org/bugs/Ground_Beetles/stag_beetles.htm
http://bugguide.net/node/view/3104/bgpage
http://www.insectidentification.org/insects-by-type-and-region.asp?

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Pronunciation of technical vocabulary
All knowledge of biology I have comes from online and after speaking for a brief period of time with someone from a biological education it is very clear that I have no knowledge of the pronunciation of all the necessary jargon I have learnt.
For example: Chordae Tendineae, Squamous Suture, Loop of Henle
How have people overcome this issue? I have searched online for pronunciation videos and whatnot, but very often they pronounce them differently to each other and it is impossible to know who is correct. I also do not want to learn the IPA for English.

"I also do not want to learn the IPA for English." - Yet this is clearly the best way to pronounce words where 1) you can find an IPA transcription for the word, and 2) you can't find a suitable audio source.

What's wrong with an online medical dictionary? E.g. hĕn′lē (sounds like HEN-lee), or  [kor´dah] (pl. chor´dae) (L.) Pl. sounds like CORD-eye. I learned by hearing other people, so no other good suggestions. Eventually patterns emerge, esp. because of all the Latin.

Don't know if it'd work for you, but I handle it by basically doing all my technical communicating in writing.

Come on guys! Let's use some 21st century technology.

I would try to use the audio features of dictionaries on the internet.
Ideally you would buy a good scientific dictionary app with audio pronunciation for your iPhone, just as I have for foreign language dictionaries on mine. However, the scientific offerings I found on the app store did not fit the bill (there may be something hiding there that I missed), so I looked on the web, and what I found was:
The Science Dictionary
Now this appears not to be an actual dictionary itself, but an aggregating site. So when I searched for Chordae I got several options, mainly from Wikipedia, which did not provide audio pronunciation, but also from
Dictionary.com
which did — for both the singular (which is what is the listing) and the plural.
Dictionary.com doesn’t always provide audio pronunciations. When I tried squamous suture there was only a definition — but there were individual pronunciations for squamous and suture.
(Loop of Henle was also there with pronunciation. Perhaps going directly to dictionary.com is your best bet.)
Rider and caveat
As @JM97 mentioned in a comment, some entries in the free dictionary have audio pronunciation, although others do not. There may be other on-line facilities that do likewise. However with any on-line dictionary one should ask oneself how reliable is the pronunciation; and it is difficult to tell because one doesn’t know how it is done in the way one does with a primary dictionary with a print reputation.
For example, take the pronunciation of the word "caeca". The open dictionary pronounces this in a classical Latin style with a hard C, whereas dictionary.com. pronounces it in a mediaeval Latin style with a soft C, the way it is pronounced by scientists I know who dissect it.

The free dictionary by farlex http://www.thefreedictionary.com/ is also very good.

@JM97 — I couldn't see any audio on the free dictionary.  Did I miss it somehow?

http://www.thefreedictionary.com/loop+of+henle see this example

Its a site which gives definitions from a large number of dictionaries including dorlands medical dictionary. just like science dictionary but the user does not have click an additional click.

@JM97 — Yes, I see there is an audio pronunciation for Loop of Henle, but not for Chordae Tendineae, which is why I had assumed it didn't support audio. (Also the app). I guess it varies. Another point is how reliable the pronunciations are. Compare the pronunciation of "caeca" on the open dictionary and dictionary.com. Better add a caveat to my answer.

It is also worth noting that in my experience, "accepted" pronunciation may vary quite a bit between biological disciplines and who a given specialist might have learned it from! For terms stolen directly from Latin, for example, there is often considerable variation between people about whether they should be pronounced in a Classical Latin style, an ecclesiastical/medieval Latin style, or (most commonly) an Anglicized style that sounds about right to an English-speaking biologist.
Names like the Loop of Henle are also tricky because they require you to know that they're anatomical structures named for particular people (in this case, Friedrich Gustav Jakob Henle), work out what language the person's last name is from, and then guess at what it is for an English speaker. English speakers do not always get this "right" on the first go, and weird pronunciations not infrequently result from confusions like this.
Personally, I wouldn't worry too much about it--I might just run pronunciations by a friend first and check to make sure I have them right there if I felt embarrassed.


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Which mushroom species is this?
Which type of mushroom is this? Hope the image has enough quality to allow answering the question.
Following community rules...

Images: please find below
Location: West-Northern Germany
Size - about 7 cm height, 5 width
Prior research: very hard to undestand which species is this, therefore asking here. Maybe this could be a Gymnopus peronatus - but here the stem is darker.
Specific characteristic: hollow stem

Please see here: https://biology.stackexchange.com/tags/species-identification/info including the specific info on mushrooms as well as all the other more generic requirements.

If you had a good book, you could identify that very fast. the particular features are, irregular stem, irregular widely spaced gills, no viscous pellicle on top, tan on top, grey gills, here is a identifier which might help: http://www.mycokey.org/agaric1.shtml?language=uk&localLanguage=uk&searchMode=full&atlasmode=false&r=132029.27384465246 there are other identifiers too. it looks quite unsuitable for a home ID for culinary, i've seen those already though, very common, i think they are related to the bright yellow ones with the grey gills.

google searching by image is giving me Russula integra.

You are probably right that it is a Gymnopus, It's difficult to know which one. There's also Gymnopus Fusipes. For a difficult ID, it's best to have a cross section, a description of the scent, compare the color under the youngest specimens, as the gills often change from very light to very dark with age.

Could you please provide some sort of support for the ID method claims you make? (I understand that they're likely based on your own experience. However, to be most helpful, providing reputable support that other users can explore really would increase the broader utility of your answer). Thanks!

Genus Amillaria species may be mellea

Hello, and welcome to Biology.SE. For responses to species identification questions, please be sure to include more information about your proposed ID, which may include common characteristics that resemble the OP, species distribution, and other general info. At least one picture is also strongly desired, with a link to its source. Thanks.

@atxgis citing reputable sources is also strongly advised, especially when referring to species IDs (since so much misinformation exists online!). Thanks

It has characteristics of a Chantrelle ; I would start there to identify it. Chantrelles are usually more orange or yellow but I have mushrooms in my yard that look very similar to the picture and after checking several references I believe it is a Chantrelle .

Definitely not a chantrelle, that should have decurrent ridges.

I never downmark but that's the worst ID i ever read, especially because it's dangerous. A chantrelle has round gill folds, and a trumpet gill base, it's smaller, doesnt go translucent or grey. There is a false chanterelle that is dangerous which has more in common with that mushroom. http://www.gallowaywildfoods.com/wp-content/uploads/2016/09/trumpet-v-sinuous-e1474988442548-900x1024.jpg common chanterelle: http://tcpermaculture.com/site/wp-content/uploads/2013/12/C_cibarius02.jpg

I was concentrating too much on the branching of the gills.However , been eating wild mushrooms for 40 years and I am still here.


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Which cells produce HCl produced in stomach? Don't these cells get destroyed by HCl?
Which cells produce HCl produced in the stomach? Or is HCl produced due to the translation of proteins. Don't these cells get destroyed by HCl?

Since your first question is a quite basic one (the answer is oxyntic cells) and asking two or more questions in the same post is a reason to close ("Avoid asking multiple distinct questions at once"), I'll address only your second question:

[Why] don't these [oxyntic] cells get destroyed by HCl?

First, it's important to understand that oxyntic cells (from the greek ὀξύς, meaning "sharp" or "acid") do not produce HCl. They actually secrete two separate ions, Cl− and H+ (and, since HCL is a strong acid, one can say that technically there is — almost — no HCL in the lumen, because the ions keep dissociated).
You can find this in any physiology book, but there is a good explanation of the steps in Scientific American (2017):

Potassium ions, K+, diffuse passively from the parietal cell into the lumen.
An active transport pump brings K+ back into the parietal cell,
simultaneously secreting H+ from the cell to the lumen. As much K+
returns by this route as leaks in (1).
Chloride ions, Cl−, diffuse passively from the cell to the lumen, and their negative charges balance the positive charges of the secreted H+.
An exchanger on the opposite face of the parietal cell balances this
loss of Cl− by importing Cl− from the blood in exchange for
bicarbonate ions (HCO3−).
Within the cell, water reacts with carbon dioxide (CO2) to form carbonic acid (H2CO3), which dissociates into H+ and HCO3−.

This image from Lodish (2000) summarises it very well:

Of course, the important factor in lowering the pH (and in eventually killing the oxyntic cell) is the H+ concentration, not the Cl− one. Regarding that, it's worth mentioning that, despite the H+ concentration in the lumen keeps rising, cytoplasmic H+ concentration is never as high as the luminal one, because H+ is being pumped out of the cell.
Second, why don't the HCl (actually Cl− and H+, as explained above) already present in the lumen destroy the mucosa? The answer is the mucus layer.
Still according Scientific American (2017):

HCl in the lumen doesn't digest the mucosa because goblet cells in the mucosa secrete large quantities of protective mucus that line the mucosal surface. Basic electrolytes, such as HCO3−, trapped inside the layer of mucus neutralize any HCl that penetrates the mucus.

