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Which fruit compounds affect the speed of fructose absorption?
Blood fructose levels are not regulated by insulin in the human body. This means that the body absorbs pure fructose very fast, and it raises the blood fructose levels rapidly.
Do fruits/ vegetation contain compounds, which help the digestive system to regulate the absorption of fructose? If so, what are they?

What do you mean by "fructose-regulating factors"? Hormones/substances which control the amount of fructose in the plants or something else?

Are there substances in fruits which help the body regulate fructose absorption?

Do you mean substances produced by the plants, for the humans/animals who eat the plants? If you don't mind me asking, what's in it for the plant?

@user8669 Please tell me, that this edit is valid, or did you mean something else?

http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=919892&fileId=S0007114505001431

@Resonating as far as I remember digestion, this is a reasonable question. The speed of sugar absorption depends on the chyme contents, not just the percentage of sugar present in them. This is why the same food in different preparations has a different GI index, and although I don't remember if it applies to fructose as well, it's not too far fetched to ask if it applies, and what's the mechanism behind it. It doesn't matter what's the reason for the plant to contain whatever it contains. But I agree that the question as written is hard to understand, and possibly way too broad.

Drawing an analogy to other sugars, what would the absorption-regulating factors be for those sugars? General things like pH, salt content, etc or some specific signaling moecules?

@inf3rno Yes, this is exactly what I meant. Thank you very much for your edit.

Probably tannins inhibit the absorption of fructose, but that's just something I read in a post. Visit my link above, it claims, that eucalyptus leaf extract inhibits intestinal fructose absorption in rats, so that is one match. I don't have time to find more related articles, but ofc. there are compounds in fruits which makes them more healthy than processed food e.g. with corn syrup and other fructose containing components.

Yes they do. The answer is glucose.
Let's begin at the beginning: you eat a piece of fruit. The fruit contains many different kinds of sugars, including fructose and glucose. One of the immediate effects your digestion of this fruit has is to raise the levels in your blood of every type of sugar that was present, and the blood levels of many other types of nutrients as well. This has nothing to do with how well your body does/doesn't absorb fructose, it is simply a normal step in digestion.
Next, GLUT2 transporters in the insulin producing cells in your pancreas import glucose. This acts as a signal that tells those cells to start producing insulin. Insulin then diffuses around the body and produces myriad effects, including upregulation of GLUT4  activity across the body. These GLUT4 transporters are present on cells in many parts of your body and are what are responsible for taking up most of the glucose from your blood.
Now on to fructose. GLUT5 is the main fructose transporter. Just like GLUT4, GLUT5 activity is also regulated by insulin, but in a less quick and dramatic fashion than with GLUT4. Although there's a large body of work showing that GLUT5 does not respond quickly to insulin, recent work has shown that, for example, high levels of insulin lead to increased GLUT5 activity in skeletal muscle over a period of 24 hours.
So if what your trying to get at is some reason why eating an apple is better for you than chugging an equivalent volume of Auntie Jemimah's pure corn syrup, it's always going to be some reason like this where you have co-metabolism of several nutrients that tend to show up together in "natural" food. It is unlikely that there are any complex plant substances that would be primarily responsible for the health benefit of fresh fruit in general.

Dietary fibers and antioxidants (e.g. polyphenols) make fruits healthier in general, so your last paragraph is very wrong... Btw. the question was very specific about fructose absorption modifiers, which exist, e.g. eucalyptus leaf extract contains them: http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=919892&fileId=S0007114505001431

@inf3rno Your thing only really applies to fruit wrapped in Eucalyptus leaves. Unless you're claiming that the magical unidentified substance within eucalyptus leaf extract that is supposed to suppress adiposity is present in all fruits, which the authors certainly don't

We don't know what this "magical substance" is, so it might be there in fruits as well. Unless you have a proof about the opposite... ;-)

@inf3rno look up the teapot fallacy

The only problem here, that I don't want to answer this question, because I don't want to earn points with a question I edited. But as you wish...

-1, we have already talked about it why... :-) It took a while to write my own answer, I needed to do some research in the topic.

Do fruits/ vegetation contain compounds, which help the digestive
  system to regulate the absorption of fructose? If so, what are they?

Yes, many polyphenols (e.g. resveratrol, curcumin, quercetin, anthocyanins, phloretin, etc.) do this and much more. Each fruit and vegetable has its polyphenol composition. There are other beneficial fruit and vegetable compounds as well, but I'll talk only about polyphenols in the current post.
Sucrose is split by digestive enzymes (sucrase, glycoside hydrolase) in the small intestine into fructose and glucose. These enzymes are inhibited by polyphenols.
Glucose is transported by SGLT1, while fructose is transported by GLUT5 into enterocytes in the intestines. After that the cells transport these sugars with GLUT2 into the blood. Polypheonls can inhibit these transporters and decrease their expression.
Fructose and glucose is transported to the liver from the blood, with GLUT2, and they do nasty things in there. Fructose is more dangerous than glucose, because it is transformed without any regulation. It uses the same pathways as glucose and mostly fatty acids are created from it, which increase the blood VLDL, LDL, FFA level and cause insulin resistance. The byproducts are urate and free radicals, which cause hyperuricaemia and oxidative stress. Hyperuricaemia cause decreased NO levels (by counteracting with eNOS and reacting with NO directly), which cause increased blood pressure due to vasoconstriction. Hyperuricaemia damages the liver and the kidney too. Too high urate levels enhance LDL oxidation as well, which cause atherosclerosis. The free radicals deplete the antioxidants of the body and cause cancer. Polyphenols prevent atherosclerosis, restore NO levels, restore urate levels, scavenge free radicals, counteract with insulin resistance and prevent liver and kidney damage. So they can fix most of the problems fructose cause.
References:

The interactions of gallic acid and tannic acid with purified brush
  border sucrase (EC 3.2.1.48) from mouse intestine have been studied.
  These findings indicate that both gallic acid and tannic acid inhibit
  sucrase activity, which is pH dependent.

http://dx.doi.org/10.1042/BSR20090012

The effects of tea polyphenols on the sucrase activity are shown in
  Table .1. Among 10 compounds, esterified (gallated) polyphenols (ECg,
  EGCg, TF2A, TF2B, and TF3) were potent inhibitors.

http://dx.doi.org/10.1271/bbb.57.123

Quercetin reduced the effect of sucrase and maltase in the in vivo and
  in vitro treatments.

http://dx.doi.org/10.1016/j.nut.2011.01.008

In conclusion quercetin and its glycoside derivatives have alfa-glucosidase inhibitory activity and high peroxyl radical scavenging-linked antioxidant activity. The above benefits (anti-hyperglycemia and antioxidant activity) of quercetin and its glycoside derivatives taken together could support the evidence that diets rich in fruits and vegetables are associated with lower incidences of oxidation-linked diseases such as diabetes

Comparison of Antioxidant Potential and Rat intestinal alfa-Glucosidases inhibitory Activities of Quercetin, Rutin, and Isoquercetin - http://ijarnp.org/index.php/ijarnp/article/viewFile/41/41

Phloretin (Ph), which can be obtained from apples, apple juice, and cider, is a known inhibitor of the type II glucose transporter (GLUT2).

http://dx.doi.org/10.1002/mc.20480

The ATPase inhibitor quercetin, which inhibits tumor glycolysis, was shown to be a glucose transport inhibitor like the chemically related compound phloretin.

Preferential inhibition by quercetin of mitogen-stimulated thymocyte glucose transport. - http://www.ncbi.nlm.nih.gov/pubmed/220448

Glucosides of some other flavonoid classes such as naringenin-7-O-glucoside, genistein-7-O-glucoside and cyanidin-3,5-O-diglucoside were ineffective as well. Thus, dietary quercetin monoglucosides, for example, Q3G and Q4G, have an impact on intestinal nutrient transporters such as SGLT1 and related systems.

http://dx.doi.org/10.1079/BJN20041128

Excessive post-prandial glucose excursions are a risk factor for developing diabetes, associated with impaired glucose tolerance. One way to limit the excursion is to inhibit the activity of digestive enzymes for glucose production and of the transporters responsible for glucose absorption. Flavonols, theaflavins, gallate esters, 5-caffeoylqunic acid and proanthocyanidins inhibit α-amylase activity. Anthocyanidins and catechin oxidation products, such as theaflavins and theasinsensins, inhibit maltase; sucrase is less strongly inhibited but anthocyanidins seem somewhat effective. Lactase is inhibited by green tea catechins. Once produced in the gut by digestion, glucose is absorbed by SGLT1 and GLUT2 transporters, inhibited by flavonols and flavonol glycosides, phlorizin and green tea catechins.

http://dx.doi.org/10.1002/mnfr.201200511

In addition, curcumin suppressed glut2 expression by stimulating the activity of peroxisome proliferator-activated receptor-gamma (PPARγ) and de novo synthesis of glutathione. In conclusion, hyperglycemia stimulated HSC activation in vitro by increasing intracellular glucose, which was eliminated by curcumin by blocking the membrane translocation of GLUT2 and suppressing glut2 expression.

http://dx.doi.org/10.1016/j.mce.2010.12.028

This study investigated the effects of an anthocyanin-rich berry-extract on glucose uptake by human intestinal Caco-2 cells. Acute exposure (15 min) to berry extract (0.125%, w/v) significantly decreased both sodium-dependent (Total uptake) and sodium-independent (facilitated uptake) 3H-D-glucose uptake. In longer-term studies, SGLT1 mRNA and GLUT2 mRNA expression were reduced significantly. Polyphenols are known to interact directly with glucose transporters to regulate the rate of glucose absorption. Our in vitro data support this mechanism and also suggest that berry flavonoids may modulate post-prandial glycaemia by decreasing glucose transporter expression.

http://dx.doi.org/10.1371/journal.pone.0078932

RES increased SIRT1 expression, but decreased the expression of GLUT5 and aldolase B in aortas from HFr-fed rats. These results suggest that RES contributes to the restoration of HFr-induced vascular dysfunction in rats, at least in part, by up-regulation of SIRT 1 and down-regulation of GLUT5 and aldolase B in the aorta. Moreover, RES may have a positive influence on vasculature by partly restoring the plasma arginine:ADMA ratio and leptin levels.

http://dx.doi.org/10.1139/cjpp-2014-0245

High dietary fructose intake: Sweet or bitter life? - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3158875/
A causal role for uric acid in fructose-induced metabolic syndrome - http://ajprenal.physiology.org/content/290/3/F625
Gut microbial adaptation to dietary consumption of fructose, artificial sweeteners and sugar alcohols: implications for host–microbe interactions contributing to obesity - http://www.drperlmutter.com/wp-content/uploads/2014/04/Payne-et-al-2012-Obesity-reviews.pdf
Early Life Exposure to Fructose and Offspring Phenotype: Implications for Long Term Metabolic Homeostasis - http://dx.doi.org/10.1155/2014/203474
Dietary fructose, salt absorption and hypertension in metabolic syndrome: towards a new paradigm - http://onlinelibrary.wiley.com/doi/10.1111/j.1748-1716.2010.02167.x/abstract?deniedAccessCustomisedMessage=&userIsAuthenticated=false
Toward a Unifying Hypothesis of Metabolic Syndrome - http://pediatrics.aappublications.org/content/129/3/557.short
Uric acid transport and disease - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2877959/

The present study demonstrates that resveratrol is more effective than metformin in improving insulin sensitivity, and attenuating metabolic syndrome and hepatic oxidative stress in fructose-fed rats.

http://dx.doi.org/10.1016/j.phrs.2012.05.003

Quercetin supplementation improved some risk factors of cardiovascular disease, yet exerted slightly pro-inflammatory effects.

http://dx.doi.org/10.1016/j.numecd.2011.08.010

In conclusion, dietary HFCS causes vascular insulin resistance and endothelial dysfunction through attenuating IRS-1 and eNOS expressions as well as increasing iNOS in rats. Resveratrol has capability to recover HFCS-induced disturbances.

http://dx.doi.org/10.1016/j.fct.2013.07.026

The major flavonoid is Quercetin, which belongs to the class called flavonols and is mainly found in apples, tea, onions, nuts, berries, cauliflower, cabbage and many other foods. It exhibits a wide range of biological functions including anticarcenogenic, anti-inflammatory and antiviral; it also inhibits lipid peroxidation, platelet aggregation and capillary permeability. This review focuses on the main effects of Quercetin on obesity and diabetes.