By the way, a similar mechanism explains why doesn't the lysosome has its membrane destroyed by the enzymes it contains.
Sources:

Lodish, H. (2000). Molecular cell biology. New York: Scientific American Books.
Scientific American. (2017). Why don't our digestive acids corrode our stomach linings?. [online] Available at: https://www.scientificamerican.com/article/why-dont-our-digestive-ac/ [Accessed 30 Jul. 2017].


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Can there be an equilibrium between humanity's increase of carbon dioxide output with plants since plants harness CO2?
Is it possible that, prior to hitting a thermal equilibrium in the atmosphere, the increase in CO2 that humanity puts out every year will come to an equilibrium due to the consumption by the world's plants, which may respond by growing, reproducing and feeding more off of the additional CO2 in the atmosphere at a faster rate?

Wow this is one single long sentence! Do you mind splitting up your question is several sentences in the hope of clarifying it? Note that a forest at its climax does not intake more carbon than it outtakes. Plants intake carbon from the atmosphere as they grow but this carbon is being released when they die. Definitely, not all forests are carbon sinks.

Also consider that even if plants could lock the CO2 produced by mankind's use (which doesn't necessarily work that way as Remi.b notes), there's more deforestation and more urban development worldwide. We have less plants and trees so where will they come from? Plant growth is set at a certain rate by its genetic code even at optimum conditions. More CO2 doesn't speed up growth.

Well, what you should also consider isn't just the static environment that exists today, but rather how plants evolve, which maybe  to intake more CO2.

Oceans, rather than forests, are actually the largest carbon sink

Yes, with 2 caveats.
More CO2 encourages plant growth up to the local plants' limit. After that limit, the plants are saturated and extra CO2 backlogs into the air. If you intend to prevent atmospheric CO2 buildup, you're better off gradually supplying CO2 rather than deploying it in large surges.
The other caveat is dead trees and other plants that should be harvested or logged to make way for new growth (while providing lumber, fuel, and employment).


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Why don't mosquitoes target the visible blood vessels under the skin?
We can see numerous veins under our skin. Why don't mosquitoes suck blood from those vessels?
Why don't they use better option?

This is unclear. Where do you think mosquitos get their blood from?

they suck only plane skin but not the skin which is elevated by large vessels underneath it. Large vessels will definitely provide more blood.

Mosquitos suck blood from small capillaries. And they don't suck very much, only about 5 µl.

Why not from large vessels?

Is there a reason why you assume mosquitoes even have the ability to identify and attribute meaning to larger blood vessels that subsequently elevate skin? Also, why do you think that accessing larger blood vessels is "better", if the mosquito can obtain the same amount of blood from other, smaller vessels? Perhaps it's in fact easier for the mosquito to go undetected by accessing smaller blood vessels, due to the possibility of increased skin sensativity in the region of larger blood vessels. This is of course, just speculation/conjucture.

large blood vessels have more pressure so in less time mosquito can suck the required amount of blood and would also require less energy, since blood will ooze out unlike capillaries where the mosquito might have to suck actively.

@Test_1 I think you are assuming that the mosquito doesn't already experience the maximum throughput of blood from smaller blood vessels when harvesting. Conversly, it could be that the higher pressure from larger vessels is too strong for the mosquito, so they tend to harvest from smaller vessels. Lastly, I would like to assert that beggers can't be choosers, and I'm sure that (most all) mosquitoes will take blood wherever they can get it, just like with most other living (surviving) organisms behave when attempting to gather environmental resources (for whatever reason).

The smart mosquitoes that have been through a phlebotomy course do go after the large veins closest to the surface. However, at times, they mistake an artery for a vein, and blow themselves up. It's a nasty affair. Most mosquitoes who've witnessed this just stick with dermal capillaries.

@anongoodnurse What a sense of humour!

@anongoodnurse how do these mosquito pass on this information to next generation and the other mosquitoes of existing generation?( just for humour)

Related: https://pbs.twimg.com/media/BF_Ua1xCAAAKMYf.jpg :)

Perhaps for the same reason that you can drink from a drinking fountain, but not a fire hose :-)

For a mosquito, there is really no benefit to targeting those visible blood vessels. Mosquitoes take only a small amount of blood, and their proboscis is going to be a limiting factor anyways.
However, mosquitoes also aren't just blinding sticking their proboscis into the extracellular space. They actually do target individual vessels, and scientists have actually been able to video the process. Capillaries are good targets because they are found in all the tissues, so the mosquito doesn't need to find a surface vein.
See the videos with the original paper here: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0050464 (in the "Supporting information" section)
There are also versions on YouTube, like here:
https://www.youtube.com/watch?v=MbXSPacvuak
Choumet, V., Attout, T., Chartier, L., Khun, H., Sautereau, J., Robbe-Vincent, A., ... & Bain, O. (2012). Visualizing non infectious and infectious Anopheles gambiae blood feedings in naive and saliva-immunized mice. PLoS One, 7(12), e50464.

In the video , the mosquito is squeezing blood from capillaries so hard that capillary is collapsed, then why do you think that proboscis is a limiting factor?


text:
Are we deaf to water's taste/smell?
If we hold a rose in front of our nose for an hour, we can barely notice the smell after that duration, since the smell receivers ( Or the brain, I'm not an expert ) get used to it, and become sort of deaf.
Now my question is, are we deaf to the smell or taste of water simply because our body is consisted mostly of water and we are deaf to it, or is it because we do not have any receiver for this liquid?
If so, is this shared between all the living organisms?
UPDATE
By water, I mean pure water. Now what we practically have is never 100% pure, but a good place to start is distilled water.
I've come across multiple articles about this, but they lack of evidence and scientific proofs.
These are 3 of them:

Ask Anything: What Does Water Taste Like?
Does ordinary water really have no taste [...]
Water taste in man

Have you done any research into this, and if so, can you include it? And what do you define as "water"? Pure (e.g. twice distilled) water? Tap water? Spring water? Because water isn't pure. FWIW, I used to laugh at the bottled water industry; my well water tasted just fine. Until 15 years later when I had a deacidifier added, then I really disliked it (but still didn't buy it, just filtered it.) Recently I moved, and I refuse to drink what the township calls drinking water (tastes terrible!) I found a bottled water that I absolutely love. Anecdotal? Yes. Rare? Not at all.

@Jack Johansson like u said " body is consisted mostly of water " if this were true what implication would it have to bear gustato or olfactory receptors which would permanently be in its adaptive form (about which u meant by the smell of rose part) throughout one's life?secondly there are osmoreceptors in the hypothalamus and in kidneys too that handle body water content changes.

...besides there is a constant secretion of mucus in the nasal epithelium and saliva in the tongue both of which have water.so dont u think that water receptors (even if present) would always remain in adaptive state.Thus holds no meaning i think

Just anecdotat, but if you spend a lot of time in the outdoors in semi-arids areas, as I do, you learn to smell water.

@jamesqf i know what u mean...in my place (kolkata) summer temperatures can be as high as 45 celcius and u would literally love to smell the water of the first rain of kalbaiskhi...its a very nice feeling...but i think this too has something to do with the hypothalamus...its jst a guesswork though.

@CATHARANTHUS: Though I think you may mean something a bit different, "the smell you get after rain": http://discworldtour.tumblr.com/post/158020764568/then-rincewind-caught-the-smell-too-rincewind  But you can smell rain coming, too.

Related: https://biology.stackexchange.com/questions/41364/why-is-water-flavorless

It appears that little is known regarding how water is detected in mammalian mouth and throat. However, a recent study published in Nature Neuroscience(1) showed that acid-sensing taste receptor cells (TRC) participate in taste responses to water.
First, the team screened knock-out mice in order to identify which TRC were involved:

They used genetic knockout mice to look for the cells, silencing different types of TRCs, then flushing the rodents’ mouths with water to see which cells responded. “The most surprising part of the project” was that the well-known, acid-sensing, sour TRCs fired vigorously when exposed to water, Oka says. When given the option of drinking either water or a clear, tasteless, synthetic silicone oil, rodents lacking sour TRCs took longer to choose water, suggesting the cells help to distinguish water from other fluids.(2)

Then, the acid-sensing TRCs thus identified were artificially activated using optogenetics techniques:

They bred mice to express light-sensitive proteins in their acid-sensing TRCs, which make the cells fire in response to light from a laser. After training the mice to drink water from a spout, the team replaced the water with an optic fiber that shone blue light on their tongues. When the mice “drank” the blue light, they acted as though they were tasting water, Oka says.(2)

Source:
(1) Zocchi, D., Wennemuth, G., Oka, Y., The cellular mechanism for water detection in the mammalian taste system, Nature Neuroscience 20, 927–933 (2017) doi:10.1038/nn.4575
(2) Scientists discover a sixth sense on the tongue—for water, Science

Thanks for the links. However, it would be nice to include some important sections of the articles as quotes, for further visitors.

@JackJohansson I tried to do so. Hope it's better now. However, I don't quote the original study, because I don't have full access...

@JackJohansson If my answer is now satisfactory enough to you, will you please consider accepting it? Thanks! :)


text:
How is a portion of DNA selected and unwound from nucleosome?
If I understand this correctly during interphase most of the DNA strand is tightly wound around histones in the form of nucleosomes, to conserve space in the nucleus. Yet RNA polymerase in order to work needs a part of DNA to be temporarily unwound. How does the polymerase find the particular part of the DNA (and especially the promoter for a gene coding the protein needed to be synthesised) in this mass of tightly wound DNA?