Beneficial Effects of Quercetin on Obesity and Diabetes - http://benthamopen.com/tonutraj/articles/V004/189TONUTRAJ.pdf

These results indicate that resveratrol ameliorated FF A-induced insulin resistance by regulating mTOR and p70-S6K phosphorylation in skeletal muscle cells, through a mechanism involving sirtuins.

Attenuation of skeletal muscle FFA-induced insulin resistance by the polyphenol resveratrol. Elucidation of the mechanisms involved - https://dr.library.brocku.ca/handle/10464/2832

Resveratrol, trans-4-hydroxystilbene, pterostilbene, polydatin, and mulberroside A were found to have antihyperuricemic activities. The uricosuric and nephroprotective actions of resveratrol and its analogues were mediated by regulating renal organic ion transporters in hyperuricemic mice, supporting their beneficial effects for the prevention of hyperuricemia.

http://dx.doi.org/10.1002/mnfr.201100828

Adult male Wistar rats were treated with a normal or high-fat/sucrose diet (HFS) with or without Res for 13 weeks. HFS and in vitro treatment with high glucose increased hyperpermeability in rat aorta, heart, liver and kidney and cultured bovine aortic endothelial cells (BAECs), respectively, which was attenuated by Res treatment. Application of Res reversed the changes in eNOS and Cav-1 expressions in aorta and heart of rats fed HFS and in BAECs incubated with high glucose. Res stimulated the formation of NO inhibited by high glucose in BAECs.

http://dx.doi.org/10.1371/journal.pone.0113716

In summary, all 3 tea polyphenol extracts induced weight loss and anti-inflammatory and angiogenic effects, although the tissue content of polyphenols differed significantly.

http://dx.doi.org/10.3945/jn.114.191007

Blackcurrants and lingonberries, as either whole berries or nectars, optimize the postprandial metabolic responses to sucrose. The responses are consistent with delayed digestion of sucrose and consequent slower absorption of glucose.

http://dx.doi.org/10.3945/ajcn.112.042184

Resveratrol prevented the HFS-induced arterial wall inflammation and the accompanying increase in PWV. Dietary resveratrol may hold promise as a therapy to ameliorate increases in PWV.

http://dx.doi.org/10.1016/j.cmet.2014.04.018

Taken together the data suggest that dietary flavonoids exhibit three distinct modes of action with regard to cancer prevention, based on their hydroxyl and methoxy decoration: (1) inhibitors of CYP1 enzymatic activity, (2) CYP1 substrates and (3) substrates and inhibitors of CYP1 enzymes.

http://dx.doi.org/10.1016/j.bmc.2011.03.042

These data demonstrate that resveratrol inhibits CYP1A1 expression in vitro, and that it does this by preventing the binding of the AHR to promoter sequences that regulate CYP1A1 transcription. This activity may be an important part of the chemopreventive activity of resveratrol.

http://www.ncbi.nlm.nih.gov/pubmed/9865727

As a chemoprevention agent, resveratrol has been shown to inhibit tumor initiation, promotion, and progression, as well as inhibit the growth of cancerous cells through increased apoptosis and/or cell cycle blockage. Inflammatory processes are associated in the pathogenesis of many chronic diseases including heart disease and cancer. Resveratrol has been shown to reduce inflammation via inhibition of prostaglandin production, cyclooxygenase-2 activity, and nuclear factor-кB activity. In addition, the estrogenic activity of resveratrol may help prevent post-menopausal bone loss.

http://dx.doi.org/10.1111/j.1541-4337.2006.00001.x

These findings suggest that fructose-induced metabolic syndrome is attenuated by the polyphenol-rich fraction of amla.

http://dx.doi.org/10.1017/S0007114509991978

Man, your answrs are so long!

I'm unsure currently about the empirical data surrounding inhibition of GLUT5, but with regards to GLUT2, some data exists to point out flavonoids and phloretin as potential inhibitors found in diet. The following articles should provide some sort of starting point to dig a little deeper on the matter.
http://www.ncbi.nlm.nih.gov/pubmed/17699876
http://www.ncbi.nlm.nih.gov/pubmed/17172639

http://www.ncbi.nlm.nih.gov/pubmed/25392295 resveratrol reduces the expression of transporter genes.

authors: Полина Рябенкова


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Why isn't vomit corrosive?
Vomit comes from gastric acid, right? And in gastric acid there is HCl and HCl is corrosive (strong), how come when I vomit, it doesn't destroy things that it (as the vomit) hits (such as floor, table)?

First of all, it is corrosive. People which are bulimic often get problems with their teeth getting damaged by the permanent exposure to the acidic stomach fluids. See the paper for more information:

Bulimia and tooth erosion

Then it is a matter of concentration. According to Wikipedia, the concentration of the acid in the stomach is around 0.5% which is a pretty low concentration. Additionally the acid gets diluted when you eat or drink things. And last but not least not all things are very susceptible to a fast degradation by acids. Thing tend also not to disappear suddenly, if they come in contact with acids.

so, the Hollywood "acid spill = instant shaft" is completely false?

In the way it is usually displayed in films, yes. Take metals for example. A lot of commonly metal will not dissolve (or only slowly). Of course, if you subject Magnesium or pure Aluminium to a strong acid, it will react rather fast. But who uses these metals in this form to build things?

Is the Aluminum/Magnesium used in many laptop/tablet/phone bodies alloyed to be much more corrosion resistant than purer forms of the metal?

Magnesium is usually used as an alloy, since it is otherwise to hard to work with. Both metals form an oxidative cover on the surface which protects them from further oxidation. And in the case of tablets/phones etc. the surfaces are additionally treated to be much more resistant.

@JanDvorak Hollywood lies and exaggerates? Heaven forbid... :)

Link behind paywall.