I was told that during interphase the DNA is actually looser and more accessible to RNA polymerase, and that it is wound up in chromosomes only during mitosis?

Though this publication doesn't directly answer your question of how RNA finds a particular portion of DNA, it does address how DNA is unraveled from a previous, tighly wound conformation. https://pdfs.semanticscholar.org/64b4/a257e7263d54706521e6b06e527481928a97.pdf

This answer will be a very broad overview and is based largely on information from the textbook "Molecular Biology of the Gene" by Watson et al. (which I highly recommend).
Nucleosomes are dynamic structures.
The interactions between DNA and histones are non-specific and dynamic. Regions of DNA can be transiently unwrapped from the nucleosome and thus recognized by DNA binding proteins. In fact, because of the non-specific nature of the interaction, DNA can slide relative to the histone core and expose different sections of DNA. This can be facilitated by nucleosome remodelling complexes which can also catalyze complete ejection of histone octamers to expose even more DNA.
Nucleosomes can be positioned specifically.
The association of DNA binding proteins with specific sequences can prevent or control nucleosome formation at specific loci and leave tracts of exposed DNA accessible to the transcription machinery. Additionally, certain DNA sequences that form bent helices are preferentially bound by nucleosomes.
Chromatin compaction is highly regulated.
Two broad classes of chromatin are present in the interphase nucleus: highly condensed, transcriptionally inactive heterochromatin and less condensed, transcriptionally active euchromatin. Chromatin compaction is regulated by post-translational modification of histone tails, and modifications such as acetylation and phosphorylation, especially of the N-terminal tails, can prevent higher order, repressive chromatin compaction. The specific pattern of histone modification is referred to as the histone code and certain modifications are associated with gene expression. These modifications can be recognized by remodelling complexes and even transcription factors.
Further Reading:
Becker PB, Workman JL. 2013. Nucleosome Remodeling and Epigenetics. Cold Spring Harb Perspect Biol 5(9):a017905.

There are a number of different ways. The histone may be marked through some histone modification (a form of epigenetic modification) that relaxes the DNA and makes it more accessible.
For example certain forms of acetylation "remove the positive charge on the histones and decreases the interaction of the N termini of histones with the negatively charged phosphate groups of DNA. As a consequence, the condensed chromatin is transformed into a more relaxed structure" this then makes it easier for RNA polymerase to access it and find the promoter for example

Nucleosome is a structure formed when negatively charged DNA is wrapped around positively charged histone octamer.
Now, for transcription only one strand of  DNA is copied to RNA having polarity 3'-->5' known as Template strand, the other strand known as Coding strand (5'-->3') has same sequence as RNA (except thymine at place of uracil)
Promoter is located towards 5' end(all references are made with coding strand) while terminator end is at 3' end.
The presence of PROMOTER in transcription unit defines the template and coding strand. In transcription only a segment of DNA is copied.
For unwrapping of DNA there are special enzymes like helicases(for unwinding helix), DNA Gyrase(for relaxing strain and supercoiling), Telomerase and holoenzyme.


text:
Why won't this spray kill this bug (household insecticide); could it be so selective?
I have a can of bug spray. The label is in another language which I can not even type in order to do an online translation, but the ingredients are in romanized writing:
Metofluthrin  0.012% w/w
Phenothrin    0.100%
Cyphenothrin  0.100%

Wikipedia: Metofluthrin, Phenothrin, Cyphenothrin
I've been seeing small (3~4mm) dark flying bugs that seem to be able to take a direct hit. They may be grounded, but after a minute or two walking around and cleaning their wings, they fly away.
The spray worked very effectively on the cockroach I bought it for; this kind of thing happened about 90 seconds after a direct hit. Here they don't really infest as much as just wander in off the street and can't find their way out again.
I assume if I get rid of any residual sources of food or water the little flying things should die off. But I was really shocked to see them fly away undaunted after some serious aerosol action.
Here are some snapshots I took of the small bug trying to eat my spicy noodles. It's actually not so dark. Please please tell me it's not a tiny baby cockroach!

It's a tiny baby cockroach.  Sorry.

http://animalia-life.club/other/german-cockroach-nymph.html
I looked up your chemicals; the first (metofluthrin) is mosquito repellant and the others are for fleas and mosquitoes.  The combo makes me think that this is something intended for spraying on the body or on animals.  It is not strong enough.
You need to get a bigger boat.  Get a spray made for roaches.

aaaaahhhhhhh!!! OK thank you for the ID. It looks like I'll have a busy day today, starting with some shopping. I added a snapshot of the can. While the Wikipedia article for the last ingredient Cyphenothrin  says it's supposed to be for cockroaches, and the middle one "Phenothrin is the active agent in the branded product Raid Fly & Wasp Killer", this seems like a non-optimal mix now that I know the pest I'm after, and the repellant doesn't make sense to me. Thanks!

I've got them again, and these guys really spend a lot of time flying around like fruit flies do. They never get very big, and I think baby cockroaches don't spend their time flying around like this. So I've just asked Is this likely to be a type of fruit fly?


text:
Validity of the August Weismann mouse-detailing experiment refuting Lamarckism
Weismann conducted the experiment — described in Wikipedia — of removing the tails of 68 white mice, repeatedly over 5 generations, and reporting that no mice were born in consequence without a tail or even with a shorter tail. This was intended to refute the Lamarckian idea of of acquired characteristics.
However, surely five generations is too short a time to observe a change in an organ when the fossil record indicates that such changes in animals took millions of years. Was this not known at the time and does it invalidate the experiments?

This is not a site for discussions where people can exchange opinions, it is  site about biological questions, to which people give factual answers. Your question is particularly bad in that you give no literature reference to this experiment so if this question were on topic there would be no way for people to judge. And if this person (whom I know nothing about) was such a novice, why are you so concerned?)

@David It's a very famous experiment in evolutionary biology.

@BryanKrause — But it is not even referenced in the question and the OP is asking about a specific experiment. I am an intelligent scientist in a different area of biology and have never heard of this experiment and have no way of finding out from the question. Hence it is an unsatisfactory question on the basis of SE Biology.

@david "I am an intelligent scientist in a different area of biology" very honestly (no offence), that leaves you with very little right to say that the question is unsatisfactory for Biology.SE. I too belong to the field that you do, yet I know about this experiment. Also, how many questions have you seen on Biology.SE that are satisfactory to all the aspects of biology? As is clear from the wordings in question, it is about evolutionary biology, so biochemists, like both of us, are not supposed to answer this.

@BryanKrause — I am not interested in answering it, I am interested in understanding it. The question is incomprehensible to anyone unfamiliar with the experiment. I am fairly sure the experiment is within my comprehension, but, in either case the question does not allow me to find out. There is absolutely no justification for this and questions that ignore  whose posters ignore requests for clarification should be removed regardless of whether others recognise which Great White Chief is in the OP's mind. I am amazed that you can defend it.

@David That wasn't me you were responding to. My point in noting that it is famous is that if you Google, for example, "Weismann mice experiment" you will get dozens of results in the very top on exactly this experiment, even without any mention of tails, like referring to "Darwin's finches" or "Watson and Crick's (Franklin's) x-ray crystallography" - it's an experiment that many students of biology (even non-majors with just 1 bio course) would know, not just evolutionary biologists. You can still request the OP add some better referencing but your initial comment was quite abrasive.

@BryanKrause — Sorry. On my phone. But my initial comment was well justified. The whole tone radiated the arrogance of ignorance borne out by the poster's inability or unwillingness to document his question. And the title still presumes the answer in a most unacceptable manner. Why has nobody in the magic circle bothered to amend the question so it conforms to the SE model? I suppose I'll have to do it myself.

@another'Homosapien' — my comment to Bryan Krause was meant for you.

@BryanKrause — Actually see you have edited the question, presumably to describe the experiment. If so, well done. I'll fix the title and the last sentence when I have a moment.

I have started making your question acceptable by rewriting the title. Previously it was phrased in a manner that presupposed an answer ("Isn't" or "Wasn't") and involved a subjective emotive adjective — "senseless". As such it comes under the category of "What types of questions should I avoid asking?" — rant in disguise: “______ sucks, am I right?”. The revised version is neutral — "validity" — and actually indicates, for those not familiar with this Weismann, what the experiment was about.

I have now added a reference to the question (one shouldn't have to look for such in answers), added the purpose of the experiment and a link to Lamarckism, and phrased the query in a measured manner. If what I have written is not completely correct, could one of the elite take the trouble to amend it please. Rolling back to the previous version would do nobody a service.

@David I appreciate the changes you've made in the question. I'm just learning how to question at SE. Also, I'm an 11th grade student from India.

@David also, you'd find it surprising that this Germplasm experiment done Weismann is taught to every high school student here, right in the 11th grade. So, i presumed that it's famous enough (no offence)

@david oops, I wasn't defending the question. The question is, obviously, poorly written. All that I was saying is that 'I am an intelligent scientist in a diferent area of biology' doesn't necesaarily give an explanation for you saying that the question is about discussion and not factual answer. I didn't know I was indirectly defending the question (；一_一)

If you are reading this after 31st July 2017 it will seem somewhat disconnected from the question. This is because the question has been extensively edited since I wrote this answer.

Anyone who is interested in the work of August Weismann should start by reading the corresponding Wikipedia page.

Ernst Mayr ranked him as the second most notable evolutionary theorist of the 19th century, after Charles Darwin.

As far as the mouse tail experiment is concerned, we learn that Weismann was concerned with disproving Lamarckianism, and that:

Weismann was aware of the limitations of this experiment, and made it clear that he embarked on the experiment precisely because, at the time, there were many claims of animals inheriting mutilations (he refers to a claim regarding a cat that had lost its tail having numerous tail-less offspring).

My grandfather used to claim that his mother was frightened by a bear whilst pregnant, which was was why he was born with bare feet but that's more likely to be due to an epigenetic effect I suppose.

Added later in response to Remi.b
I see that Charles has already addressed this to some extent, but since I have already done the research I'll post what I found:
from August Weismann, Essays Upon Heredity. Clarendon Press, Oxford, 1889
(Volume 1, Chapter 8, p. 431)

But now, after this little digression, let us return to the transmission of mutilations.
We have seen that the rudimentary tails of cats and dogs, as far as they can be submitted to scientific investigation, do not depend upon the transmission of artificial mutilation, but upon the spontaneous appearance of degeneration in the vertebral column of the tail. The opinion may, however, be still held that the customary artificial mutilation of the tail, in many races of dogs and cats, has at least produced a number of rudimentary tails, although, perhaps, not all of them. It might be maintained that the fact of the spontaneous appearance of rudimentary tails does not disprove the supposition that the character may also depend upon the transmission of artificial mutilation.
Obviously, such a question can only be decided by experiment: not, of course, experiments upon dogs and cats, as Bonnet rightly remarks, but experiments upon animals the tails of which are not already in a process of reduction. Bonnet proposes that the question should be investigated in white rats or mice, in which the length of the tail is very uniform, and the occurrence of rudimentary tails is unknown.
Before this suggestion was made, I had already attacked the
problem experimentally. Such a course might, perhaps, have been more natural to those who maintain the transmission of mutilations, to which I am opposed. Although I undertook the experiments expecting to obtain purely negative results, I thought that the latter would not be entirely valueless; and since the numerous supporters of the transmission of acquired characters do not seem to be willing to test their opinion experimentally, I have undertaken the not very large amount of trouble which is necessary in order to conduct such an experimental test.

Nice quote +1. Would be great an original's Weissmann's quote as well. Also, you grandfather was a funny guy!

@Remi.b Thanks. I've added a quotation, as you suggested - it's rather long. The last sentence is a great put-down.

As has been mentioned, the study that you're referring to was conducted as to debunk the notion that mutilations (acquired characters) of a parent were able to be inherited by their offspring (referred to as Lamarckian theory). More specifically, Weismann set out to demonstrate that only germ cells contribute to inheritance. That, somatic cells are produced by germ cells, but that somatic cells do not influence the production of germ cells. Today we believe this to be true, and refer to it as the "Weismann barrier".
To provide a few quotes of Weismann from his Essays Upon Heredity:

If acquired characters cannot be transmitted, the Lamarckian theory completely collapses, and we must entirely abandon the principle by which alone Lamarck sought to explain the transformation of species,--a principle of which the application has been greatly restricted by Darwin in the discovery of natural selection, but which was still to a large extent retained by him.

..

I believe that I am able to show that the actual existence of transmission of acquired charaters cannot be directly proven; that there are no direct proofs supporting the Lamarckian Principle.

..

It can hardly be doubted that mutilations are acquired characters: they do not arise from any tendency contained within the germ, but are merely the reaction of the body under external influences. They are, as I have recently expressed it, purely somatogenic characters, viz. characters which emanate from the body (soma) only, as opposed to the germ-cells; they are therefore characters which do not arise from the germ itself.

So, the (currently accepted to be) mechanics of evolution and heredity most definitely weren't known during that time, but instead were just being discovered/established! As can be observed from the first quote, even Darwin wasn't fully convinced that Lamarckian theory was incorrect, though it directly conflicted with his own findings. Also during that time, Mendel was alive and conducting his own experiments. Pretty cool, huh??

Lastly, here's another (this time loosely translated) quote from Weismann regarding Lamarckian theory; one that I like quite a bit:

If you came across a case of an inherited acquired character, it's as if a man sent a telegram (written in English) to China and it arrived translated into Chinese.

Good answer. I edited the first quote to fix grammar. In sources I found, the actual essay didn't have these errors, but feel free to roll back.

[D]oesn't it take around millions of years for an organ to disappear or appear

No, not necessarily. But whether this claim is true or not is not so much the point of your question.
False Negative Result
Weismann did not observe an effect of cutting a rat tail on the length of the tail of rats at birth. It is what we call in statistics a negative result. Any negative result can be a true negative (cutting rat tail really does not affect the length of the tails in the offspring) or a false negative (maybe Weissmann had too a small sample size or maybe the experience should have been conducted on a longer time scale).
This is true for any experiment. It is the basis of the philosophy of knowledge. You can't show evidence of absence, you can only show evidence of existence. So, if an effect does not exist (if the result should be negative), then the only thing one can do is to fail to show evidence for the existence of this thing.
So, Weismann was in no way naive. Just like any other scientist, he just accepted the very nature of how knowledge can be acquired about the world. Actually, from @AlanBoyd's answer, Weissmann did comment on the limitations of his study.
This section was more about philosophy of knowledge than about biology. You should maybe learn a bit more about philosophy of knowledge, philosophy of science and typically about some key concepts such as Russel's teapot and evidence of absence.
So was it a false or a true positive
It was a true positive! We today understand a lot about genetic mechanism of inheritance and know that modifying the phenotype will not affect the DNA sequence (although it may affect the surrounding of the DNA sequence but this is a story for another time).
Introduction to genetics
You might want to follow an intro course such as Khan Academy > Classical and molecular genetics, Khan Academy > DNA as the genetic material and Khan Academy > Central dogma.


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UK - What type of spider is this?

Location: East Anglia, UK.
Approximate size (including legs at full span; like in the image): about 3cm.

It appears to be a Noble False Widow Steatoda nobilis

From http://britishspiders.org.uk/wiki2015/index.php?title=File:Steatoda_nobilis.jpg
It apparently is thought to be introduced to the UK, and there are some reports that the bite has caused some issues for some people.
https://en.wikipedia.org/wiki/Steatoda_nobilis

I had suspected as much but I wanted to see if someone else would come to the same conclusion. In fact the spider in the image you have provided is pretty much a carbon copy of the one I have shown (although mine had a smaller abdomen). I have caught ~5 of these spiders this year so far; all of which have reasonably small abdomens compared to what I would expect on a false widow; I'm assuming that makes them males? I have caught one with a very large abdomen which was unmistakeably a False Widow Spider, but that was 2 years ago.


text:
Does cocaine bind competitively or non competitively to DAT?
I was just wondering whether cocaine, once reaching a synapse, binds to a DAT (Dopamine transporter) competitively or non competitively, or neither of them?

Cocaine binds competitively to DAT, though not in precisely the same binding site, rather there is overlap, and many of the same amino acids are involved in binding of each.
Amphetamine and benztropines also bind in the same region.
Beuming, T., Kniazeff, J., Bergmann, M. L., Shi, L., Gracia, L., Raniszewska, K., ... & Loland, C. J. (2008). The binding sites for cocaine and dopamine in the dopamine transporter overlap. Nature neuroscience, 11(7), 780-789.

Just to further support this answer..from the last sentence of the abstract in the article: "Our data demonstrate the molecular basis for the competitive inhibition of dopamine transport by cocaine."

Is this overlap also present when dopamine binds to the dopamine transporter?

@ModoUnreal I'm not sure what you are asking- this is all referring to competitive binding with respect to binding of dopamine. When you have competitive antagonism you can't really bind substrate and antagonist simultaneously, that's the whole meaning of competitive binding: they sit in the same place.

As in does dopamine overlap with the dopamine transporter when it binds to it, like cocaine does? Apologies for the confusion.

Overlapping is referring to the binding sites for dopamine and the binding sites for cocaine on the transporter. Each binds to some of the same amino acids so we say they are overlapping. It doesn't make any sense to say whether either overlaps with the transporter: the transporter isn't binding itself.


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Which fish species is it?
Today we found this kind of fish on the shore of Baltic Sea near Gdansk (PL). It is a very thin "fish" with some kind of a needle in place of nose. It was about 5 cm long and very lively. What is the name of the species?

PS. Kids caught it into a bucket just to take a pic - we released the creature just after the photo session :)

I am super super sure it is a straightnose pipefish which is usually found in the baltic

Yes, but are such long needle noses common in that species?

This looks like a pipefish, possibly a straightnose pipefish.
See also. But the size suggests a juvenile?

Thank you @alan-boyd for your answer. The one you suggest has however much shorter "needle" than the one on my photo, at least compared to the photos over the web. Could it be Syngnathus typhle perhaps?