@Thorbjørn: At least you can still read the abstract without paid access.

@ThorbjørnRavnAndersen Do want to read the paper? Then I will make this possible...

I am mentioning it so others know immediately without having to go and have a look.  I do know about the problem - I just wanted to skim the conclusion.  The only thing you need to do is to mention in a parenthesis after the link how the information is restricted.  I would, however, recommend that if you want people to find your answer helpful, that  you make it possible to actually read the information you link to.

As Chris said it's a matter of a low concentration for a small amount of time. Most people clean up their vomit rather than leave it to sit. Most people who vomit also have recently eaten something which triggers the reflex but also dilutes the acid or may neutralise it.
To further add to Chris' answer. Even heartburn or gastro-oesophageal reflux disease, is particularly corrosive. Damaging cells that line the oesophagus, it causes changes in the cells that make them pre-cancerous (Barret's oesophagus) and can lead to full blown cancer (carcinoma). This is because the cells change type to try to protect themselves.
Even in the stomach a thick layer of mucus is required to prevent the stomach from eating itself. This is not only to protect the lining against its own acid, but the enzymes which are made are seriously dangerous and will digest our body if able, only work in acidic environments. To understand how dangerous they are, when the pancreas which makes these enzymes is blocked releasing these enzymes it can digest nearby structures such as major blood vessels and cause seriously dangerous bleeding.

Chris is right, I just want to extend his answer a little bit more.
The presence of corrosion and the corrosion speed highly depends on the concentration of the acid, which is very low (0.5% according to Chris) in this case (considering that ccHCl is about 35-40%). According to wikipedia the vapour pressure of water is about 2645 kPa while the vapour pressure of HCl is about 4352 kPa on 22°C. The atmospheric pressure is about 1000 kPa, so one part of the (few) HCl will evaporate before the water does, which makes, the concentration even lower. So I highly doubt that it can cause any damage to a regular floor or metal/wood table in an open environment.

so, the Hollywood "acid spill = instant shaft" is completely false? –
  Jan Dvorak

It is possible to do that with much more concentrated acid. E.g. a bottle of hot concentrated sulfuric acid can cause very serious damage to people in a short time...

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How do I tell if the mosquitos in my New York City apartment can carry Zika?
The species that carries Zika, A. aegypti, is unlikely to be found in New York. However, the related species A. albopictus is prevalent and quite concerning. So this question is focusing on A. albopictus (if I may editorialize I would suggest leaving the title closer to the real question of interest, and disambiguating the species as the first step in resolving it).
According to the CDC

Zika virus is transmitted to people primarily through the bite of an infected Aedes species mosquito (A. aegypti and A. albopictus).

I understand New York has IIRC the aegypti species and Zika has appeared.
My apartment gets mosquitos rather randomly every couple months. Understandably I want to figure out how much effort I should put into preventing or getting rid of them. I can describe their behavior here and maybe that's enough information. If not, do I need to get out a magnifying glass or sequence DNA? (Which I did once in college but I wasn't very good at it).
Their behavior:

I get "bursts" of them at random times in the year - more in the warm months but also in November. We had a warm winter but this still surprised me.
They seem to bite me at night but I've never had a mosquito bite on me. I've had mosquito bites from being bitten by mosquitos before, so unless I've developed a resistance to that in the last few years, that's strange.
I haven't found any evidence of standing water nearby. They don't hover around my sinks or toilets. I read once the Zika carrying strain is on the hardy side and can live off of moisture in walls so this is troubling.

If you're curious my preferred life hack is keeping my living room slightly warmer than my bedroom. And also, you know, killing all of them.
So, are these behavior traits useful? Can I identify them as opposed to other New York inhabiting mosquitos? Is a DNA test necessary?

This is a reasonable question, and I was surprised to find that official information on whether Aedes aegypti is present in NYC isn't very clear. I personally would have thought that NYC was quite far beyond the range of Aedes aegypti (the 'yellow fever mosquito', believed to be the main vector of Zika virus in the ongoing emergence event in South America), and the New York City Department of Health apparently agrees with me:

Aedes aegypti has not been found in New York City.

...(emphasis theirs) which seems pretty clear cut. However, the CDC recently published a map claiming that NYC is within the potential range of Aedes aegypti.

It's not really clear exactly what they mean by this. From the webpage:

The new estimated range maps have been updated from a variety of published and unpublished sources.
These maps show CDC’s best estimate of the potential range of Aedes aegypti and Aedes albopictus in the United States.
These maps include areas where mosquitoes are or have been previously found.

A related species, Aedes albopictus, is sometimes found in NYC during the summer and is probably capable of transmitting the strain of zika virus currently circulating in the Americas (see for example this recently-published experimental infection study). Aedes albopictus has been the major vector in some previous zika outbreaks in other parts of the world.
(Edit (14th June): A group of mostly-CDC entomologists just published a map of locations where Aedes aegypti and Aedes albopictus have actually been collected between 1995 and 2016 here, and there's an NPR article explaining why the maps are different here).
Whether the density of this species or the temperatures are sufficient to sustain transmission for any length of time in a climate like that of NYC is a more complicated story. The CDC even adds:

Maps are not meant to represent risk for spread of disease.

But you've asked whether the mosquitoes in question can carry zika, not whether they're likely to be good at it, so I'll leave it there. The short answer is that if they're Aedes mosquitoes, then they might be able to.
So how do you know if they're Aedes mosquitoes? Aedes are visually quite distinctive; they have black bodies with white stripy abdomen and legs:

(Image taken by Muhammad Mahdi Karim; details and license here).
Aedes are also generally day-biters, so if you're getting bitten at night that makes me suspect you've got something like Culex mosquitoes instead (which might be able to spread West Nile virus, although that's a different story). These are dull brown.
If you do find you have Aedes and you'd like to try to identify them to species level, you could collect some dead ones and look at their thorax. If you take some photos and post them here as a species-id question you'll probably get an answer pretty quickly, but this figure illustrates the difference between aegypti and albopictus:

(Image from WHO (1995) Guidelines for Dengue Surveillance and Mosquito Control, Second Edition)
There are better images here but I think these are under copyright.

You're very much out of range of Aedes Aegypti, which is the primary carrier of Zika. Albocitus is a much more theoretical carrier, whose potential for spreading disease is much less. There have been no locally acquired cases in the mainland US this year. The odds of a New Yorker being the first to catch it are ridiculously long.

Well, there are 78 reported cases of Zika in New York so far. Apparently the concern is Aedes albopictus.

Edited question to note that the CDC is concerned of A. albopictus. I don't know the state of the research on A. albopictus + Zika but I can only hope the city has looked into it given they're about to spend millions of dollars fighting it.

This does not provide an answer to the question

New York is an international hub, just because there are reported cases doesn't mean that it came from the native mosquito population.

From the link: "All cases contracted Zika while visiting other countries"

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Which disorders are fully concordant?
I work in neuroscience, mostly Alzheimer's disease (AD), with some work in autism spectrum disorder (ASD). The work is in gene regulation and epigenomics. I'm familiar with monozygotic twin (MZ) discordance for AD and ASD and the methylome studies done in discordant MZ for those disorders. I began to become curious.
What disorders have never had MZ discordance reported in the literature? Even sickle cell has MZ discordant progression (Amin et al. 1991. Hemoglobin. 15:247-56). Do any disorders lack MZ discordance?

For those that don't know about it, could you expand a little on what MZ discordance is and what it means for a disease?

MZ discordance is when MZ twins do not have the same phenotype. Twin A gets Alzheimer's. Twin B does not. If Alzheimer's were fully genetic, both twins would get it, since their genomes are (very close to) identical. The higher MZ discordance for a disorder, the more effect environment is presumed to play. What is interesting is when a very Mendelian disease, like sickle cell, still shows MZ discordance on symptoms or a disorder with high genetic risk, like ASD, still shows non-patient/patient MZ discordance. My question means "Do any diseases have airtight evidence as being 100% 'genetic'"?

Complete concordance is generally rare because environment will always have some influence on the trait. In general all disorders that are not quite lethal are susceptible to environmental effects and buffering


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Rationale for helper T cells?
If my understanding is correct, helper T cells have two main functions:

stimulating macrophages at the site of infection
activating B cells and helping them undergo somatic hypermutation

What advantages do Helper T cells in mediating this process, instead of macrophages and B cells activating on their own?
In particular, I could imagine:

macrophages always being "on duty" to swallow pathogens that do not present self-antigen.
B cells already require a first activation by free-floating antigen, so they could just have evolved to not require the second activation by helper T cells.

Would this have disadvantages I have not considered, or have had evolutionary problems?

@anongoodnurse good question! I think that is because that requires a more complex evolutionary path. But in the case of T cells, the immune system evolved a whole new type of cell instead and complex secondary activation mechanisms instead of what seems like a more straighforward strategy, which seems very mysterious to me.

@anongoodnurse I skimmed the link and still don't understand. What do you mean?

https://www.ncbi.nlm.nih.gov/books/NBK27138/ Don't skim. Read carefully. Present your findings (research into answering your own question.)

I have edited this question by applying Occam’s razor to it, as is required in many questions here posed in terms of “why did this evolve”, which in any case generally can only be answered by subjective conjecture. By focusing on the systems in question one can answer by make objective scientific points about the mechanisms, or, if necessary, the problems in their evolution (number of events for example). But in asking this question, focus on the mechanistic question — keep other things out, allowing users to supply them in answers only if they see them as relevant.

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text:
Do ATP generated aerobically and anaerobically have different phosphorylation potentials?
We have recently postulated that ATP generated by substrate-level  phosphorylation may have a different phosphorylation potential to the ATP generated by oxidative phosphorylation. This  could be because ATP generated via ATP synthase is released into a more basic environment than the cytoplasm.
My question is:
Has anybody measured the phosphorylation potential of ATP during the growth of  E. coli under anaerobic conditions, and,
if so, how does it compare with the phosphorylation potential of ATP during the growth of E. coli under aerobic conditions?

Please tell us the results of your own research to try to answer this question.

@David my cynical side says this question is purely to raise the profile of the OPs paper linked in the question.

@bob1 — One has to take questions of this sort at face value, and respond by making sure they fulfil the usual prerequisites. Anyone trying to publicize their own published science on this list — especially on this type of subject — is wasting their time, in my opinion, as I think they are addressing the wrong audience. But that’s their problem.

Do you have an open-access version of your publication?

https://www.alliedacademies.org/conference-abstracts-files/switches-thresholds-and-flux-signals-in-the-control-of-central.pdf

https://www.alliedacademies.org/conference-abstracts-files/switches-thresholds-and-flux-signals-in-the-control-of-central.pdf

Welcome to Biology.SE. Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, reference information should be added to the body of your question rather than being placed in a comment — comments are for discussing improvements to posts. Consequently they are ephemeral and often overlooked.

@MansiEl-Mansi You are probably the best person to answer your own question. This site is for biologists as well as general public but there are only a handful of experts who study different fields of biology. You ask a question about a very specific topic (that too asking for literature evidence for something). You have better chances of finding an answer yourself than relying on users here, because this is your research topic. Did you check out google scholar?

I thank you for the effort and time.

Based on the way this question is phrased, the answer is trivially no. No matter how you make an ATP molecule, if you measure hydrolysis in a consistent manner there will be no difference.
A fundamental axiom in chemistry is that identical molecules are indistinguishable from each other. Specifically, I mean that the entropy and enthalpy are State Functions - they only depend on the current state of the system and not how the system got there. This is best summed up with Hess' Law.
The only things that could change the free energy of hydrolysis of an ATP molecule are:

A change in the isotopic makeup of the ATP molecule
A change in the environment in which the hydrolysis is occuring

The first is very, very unlikely to be dependent on aerobic vs. anaerobic respiration. I mean I guess the isotopic makeup of the oxygen could be ever-so-slightly different or something, but I would be shocked if it was. Even then it almost certainly wouldn't make much of a difference in energy of hydrolysis.
The second, is actually very likely to occur. Changes in temperature will always affect any reaction for which the change in entropy is non-negligible (remember $ \Delta G = \Delta H - T \Delta S $). As you suggest, changes in pH would certainly effect a measured change in energy due to a change in the abundance of the various protonated forms of ATP (and keep in mind  hydronium if you're considering spontaneous hydrolysis). Indeed, almost any change in the environment could affect the measured energy.
But, importantly, these are not due to differences in the actual ATP molecule. These are due to differences in the environment that the reaction is taking place in, not the environment it was produced in. If you take two ATP molecules and place them in an identical environment they will always have the same energies (isotopic differences excluded). Any evidence contradicting this is either wrong or a suggestion of a fundamental paradigm shift upending years of basic physics and chemistry.