Agreed, that looks like a possible match, but size is still a problem. Mine was a quick-and-dirty answer - I assumed that a Baltic pipefish expert would be along to clarify. Without a better image you may never know exactly what species it was.

Hi. I also found Microphis brachyurus aculeatus on the web, which looks at most similar to the one we found. However, according to the sources, it does not appear in Baltic Sea , only in Senegal, Angola, etc...


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What animal does this skeleton belong to?
I was exploring around the outskirts of a local lake this afternoon (central Kentucky, USA), and came across the following skeleton:

The length of the remains is somewhere between 9-12".
Can someone tell me what animal this is from, and what part of the body it is?

It could be the synsacrum from a bird. 9-12" means it would have to be a rather big one. Goose?


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During acid reflux and vomiting, is the burning sensation from pepsin or acid?
When one's stomach contents enter one's esophagus, a burning sensation usually ensues. Is this from the enzyme pepsin breaking apart your cells or just from the acid?

It is the acid that causes the burn
Medicines like proton pump inhibitors (e.g. Prilosec), or H2 receptor antagonists (like Zantac) that reduce acid secretion reduce the burning sensation.  Medicines that neutralize the acid like calcium carbonate (e.g. Tums) also reduce the burn.  These medicines do nothing to the secretion of enzymes.
ADDENDUM. @anongoodnurse wants references.  Maybe in exchange she will remove that pesky down vote.
Cimetidine won the team that developed it the Nobel prize - the first rationally (as opposed to empirically) designed drug.  It was designed to very specifically reduce stomach acid.
https://www.acs.org/content/acs/en/education/whatischemistry/landmarks/cimetidinetagamet.html

Smith Kline & French's multidisciplinary research team first looked at
  the physiological cause of acid secretion. They confirmed that a
  molecule found in the body called histamine triggers the release of
  acid when it binds to a specific receptor (now called the H2-receptor)
  in the stomach lining. Their aim was to find a molecule that
  successfully competed with histamine in combining with the receptor,
  but then blocked, rather than stimulated, acid release. Such a
  molecule was called a histamine H2-receptor antagonist and represented
  a new class of drugs.

This and the successor class of drugs (proton pump inhibitors) are very specifically designed to decrease acid secretion and do little else.
The fact that billions of dollars worth of these drugs are sold means that persons suffering from reflux pain / stomach ulcer perceive that their pain is reduced by a decrease in acid secretion, and so are willing to pay.

Tagamet® was greeted with great enthusiasm by doctors and patients
  alike. Ten years after its introduction, it had achieved sales of one
  billion dollars and had become the world's number one prescription
  drug.

You need a source for this answer, and truthfully, the pathophysiology of reflux pain is incompletely understood.

@anongoodnurse - adequate references?

I didn't DV! Thought about it but didn't; commented instead. That's the problem with commenting when there's a down vote. :( People make assumptions. (I did DV the other posted answer, however.) But good job adding sources!

Actually, I also just decided to upvote because of the improvement of the answer. (I still maintain that the pathophysiology of reflux pain is incompletely understood.) But still, did not DV. Therefore my UV only counters one DV.

@sorry anongoodnurse.  Actions of any kind are sparse on these bio stack questions and I jumped to conclusion.  BTW: I appreciate the double entendre in your moniker.

Pepsin is a protein breaking enzyme which is most active in acidic pH. Stomach is protected from its effect by mucus, but oesophagus and larynx don't have much mucus so pepsin reflux will cause injury. So burning sensation is from both acid and pepsin.
{In contrast, if pepsin refluxes into the oesophagus and above it is damaging as there is no protective mucus layer and also the squamous tissue (the cells that line the oesophagus) is more sensitive. Research has shown that the surface cells of the larynx and airways are even more sensitive than the oesophagus to injury by reflux and pepsin specifically.} ( an excerpt from  https://www.peptest.co.uk/reflux-the-role-of-pepsin-explained/ )

Your source is a for-profit advert for a diagnostic test that measures pepsin. For profit sites are not a reliable source of information. It's true that pepsin most likely damages the larynx, but it's role in the pathophysiology of "heartburn" (typical reflux pain) has not been proven.

Read this https://www.hindawi.com/journals/ijoto/2012/646901/ Don't say that this is also for profit. Do you have any proof for your claim?

Yes, I do, but commenters don't need to prove they are correct. I actually read that paper you linked to in the comment before you commented; did you? It discusses the role of pepsin in damage of various kinds but not in symptomatology.

Its damaging along with acid so the burning sensation is cumulative. DO you have any proof for your claim?

Again, yes, I do. Your comment is only your opinion; your link doesn't support it. Did you know that a lot of GERD is painless? Sometimes the only symptom is a cough. I suspect pepsin may have something to do with that. Other non-pain symptoms also occur. Yet the acid (and pepsin) is there. Hmm.


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What is a good set of notes to study human's eye mathematically?
I want to learn about the human eye. I could read a lot of online literature about it.
However, ideally I would like to study human's eye by solving some maths exercises. I suspect people have done this before. How would we have glasses otherwise?
Maybe you know good maths notes + PROBLEMS that would give me an insight into how an eye works?
The notes don't have to comprise a whole course. One chapter is enough, as long as there are some maths exercises attached.

Mathematical models of the human eye

Fluid mechanics

Mathematics of Eye

Physics of blinking
Thin layer approximation (lubrication theory)
Aqueous flow in eye chambers
Tonometry

Those two links provide quite a sufficient description of how to mathematically describe/analyze the human eye. It seems that you need to be fairly familiar with (at least) differential, integral and vector calculus in order to competently study the eye, mathematically. If you can get through (and understand) the fluid mechanics then you'll be well off.
And as for practice problems, aside from the examples in those links, I'm not sure you'll so easily be able to find sets of mathematical practice problems that specifically describe the eye. Or at least, I wasn't able to find any such  repository.


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Rate of Diffusion Through Cellulose Membrane
From what I understand, the larger the molecular size, the slower the rate of diffusion and vice versa. However, after doing a lab (similar to this one) about diffusion through a cellulose membrane, my instructor said that despite substances having different molecular sizes, the rate of diffusion (thru the membrane) will be the same. Could someone further explain or did I hear incorrectly?

Yes, diffusion coefficient varies with molecular size, so it is difficult to imagine a mechanism whereby a membrane would precisely nullify this relationship, but could you describe your experiment in a little more detail?

@AlanBoyd
http://mayhewbiology.com/laboratory/Diffusion%20lab.htm
This is essentially what we did

I think that your instructor was wrong.
For the type of experiment that you describe the dialysis tubing (cellulose acetate with pores) is acting as a semi-permeable membrane which can block the diffusion of a polymer (starch) but will allow the passage of a small molecule (glucose). The molecular weight cut-off of the tubing was probably 10 kilodaltons or greater, so glucose (180 daltons) would diffuse through the pores without hindrance, as would sucrose (342 daltons). But would the monosaccharide and the disaccharide move through the membrane at different rates?
This table gives values for the diffusion coefficient (D) of these two sugars as:

glucose 6.7 cm² s⁻¹ × 10⁻⁶
sucrose 5.2 cm² s⁻¹ × 10⁻⁶

The time τ to travel distance L by diffusive movement is given by
τ = L²/6D
Here all that matters is that τ is inversely proportional to D, so we can estimate that glucose 'diffuses' approximately 30% faster than sucrose.
Bulk diffusion is, of course, driven by a concentration gradient: if you were to start with, say, 0.1 M each of glucose and sucrose in a dialysis tube the glucose should reach equilibrium with the surrounding liquid faster than the sucrose.


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How did giant sauropods satisfy their daily energy needs, considering their relatively small mouths?
Gigantic sauropod dinosaurs had relatively small heads (and consequently small mouths) in comparison to their overall body mass.
In the book "Dinosaur Odyssey: Fossil Threads in the Web of Life" (by Scott D. Sampson) the author says (on pp. 218-219) that

The sheer size of the biggest sauropods has long shrouded them in
  mystery. How could such gigantic animals with such small heads (at
  least compared to their body sizes) manage to consume enough food to
  sustain themselves? The mystery deepens when we look inside the
  mouths of sauropods. Cows are typical of big mammalian herbivores
  (e.g. elephants, deer, antelope, and the like) in possessing oversized
  teeth well suited for processing large amounts of fodder. Chewing
  serves not only to break food-items into bite-size chunks' it also
  grinds up the plant matter and begins the process of digestion by
  making the bits of vegetation more susceptible to chemical attack. By
  comparison, sauropods have puny teeth well suited to tearing or, at
  best, slicing, but not for grinding.

(emphasis added)
I don't remember Dr. Scott providing an explicit answer to the question "How could such gigantic animals with such small heads (at least compared to their body sizes) manage to consume enough food to sustain themselves?" but somewhere in the book he did mention that the earth's ecosystem may have been rather different back then.
However, since the book came out nearly a decade ago, I was curious on whether any other findings have been made since then.
How did sauropods manage to consume enough food to sustain themselves? Was it because of some differences in the ecosystem that are now lost?