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Please help ID this plant
Can anyone please identify this plant and confirm if the species is Synsepalum dulcificum (Miracle fruit)? Pics were taken near my house in Bangalore. Because the miracle fruit plant is not native to India, I'm guessing it is a different species.

Looks like miracle fruit.

No, I don't think it's an S. dulcificum, the leaves are very different. It might belong to a related species.

Thanks for the comment guys!! really appreciate it! is there anyway to be completely certain of the species. I'll try eating a tiny bit of the fruit today just to see if it works. can anyone who has tried the fruit tell me how it tastes like and whether the effect is seen if a tiny amount is ingested.

Hmm could it be nightshade berries?


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Why isn't the sticky bud plant more widespread
Why isn't the sticky bud plant (Galium aparine) everywhere around the world? Because to me it seems that it has the best method of seed dispersion/transportation (wiki link: https://en.wikipedia.org/wiki/Galium_aparine)

Can you link up something on the "sticky bud" plant?  I would like to read more about it.  I suspect there may be more than one plant with sticky buds.

Cleavers are distributed all over the world. The link you provide answers the question. (They shouldn't be able to grow in the desert.)

As already pointed out in comments, Galium aparine is actually very widespread, according to wikipedia it occurs in "a wide region of Europe, North Africa and Asia from Britain and the Canary Islands to Japan. It is now naturalized throughout most of the United States, Canada, Mexico, Central America, South America, Australia, New Zealand, some oceanic islands and scattered locations in Africa."
Because it occurs on moist and rich soils, it doesn't occur everywhere. It is unable to grow on dry and nutrient-poor soils (like deserts and steppes). But it is also absent in frequently mown grassland.


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Is there a specific suffix for "within a cell"? i.e. in a similar manner to how -aemia refers to within the blood
Words like hyperglycemia and hyponatremia refer to the relative level of each component in the blood, not in the cell. Is there a suffix for within the cell? For reference I would like one word as an alternative to "hyperglycemic cell".

I'm voting to close this question as off-topic because it is an English Language question that could have been answered by reference to dictionaries and scientific literature.

It is not present in dictionaries, nor scientific literature per se. In fact, the question arose after noticing that many authors wrote out the full phrase. I still agree it might also suit the English Language exchange, but on reconsideration it is just as relevant here. Biology is after all the main, if not only, context in which the word could ever be used. See below.

"Cyto"/"cytic" and similar are common prefixes/suffixes to refer to things associated with cells; however they don't necessarily specify intracellular space, they are more often referring to specific cell populations, counts, etc.
The word "intracellular" is, however, commonly used terminology for "inside the cell."
For the specific case you mention, I would simply write "high/elevated intracellular glucose" - I am unaware of any reference that uses a individual word for the same meaning. Some others have referred to "intracellular hyperglycemia" which may be a bit odd since the -emia refers to the blood, but they are specifically referring to the case where high intracellular glucose is a direct consequence of overall hyperglycemia.

i wouldn't say intracellular hyperglycemia. I'd say high or elevated intracellular glucose. The -emia suffix is still going to mean in the blood

@DeNovo Hmm that's a good point. I found a lot of cases where people used the term "intracellular hyperglycemia" but I've edited accordingly.

Just for reference I went with hyperglucous cells as it is more accurate than intracellular hyperglycaemia; much more useable than the triple combos: hyperglucocyte, hyperglucocyst, hyperglucocytic, hyperglucocytal.

There are very few medical terms that have  suffixes for body parts or compartments. The only 4 I'm aware of are -emia (in blood), -uria (in urine), -rhachia (in cerebrospinal fluid, rarely used) and -dactyly (arrangement of fingers) (medical term suffixes). For organs, prefixes are typical: gastro- (stomach), spleno- (spleen), cardio- (heart), cerebro- (brain), etc.


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Does the complimentary base pairing of rRNA with itself play a role in its transcription?
I have read that the termination of the transcription of mRNA involves a termination sequence in the form of a stem loop. As the structure of ribosomal RNA involves extensive internal base pairing, I wonder whether part of the mature rRNA provides the termination loop for its transcription.

Your question is unclear to me. You question appears to be about the termination of transcription of rRNA, although your title seems to be about rRNA structure that can be answered from any book or Wikiipedia. Your tag of reverse-transcription was certainly wrong and I have removed it. Please clarify your question, but first do some reading. A statement that "I know rRNA must come from a gene" suggests you might benefit from this.

As you haven't replied and as nobody else followed my vote to close this question I have rewritten it in a way that now makes some sense and may be what you meant. If not please edit it. I have reversed my close vote and will answer the question if nobody else does.

Summary
The process of the termination of transcription is still not well understood. It differs between eukaryotes and prokaryotes and between mRNA and rRNA. Although it involves stem-loop structures, such structures may be necessary, but are not sufficient for termination. The idea that the termination signal might be part of the mature functional transcript — especially for rRNA comes up against a number of problems, and turns out to be incorrect. Such problems include the extensive nature of the stem loops (which to use?) and the fact that the smaller stem loops emanating from the core conserved hydrogen-bonded skeleton, are not necessarily themselves conserved (reviewed by Brimacombe). In fact the large and small rRNAs are in a single transcription unit with other genes at the end of which are specific termination signals outside the region encoding the mature rRNA.
Prokaryotic rRNA transcription
This has been reviewed by Condon, Squires and Squires (1995). The structure of the well-studied rrnB operon of E.coli is shown below, with the promoters indicated as ‘P1’and P2’ and the terminator sequences as ‘T1’ and ‘T2’. (Adapted from Pfeiffer and Hartmann.)

This transcription unit includes the 5S rRNA as well as a tRNA.
Eukaryotic rRNA transcription
This has been reviewed by Goodfellow and Zoomerdijk(2012), from which the diagram below, of the mammalian rDNA repeat, is taken. The terminator elements are ‘T1–10’.

In eukaryotes the 5S rRNA is not in the same transcription unit as the large and small rRNAs (and the 5.8S rRNA). Indeed it is transcribed by DNA-dependent RNA polymerase III, rather than the DNA-dependent RNA polymerase I, which transcribes the rDNA repeat shown.

Transfer RNAs (rRNAs), ribosomal RNAs (rRNAs) all fold back on themselves and hydrogen bond to make complementary base pairs. So yes, this is common.

I think that, despite the title, the question is about termination of rRNA transcription, not rRNA structure. On reflection, he is probably asking if the transcription termination loop (if such exists for rRNA — I don't know) is part of the rRNA transcript and (perhaps) the mature processed rRNA.

Apologies, but I edited the question so that your answer is no longer pertinent. As it is just a two-liner, I trust it will not inconvenience you too much.


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Dreadnoughtus: Why are new taxa named using Dog Latin?
Once upon a time, binomial nomenclature was expected to follow Latin rules: the genus had to be a noun and the species had to be an adjective that agreed with the genus according to Latin rules of adjectival agreement with the noun modified by it. That’s why we have species names like sativus, sativa, and sativum seen again and again, the exact form depending on the genus’s gender.
So if knew a bit of Greek and Latin, you could figure out something about what binomials such as Stegosaurus armatus or Dodecatheon pulchellum might be about.
Enter 2014, and with it such new binomials as the ponderous Dreadnoughtus schrani.  That looks more like Dog Latin than Classical Latin: just tack a few Latinate-looking suffixes to words that cannot be decoded using any known roots from Greek or Latin.
When I first read about it, I honestly thought somebody was making a bad joke. It’s not like the Greeks and Romans never thought of fearing nothing; one might imagine a taxon built out of actual classical roots — perhaps like *Timendumnihil — would have been more universally understandable than the Dog-Latin form Dreadnoughtus we’ve been stuck with.
Is there no requirement that new taxa have classical forms?  Was there ever, and if so, when and why did this change?  Or, if there was not, then why did everybody seem to go along with the scheme for so long?

I'm not a latinologist, but I don't think new words have been added to latin or (classical) greek in a long time. This creates a limited vocabulary, and new taxa may not fit the classical vocabulary. Additionally, classical languages are no longer widely taught, so the average person may have more exposure to pseudo latin than to real latin. Pseudo latin may also be more easily understood by the lay audience than real latin.

There is an International Commission on Zoological Nomenclature, to which submissions for new organisms' names is strongly recomended. The discoverer does have some leeway within this system if there is no Latin name that well-describes this species. Your example is one of many.
Chapter 31, for example, clearly states:

31.1.1. A species-group name, if a noun in the genitive case formed from a personal name that is Latin, or from a modern personal name that is or has been latinized, is to be formed in accordance with the rules of Latin grammar.

Examples. Margaret, if latinized to Margarita or Margaretha, gives the genitives margaritae or margarethae; similarly Nicolaus Poda, even though the name of a man, if accepted as a Latin name, gives podae; Victor and Hercules, if accepted as Latin names, give victoris and herculis; the name of Plinius, a Roman, even though anglicized to Pliny, gives plinii; Fabricius and Sartorius, if treated as Latin names, give fabricii and sartorii, but if treated as modern names give fabriciusi and sartoriusi; Cuvier, if latinized to Cuvierius, gives cuvierii.

31.1.2. A species-group name, if a noun in the genitive case (see Article 11.9.1.3) formed directly from a modern personal name, is to be formed by adding to the stem of that name -i if the personal name is that of a man, -orum if of men or of man (men) and woman (women) together, -ae if of a woman, and -arum if of women; the stem of such a name is determined by the action of the original author when forming the genitive.

Example. Under this provision, the species-group names podai from Poda, victori from Victor, and cuvieri from Cuvier are admissible. The names puckridgei and puckridgi may be formed from Puckridge.

Similar rules apply for genus and family names.
Since your example was a new genus and species, it didn't "fit" into previous categories (in the future, if and when similar discoveries are made that shed light on the genus' relation to others, the name can and will be changed accordingly, with or without the authors' approval).

According to the research team that discovered the taxon, the genus name Dreadnoughtus "alludes to the gigantic body size of the (which presumably rendered healthy adult individuals nearly impervious to attack)" and to the two dreadnought battleships of the Argentine Navy, the ARA Rivadavia and ARA Moreno. Thus, the genus name also honors the country (Argentina) in which Dreadnoughtus schrani was discovered. The name of the type species, schrani, was given in recognition of the American entrepreneur Adam Schran for his financial support of the project. - Wikipedia

A "good" or "useful" taxon is commonly taken to be one that reflects evolutionary relationships. Since this one does not, in a few decades, this name may well be gone.

Brava for a well-documented answer! I hadn’t realized that it might get its name revised that easily.  And your genitive mention reminded me of last year’s new orchid species in an existing genus,  Lophiaris silverarum — “of the Silveras” in the genitive plural -arum.

Names get revised all the time, especially now with the ability to determine relationships genetically.I feel bad for pathologists, who must face the reclassification of bacteria regularly, it seems.


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Why do humans seem to be the only mammals that like spicy food?
Peppers evolved chemicals like capsaicin to discourage animals from eating them, and that chemical itself can cause internal damage if consumed in large quantities, though this is usually only a concern for the hottest of peppers (which people do eat).
Still, why is it that humans seem to be the only animal that often "like" spicy food?

Since I can't quote any literature on this I wont write it as an answer. My guess would be that other animals don't have the ability to feel the "rush" we get from punishing ourselves by eating spicy food. For example the burning sensation from chilly releases endorphins which gives you a temporary biological "high". I am also eagerly waiting for an expert to answer this.