Unlike mammals, saurischian dinosaurs don't have to chew their food. Like birds they have a gizzard to do that instead.
Look at a modern ostriches: they have a very small head because the head is only used to gather food not process it. Mammals process food in the head (chewing) so the head has to be large to support the muscles, teeth, and other apparatus for this. On the other hand, birds and sauropods use stones in the gizzard to grind up their food, so all that space is taken up in the torso instead of the head.  Ornithischian dinosaurs, which do chew, have large heads just like mammals.
Additionally since the mouth is not occupied chewing the time that would be lost chewing can be spent feeding instead. This can be a lot of time a cow spends 8 hours a day just chewing.
Source

Note several things:

Their long neck allow them access to a lot of food enabling to broswe with minimal movement and energy consumption.
The sauropods had very big and long digestive system, and they probably also used gastroliths. These allowed them to process the food without chewing it in their mouths.
I didn't relate to the question rather they were "cold blooded" or "warm blooded". If they were partially cold blooded (mesothermic) then they would need less food than a warm blooded critter of their size.
I guess the vast majority of their diurnal activity was eating... a lot.

Hope it helps.

What you say about high O2 is true for the Carboniferous. Actually through at least the Triassic and Jurassic, pO2 was below present levels. https://www.annualreviews.org/doi/10.1146/annurev.earth.31.100901.141329

Point 1 here is wrong, as @kmm says. Point 2 is speculation, based on an incorrect fact that doesn't lead to the conclusion anyway. Remove those and the remaining points would make a decent answer if any references were given; there are many references to support those points so it shouldn't be hard

I removed them.

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


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What would happen if some neurons are unmyelinated?
I know that cold receptors have myelinated axons and heat receptors don't.
From a physiological perspective, what could be the consequences if cold receptors were unmyelinated? Would that pose some detrimental effect?

i am not sure but human sensitivity to cold could become more than sensitivity to heat because the speed of impulse conduction would be higher in a myelinated fibre than an unmyelinated fibre...so coldness must be physiologically some how more detrimental than hotness specially if u consider enzyme activity and thermoregulation...

The nociceptors (pain including noxious heat and cold) are unmyelinated (and thus pain sensation is delayed). Usual sensory neurons are myelinated.

ASFAIK there is a fast component of pain which is myelinated, and this fast component include thermal and mechanical components.

Is your main question about cold receptors or about neurons in general (as your title suggests)? And exactly what do you mean with a detrimental effect?

From a physiological perspective, what could be the consequences if cold receptors were unmyelinated?

Per the resistor-capacitor model of a neuron, one would expect signals conducted through myelinated axons to be faster, more sharply localized in time (spikes don't broaden out as they propagate down the axon), and less costly of energy, vs in unmyelinated axons.
I wouldn't read too much into significance as there's all kinds of ways to accomplish the same effect at any level, e.g. faster conduction is also accomplished through larger axon diameter, and better temporal localization is also accomplished through signal coding, and energy consumption is also modulated by tweaking membrane composition of ion channels etc.

Would that pose some detrimental effect?

Generally, if it's normal for axons to be unmyelinated then one would expect things to be running normally. Demyelination of normally myelinated axons pretty much always leads to loss of function in sensation or motor control.
The question to ask here is rather "Would myelination of normally unmyelinated afferents pose some detrimental effect?" I'm actually not aware of any disorders in which there is "extra myelination" -- Even the dysmyelination disorders are all loss of function in the proteins, not extra insulating myelin or myelination in the wrong place. That doesn't mean there aren't overmyelination disorders, but does suggest that our nervous systems are less sensitive to overmyelination if it is a thing that happens.
One would expect conduction velocity and energy consumption to decrease, okay. Probably not an issue unless temporal synchronization in that signal is important; even then "plasticity" usually irons out these problems.
If the normally unmyelinated afferent axon normally has synapses homogeneously distributed along its shaft, then abnormal myelination could cause abnormal development of these synapses. As contact area would only be available between myelin "nodes," synapses would be crowded into smaller area. Also depending on how development works in the systems you're considering, overmyelination might affect the spatial pattern of secreted growth factor concentration which could affect synaptic development along the axon shaft. But this is all completely hypothetical.


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Are there animals who do things just for pleasure like humans?
In a debate my father said that only humans do things that are not directly linked to survival(painting, playing musical instruments, singing etc). He said that this is because we are "special" and not like other animals on the planet.
I said that this is only because we have much more developed brain than other animals. But now I'm also interested in one question.
Are there animals who do similar things(not exactly same, of course) not for mating/survival but just because they like it?

My answer (here in the comments, because if I write a real answer I'll get a bunch of downvotes very fast): all mammals and birds do things for pleasure, that is, just for fun and not related to survival. All mammals and birds have consciousness, and self-aware animals do those complex behaviours. Besides that, since it's possible that consciousness is a feature not only of mammals and birds but of all tetrapods or even of all vertebrates, the answer can be still more inclusive.

Isn't there an argument to be made that art is simply a form of sexual display? (Although I'm not making it!)

Dolphins and some whales blow toroidal vortices: https://www.youtube.com/results?search_query=dolphin+toroidal+vortices

There are many species of animals that purposefully get intoxicated (waiting for fruit to be a certain chemical composition during specific seasons of the year), as well as indulge in sexual foreplay (fellatio/masturbation). I'd say those two activities are (mostly) for pleasure, and don't have as much to do with direct survival strategies.

Why does my dog bring me a stick (tennis ball, Frisbee, &c), and keep poking me in the knee with it, or toss it at me and bark, until I relent and throw it for him to chase and bring back?

@jamesqf - Can it possibly be that, like humans, they want to have some purpose? My Border Collies think their purpose is to herd tennis balls, and they definitely want to work. My new dog just wants to play with squeeky things. I don't know what's up with that. I've had border collies for too long.

@anongoodnurse: And work (or at least certain sorts of work) isn't a pleasure?  And my border collie/Aussie mix loves to chase tennis balls, but won't bring them back.  She just lies there with the ball between her paws, grinning.  Now if that isn't pleasure, I don't know what is :-)

@jamesqf - Absolutely it's a pleasure. BC/Aussi: "No take ball! Just throw!"

@anongoodnurse: Though in her case, I think it's more like "Well, I chased the ball over here, now it's your turn to walk over and get it.  Fair's fair!"

Show your Dad this video of a Panda playing in the snow. It seems obvious to me that she is sliding down the hill just for the fun of it. https://www.nbcwashington.com/news/local/giant-panda-family-tumbles-around-in-snow-at-smithsonians-national-zoo/2556848/?amp&fbclid=IwAR20D6QAMTHaqRZnuo39GtWx6DZaO6Xi70xNUeHcG18rkwmiGuZVoN3CmQM

I see that Gerardo has said effectively what I was going to: animals don't do things because they have reasoned out that these things will help them survive; they engage in behaviors because these behaviors lead to reward circuitry response and animals who find general categories of behavior rewarding have tended to survive better. Sometimes behaviors that are not directly related to survival trigger the same circuitry.
(P.S.: this is exactly what is happening in humans, too.)
Masturbation is one example, as above; so are animals that 'adopt' either conspecific or heterospecific juveniles who don't belong to them, which is not uncommon in many species. (Barn cats in particular do this often; aside from all the cute Youtube pictures of cats who think ducklings are kittens, it's very common for queens with kittens about the same age to co-nurse them.) You can argue that sociality and taking pleasure in altruistic activities with no immediate personal benefit is a survival adaptation, but that's not a calculation the animal is consciously making at the time.
Animals often have strong aesthetic preferences, especially for conspecifics; female and male animals often prefer traits that don't have anything obvious to do with survival in potential mates, and there is an entire discipline of sexual selection in biology devoted to teasing out why. It's worth noting, however, that in many species it turns out that females have preferences that vary widely for a number of traits, and that female preferences do not always line up to male reality...
Outside of naturalistic social behavior, numerous examples of elephants and chimpanzees creating drawings or paintings in their enclosures without any conscious reinforcement from their keepers have proved interesting reading. There are also examples of animals who keep "pets", including the famous case of Koko the gorilla and her pet kittens. You may find this article, with descriptions and citations of several animals who may or may not be engaging "art" for its own sake, to be a useful read.

Thanks for reply, it's very interesting. Where can I find free researches(can only read abstract in last link) about animals who do art "without any conscious reinforcement from their keepers"?

I'd check ResearchGate or #icanhazpdf on Twitter.

Arguably, yes.  There numerous species of non-human animals which have been observed to masturbate wikipedia.  Non-human animals will frequently choose less-healthy foods over healthy foods.  (Offer a cat a raw fish and a can of tuna, most of them will choose the canned tuna every trial even though a diet of only canned tuna would be disastrous due to the high salt content.)
Arguably, these are just instinctive behaviors firing outside the ideal circumstances, but that plus endorphins or species-specific analogues may be as good a definition of acting purely for pleasure as any.


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Identify this insect
Please help identify this insect - genus, species and anything interesting about it. Also - please outline your general methodology for identifying such insects
Note, this is posted separately due to comments in this other thread.

Which previous thread? Your link doesn't point to a previous thread, it points to https://i.stack.imgur.com/FtdoD.png.

@arboviral https://biology.stackexchange.com/q/64042/1486

You should add the location for all species ID questions.

It is a long-horned beetle in the genus Anoplophora. Most likely A. chinensis, A. macularia or A. oshimana.

Okay, to identify to Order level you can use the key here (although it's actually not as user-friendly as I'd expect; I might suggest they revise it). The key characteristic is that the forewings are uniformly hardened. So, starting at question 1:

"Insect has wings" - yes; go to 2.
"Two pairs of wings" - yes (wing cases/elytra are the first pair); go
to 7.
"Fore wings hard or leathery" - yes; go to 8.
"Fore wings of uniform texture throughout" - yes; go to 9.
"Fore wings (elytra) hard and veinless, meeting in centre line" -
yes; go to 10.
"Abdomen without forceps: elytra commonly cover whole abdomen =
Coleoptera [beetles]".

So we know it's a beetle.
There's a key to beetle families here. Starting at question 1:

antennae are "clubbed or thickened" so go to 5.
"Elytra covering all of abdomen" yes, go to 7.
"Head not stretched forward into a beak" - go to 9.
"the last few segments [of the antennae] clearly wider than the rest" - no, so go to 24.
the elytra (wing cases aren't "soft (easily bent, folded or even
rolled up)" so go to 28.
this is a tricky one, but basically you can (just) see that all the tarsi (feet) have the same number of segments, so we go to 29.
29: "      Beetle usually elongate and parallel-sided; antennae very long often longer than head and body; most antennal segments very elongate (at lease twice as long as wide)" - sounds like our beetle, so that makes it a longhorn beetle. (Some of the other criteria - eye nothces etc - only apply to some species, but this key is a UK-specific one).

So we have a longhorn beetle (Coleoptera: Cerambycidae). In theory you shouldn't need to geographical location to get this to species level as it could be an introduced species etc; in practice most keys are specific to certain geographical regions so you might need to provide the collection location to get it to species level. You could start by Googling "longhorn beetle identification key" and give it a go though.

Well done, nice research made... +1

From overall appearance, it also looks like an Lamiinae (flat-faced longhorns).

@fileunderwater overall appearance?

would this fit the bill of Asian longhorn beetle?

@ina Flat vertical face, robust, reniform eyes etc. Still thousands of species to choose from though.

any advice on how to narrow down on the species?

Or you could just look at the picture and say "that's a longhorn beetle"


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Plant identification in UK
I need some help identifying this plant please. It is summer flowering in the UK. Its height is approximately 30cm, flowers approximately 2cm across.

I'm drawing a blank. Any chance of showing us the leaves? Is it a wild flower? Could it be a garden escape?

Unfortunately I have no better images which show the leaves Alan, however I think I may have managed to identify it after much searching. I do believe it is a variety of Viscaria oculata. I sincerely appreciate you going to the trouble of responding and trying to help though, thanks very much!

This plant has been identified as Viscaria oculata.


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Can solitary animals show extroverts traits?
So far as it is known there are solitary animals and social animals.
Does introversion exist among nonhuman primates? says that there are introverts among social animals:

Recent studies have identified extraversion/introversion in great apes, including chimpanzees, gorillas and orangutans. Chimps exhibiting greater solitary and reserved behaviors are considered more introverted, whereas those that are more playful and interactive fall on the extraverted side of the spectrum. Extraversion/introversion behaviors, such as sociability, have also been identified in species of monkeys.

Are there extroverts among solitary animals? I mean those who seek union with others although the vast majority of animals of their species are solitary?

I don't think it makes sense to talk about extraversion/introversion in anything but social animals; those are also quite anthropomorphized terms (though I have no problem applying them to other primates).

So solitariness vs sociality in animals is a little more complex than we usually give it credit for. For example, even in species previously thought to be largely solitary except for mating, sustained observation and tracking often shows that previously assumed to be solitary individuals actually do interact and sometimes develop lasting social relationships with conspecifics, just not at times when people are observing them. This is a particularly common finding in nocturnal animals among males who are assumed to be solitary, such as buck deer who turn out to be more social than does--just primarily at night!
That Wikipedia article you cited for 'solitary animal' is actually pretty shitty when you get down to it; the list of "solitary animals" include several generic terms for animals that include common species known to have variable social systems depending on region, such as badgers, moose, jaguars, cheetahs (in whom males, often brothers usually form lasting social relationships), red fox, and devils, who actually encounter each other quite frequently over kills and scavenging sites. (Citations are listed in this Collabedit file, because Stack Exchange is yelling at me for trying to provide actual links.)
In that context, I don't think many people have done behavioral syndrome/"animal personality" work on sociality, because it's not a particularly good thing to measure--you're really measuring something more like 'aggression threshold.' People have done work on species like social spiders where sociality varies significantly between individuals, however.


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Is diabetes (type 2) a genetic disease?
My friend's father has diabetes (who was diagnosed with diabetes long after my friend's  birth). The doctor told the friend that he has more chances of getting diabetes than a normal person and he must make lifestyle changes as he is more likely to get the disease. Does it mean that diabetes is genetic (hereditary)?

According to Wikipedia there is a genetic component to the risk of developing type 2 diabetes. The page cites this source at the US National Institutes of Health. There is also a Wikipedia page on genetic causes of Type 2 diabetes

Does it mean that diabetes is genetic (hereditary)?

Yes, Type 2 Diabetes most definitely contains a genetically inherited component. However, there is also a very strong environmental influence, which is the reason why your friend's doctor recommended that your friend change his lifestyle (because the onset of T2D is heavily determined by environmental factors, and is by no means 100% genetically predetermined).

According to the World Health Organization...
Genetics in the Development of (Type 2) Diabetes

It has long been known that T2D is, in part, inherited. Family studies have revealed that first degree relatives of individuals with T2D are about 3 times more likely to develop the disease than individuals without a positive family history of the disease (Flores et al., 2003; Hansen 2003; Gloyn 2003). It has also been shown that concordance rates for monozygotic twins, which have ranged from 60-90%, are significantly higher than those for dizygotic twins. Thus, it is clear that T2D has a strong genetic component.

Environmental Risk Factors

The major environmental risk factors for T2D are obesity (> 120%
     ideal body weight or a body mass index > 30 k/m2) and a sedentary
     lifestyle (van Dam, 2003; Shaw and Chisholm, 2003). Thus, the
     tremendous increase in the rates of T2D in recent years has been
     attributed, primarily, to the dramatic rise in obesity worldwide
     (Zimmet et al., 2001). It has been estimated that approximately 80%
     of all new T2D cases are due to obesity (Lean, 2000). This is true
     for adults and children. In the Pima Indians, 85% of the T2D children
     were either overweight or obese (Fagot-Campagna et al., 2000).
     Another study in the US reported that IGT was detected in 25% of
     obese children age 4-10 years, and in 21% of obese adolescents (Sinha
     et al., 2002). Undiagnosed T2D was detected in 4% of the adolescents.

..

The other major T2D risk factor is physical inactivity. In addition to controlling weight, exercise improves glucose and lipid metabolism, which decreases T2D risk. Physical activity, such as daily walking or cycling for more than 30 minutes, has been shown to significantly reduce the risk of T2D (Hu et al., 2003). Physical activity has also been inversely related to body mass index and IGT. Recently, intervention studies in China (Pan et al., 1997), Finland (Tuomilehto J et al., 2001) and the US (Diabetes Prevention Program Study Group, 2002) have shown that lifestyle interventions targeting diet and exercise decreased the risk of progression from IGT to T2D by approximately 60% . In contrast, oral hypoglycemic medication only reduced the risk of progression by about 30%.

That being said, I would strongly nudge your friend in the right direction, and start asking them to go on walks or bike rides (with you), and remind them from time to time to drink less sodas and processed foods (assuming that they do).
Just as a side note, the American Heart Association recommends that only an additional 36g of sugar be added to your daily diet (for an adult male; 25g for adult female).

The trouble with questions like this--"is this disease genetic?"--is that diseases are complicated phenotypes that arise from interactions with both individuals' genetic makeup and also the changes in gene expression that happen as a result of the environment of that individual over their lifetime.
To put it another way: neither nature without nurture nor nurture without nature are particularly interesting, because the first amounts to a little vial of DNA in a microcentrifuge tube and the second amounts to, uh, a whole lot of nothing.
In the case of Type II diabetes, there is both a strong environmental component--persistent obesity in humans is so likely to lead to diabetes that one of the two original mouse obesity model strains was named 'db' for diabetes--and also a genetic component that affects the likelihood of developing Type II diabetes in a number of ways. Some genetic variants may be less likely to develop obesity even under the high-fat diets that typically are used to create obese phenotypes in mice. Some variants may be more or less likely to develop insulin resistance even in the presence of high levels of adipose tissue. Both of these variations would affect your likelihood of getting Type II diabetes... depending on your environment and the level of body fat you carry, and that last one is going to be dependent on not only your genetic makeup but also your environment and (almost certainly) epigenetic influences from your parents.
With respect to Type II diabetes and actual specific genetic variations that have been identified, there's the twin study cited in another answer here, which was done in Danish twins and really just looked at whether there was a genetic component done at all. GWAS studies have, predictably, resulted in several candidate loci, all with relatively small effects on risk--which makes sense, because metabolism is a complex thing and many players are probably involved in competing roles. (I'd link more, but I'm new here--hitting up a Google Scholar search for "type ii diabetes genetic variance" nets you a whole bunch more GWAS studies talking about specific types of variation noted.)


text:
Longest pathway from sensory to motor neurons

How long is the longest pathway a neural signal can take starting from a
  sensory neuron and ending at a motor neuron (without loops)?

[This is a purely theoretical question concerning only the synaptic connectivity of neurons, not the propagation of real signals.]
The number I am looking for must be greater than 8 because there are 6 layers in the cerebral cortex and 2 layers of motoneurons: upper motor neurons and lower motor neurons.
The question then reads:

How long is the longest pathway from a sensory neuron to layer I of
  the cerebral cortex?
How long is the longest pathway from layer VI of the cerebral cortex
  to an upper motor neuron (which may lie in the brain stem)?
How long can be "detours" inside the system of layers of the cerebral
  cortex?

I assume that the cortex is not strictly layered, so that a neuron in layer $i$ normally projects on a neuron in layer $i+1$ directly, but possibly also via $N$ interneurons. Theoretically, the upper bound for $N$ is just the number of neurons in the brain, but in practice will be much smaller. To get a sensible number, it may be necessary to neglect detours that are too long because they are too sporadic and/or useless. (But how to define and quantify sporadicity and usefullness in this context?)
If my question doesn't make sense in the way I ask it here: How could I improve it to make it sensible?
[Of course, I am not looking for exact numbers but only for estimates, resp. estimates of lower and upper bounds.]

Theoretically the number could be huge, if you include both the sensory and motor cortices, plus cerebellum, memory areas for specific activities. But much of the processing will occur in separate areas. Would you count every synapse involved? Or every neuron? Given that a neuron can have 1000's of synapses, not all of which will be involved in the specific action. It might help to think of a specific pathway/action, e.g. reflex response to pain, sight, sound. Or a non-reflex, e.g. a chosen response to a given stimulus.


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Blood transfusion
Can we exchange the antigen present on membrane of RBC's so that it can be transfused from one person to other ?
As we face problem to find  required bloodgroup at the time of emergency especially O negative. So can we have some other technique to simplify our problem ?

In theory it's possible to change the blood types A & B into O, since the antigens for them have longer sugar chains than the O antigen (as seen on this picture from wikipedia). The problem is finding a  way of actually removing this extra sugar molecule(s) without destroying the viability of the blood cells.
An attempt was once made by a student team in the iGEM competition, but they were not successful - I don't know if anyone else ever tried it.

To be clear the iGEM team was partially successful they did remove most of the antigens,  but removing all the antigens present in the blood required an impractical amount of the enzyme being used.


text:
Mutated cell proliferation
Reading Jennifer Doudna's fascinating book on CRISPR. So she describes rare cases where a mutation in a single cell removes the gene responsible for a genetic disease. The cell proliferates and the disease is cured. What I don't understand is--aren't all the aberrant cells also still dividing and passing on the harmful mutation to their progeny? How does the single healthy cell edge out all the other cells to "cure" the patient.

There are some diseases in which a minority population of normal cells can rescue the organism, even in the presence of a majority of mutant cells.  Sort of like a group vacation to Kazakhstan with one friend who can speak Kazakh.  Very different experience from a vacation where none of you speak Kazakh.
Take for example hemophilia A.  Cells have a mutant gene for factor 8.  Without factor 8 blood does not clot properly and people have bleeding trouble.  You do not need much factor 8.  Just a little bit can prevent spontaneous bleeds.  People who are heterozygotes for hemophilia A (carriers) are fine at 50% normal.  So if you edited mutant liver cells such that they could produce factor 8, even if they were only 10% of the total cell population of the liver, having some factor 8 would sidestep the full hemophilia phenotype.
Likewise metabolic mutants - some children are born unable to handle certain substances.  Phenylketonuria is the one you read about every time you drink a diet coke.  If a minority population of cells could be produced that were able to handle phenylalanine, those would rescue these kids even if most of the cells still could not.

Are you talking about people?
Because in bacteria, a mutated bacterium with a beneficial mutation will definitely edge out the competition, or if it is in a "good mood" (cell humor lol) it will share its DNA with the other bacteria.
You're absolutely right about people, though. One cured cell won't cure the patient.


text:
Basic question about evolution
I want to understand a mechanism how at the first times when the life began on earth evolution helped the new species to arise through selection while the same organism also continued to live as not evolved. If natural selection favors survival of the fittest, than why after a living evolves to a new fittest form, the older form still exists while it should be counted as unfit for survival and extinct, I am not sure but bacteria may be an example perhaps and I am not asking about the situations where the unfit form has extinct but both organisms continued to live.

Related question.

Imagine people playing in a sports league. Some people, because of their (potentially newly developed) abilities (due to practicing), will be able to move on (evolve) to higher levels of competition within the sport, whereas those who are not developing new abilities (but perhaps are still skillful enough to keep playing in their current league) stay where they are. The question then becomes: how do some organisms gain new (more adventagous) traits, and others don't? Answer: genetic variation (either through sexual reproduction or rapid generational evolution) combined with random opportunity.

Thanks for the answer and showing the related question, I specifically didn't want to give an example like apes to humans evolution but the evolution that happened during the times when the life has begun. Could it be that life has started in different locations and in one habitat mutations that were favorable to survive through selection were not necessarily the fittest in another habitat and the same species was already fit to survive and mutations that lead to new species were not the fittest in that location?

@Charles: And some people find they aren't good at baseball, so they invent a new "evolutionary" niche like basketball instead :-)

I want to understand a mechanism how at the first times when the life began on earth evolution helped the new species to arise through selection while the same organism also continued to live as not evolved.

Well, this beginning is not grammatically correct so it is hard to make much comments on it.

If natural selection favors survival of the fittest, [..]

Selection is the process by which fitter individuals increase in frequency in the population. survival of the fittest is a layman phrasing of the process that is natural selection. Natural selection therefore does not favour survival of the fittest, but it is represented by the phrasing survival of the fittest.

[..] th[e]n why after a living evolves to a new fittest form, the older form still exists

It does not. The older form is called an ancestor. The ancestor does not exist today. If there was a speciation events, then the ancestral lineage would have giving rise to more than a single lineage today. Some of these modern lineages may 'look more' like the ancestors than others but it does not mean that any ancestor still exist.
For example, the chimpanzee is not an ancestor of humans. Chimpanzees (and bonobos) and humans share a common ancestor that is about 8 millions old. To consider another example, humans and an oak tree share a common ancestor. This ancestor was neither a human, nor an oak tree. This ancestor lived about 1.6 billions years ago.
If you want to know why I am using term 'lineage' rather than 'species', you can have a look at this post
See below linked Biology.SE posts for more information

the older form still exists while it should be counted as unfit for survival and extinct

Don't forget that different lineages may (and will be at equilibrium due to the competitive exclusion principle) be adapted to different ecological niche. As such, one lineage will not necessarily outcompete the other one.
Source of information on StackExchange
There is a lot you can learn on the subject. You should start with an introduction to phylogenetics such as the one provided in the post

Why do the ancestors of birds still exist?

You can also have a look at

Extinction of species

You should also have a look at

How does Darwinian Evolution work?

Reading your post, it sounds like you may have too a pan-selectionist view of evolution. Related to this point, you might want to read

Why don't mammals have more than 4 limbs?

Source of information external to StackExchange
Understanding Evolution is a good introductory course to evolutionary biology.

Response to comment

Thank you for the very descriptive answer, as you have figured out easily I am very new to evolution. I will read the references you have provided carefully

You're welcome!

is after evolution of a specie through natural selection,

This show again that you have too a pan-selectionist view of evolution.

unfit ancestor extinct and this is explained through phylogeny ?

From wikipedia

Phylogenetics is the study of the evolutionary history and relationships among individuals or groups of organisms (e.g. species, or populations).

A phylogeny is a tree of life of a given taxon. For example here is a phylogeny of placental mammals.
To be able to fully answer your own question, you need to understand the relationships between lineages and therefore you need to have some understanding in phylogenetics.

Thank you for the very descriptive answer, as you have figured out easily I am very new to evolution. I will read the references you have provided carefully, but I think the main answer to my question is after evolution of a specie through natural selection, unfit ancestor extinct and this is explained through phylogeny ?

It's also important to remember that "survival of the fittest" is essentially a circular definition, because organisms prove that they are "fittest" by surviving to reproduce.  Also "fittest" is variable: an orca may be a supremely fit top predator in the ocean, but it's quite unfit to survive in the Mojave Desert.

@bbbandroid See edit to address your comment.

@Remi.b I have just started by watching the video you have mentioned in your post "If you want to know why I am using term 'lineage' rather than 'species', you can have a look at this post" and there is a video in the end of that post named "What Makes a Species a Species?" and i have watched in ending says biological species concept is not an absolute rule

Yep.... any question about it?! You should maybe read the post if this is unclear to you.

Ok i got that point, so i can reshape my initial question, checking below sites link and link when a species diverge into 2 new species, does it mean that the ancestor that diverges extinct ?

In general, you can ask short follow-up questions but not too many of them and not entirely new questions. Your question here is fine. The ancestor became both descendent lineages. So it does not exist anymore as it became something else. The standard mistake would be to think that one of the descendent lineage is the ancestor.