But the observation remains the same. Humans are mammals and often like spicy food, and there are other animals comparable to humans in many ways which do not like spicy food by their seeming intrinsic physiology. The question still remains: why is it that humans to are an exception from this group? Perhaps its something similar to broccoli where some people taste it as especially bitter and others do not, but you have not provided any formally recognizable answer.

The same question could be asked about acid or bitter food. I would think the answer lies in our cognitive abilities. Somehow, we just happen to have built a culture for liking those types of food we've been selected for not liking.

Perhaps the answer is that humans seem to be the only species that is capable of seasoning its food.  Very few people eat hot peppers directly (and then it seems to be more of a test of machismo that actual liking, at least IMHO), they use small amounts to season food.  Certainly my dogs have eaten such food with every outward evidence of liking.

Only TWO known mammals like spicy food. source

There are really two questions here  1. Why do humans use spices? and 2. Why do some humans eat excessive amounts of this particular capsaicin but not other spices, or only a few others?
I will answer the second question first. The current understanding of why some humans eat so much spicy food is that it is a form of benign masochism. "Some" is the key: only some humans like spicy food in anything but the most minimal amounts. It has been shown that eating spicy food releases endorphins, but only after the burn, so eating spicy food is like going to a scary movie or riding a rollercoaster — initial discomfort followed by a rush. Humans are the only animals that do these things because we know they are not dangerous. It is thrill-seeking.
Now this is not the entire story. Spices in general have their own origins.  Many spices inhibit bacteria, and capsaicin appears to do so as well. This alone could be the reason people started using it more widely. We see that more spices are used in warmer climates, the same places where spoilage would be the biggest risk.  We also see more use of the spices with the highest inhibitory properties. Interestingly humans may not be the only animals to spice food in this way; bears and bees are both known to mix antibacterial plants into stored food.
Additionally small amounts of many spices, even capsaicin, can improve flavor  without generating the burn. This is probably the least understood aspect, but some believe it may be linked to simulating the flavor of better-quality organ meats or increasing bioavailability of some nutrients.
Lastly it has been shown that capsaicin in particular can actually trick the body into cooling itself off even when it would not do so normally. Your body responds to the false signal of heat by cooling itself, which could be a benefit in hotter climates.

Yes, I was going to answer with "benign masochism" also.. The examples of "from negative to positive" experiences are called hedonic reversal.

Here is a relevant article and a relevant excerpt about animals: "There is no
strong evidence for liking for innately negative experiences
in animals. The strongest evidence against animal
exemplars is that rural Mexican dogs and pigs that eat
food with hot peppers regularly (since they eat human
leftovers) do not develop a preference, unlike some hundred
million human Mexicans who share their diet (Rozin
& Kennel, 1983)"

Birds for instance can "ingest" spicy food, but that doesn't mean they actually perceive the spiciness in the same way or at all. If someone can't taste the acidity sulfuric acid, they could drink sulfuric acid and say they liked it.

@DaneJoe it isn't spicy to birds, capsaicin only works on mammals.  birds don't have the same TRPV receptors as mammals, which works for the plants because birds spread the pepper seeds, mammals destroy the seeds when they eat them (chewing) so the pepper want to discourage mammals but not discourage birds.

Right, so when people try to argue that birds have no problem with spicy food, the point is moot.

@DaneJoe correct, chili peppers are not spicy to birds, the closest things to spicy you have for birds is things like mustard, wasabi, or black pepper.

I think like many things spicy food became something that we used as a tool. Used mostly for preserving food, those countries where it gets very hot due to a tropical climate you'll find the food tends to be much spicer in areas where parasitic flies and other pathogens would contaminate the food faster. The spicier it is, the longer your food stocks would last. Over generations they developed a higher and higher tolerance.

Welcome to Biology SE! It'd be great if you can cite your sources. Answers with no references may be challenged or deleted.


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What kind of fish are these?
This should be pretty easy. We have a tropical fish tank, and among a few other species we have an adult pair of these guys. The female is a live-bearer, and seems to be giving birth to two young at a time. However, I can't for the life of me remember what kind of fish they are.

The male is in the foreground, and the female in the background. Any ideas?

I believe it is a Red Wag Platy (Xiphophorus maculatus)

This looks like a Red Wag Platy (Xiphophorus maculatus). Apparently it is a common tropical aquarium fish. Wikipedia does not show a picture of this variant. However a google image search with this will return the images of fish that you have shown.

Thanks for the confirmation, you are correct. I accepted the other answer because yours was posted 10 seconds too late - I doubt you'll mind, though :)

@MattDMo No prob. I realized that after a few minutes and I thought I'll delete mine but someone upvoted. So I thought I'll let it stay :P


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DNA extraction from oil-containing seeds
Which protocol of DNA extraction from plant oil-containing seeds take fast and good result in purity that can use in RT-PCR(Real Time polymerase chain reaction)?

I guess you mean realtime with RT, right?

@Chris yes that's right

Maybe this is interesting for you.

@Chris you should post that as answer. You can copy paste the protocol

The paper "Modified method for combined DNA and RNA isolation from peanut and other oil seeds." has a nice protocol for isolating DNA and RNA (which later can either be differentially digested or precipitated) from oil seeds for PCR. You can find the complete paper in the link above, the materials and methods sections says the following for the extraction method:

RNA and DNA isolation
Approximately 1–1.2 g of dried seed of each genotype was utilized in
  extraction. Seeds were frozen with liquid nitrogen and pulverized by
  grinding with mortar and pestle until a fine powder. Tissue was placed
  into 10 mL solution I (100 mM Tris, 150 mM LiCl, 50 mM EDTA, 1.5 %
  SDS, 2 % PVP-40, 1.5 % b-mercaptoethanol) buffer, pH 7.5, and mixed
  thoroughly by vortexing or inversion.
To the homogenized tissue, a 5
  mL acid phenol, pH 4.3 (Fisher Scientific, Pittsburg, PA) was added
  and tissue was mixed thorough for 5 min, followed by the addition of 5
  mL chloroform:isoamyl alcohol (24:1) and mixed for an additional 5
  min. The homogenate was centrifuged for 10 min and the upper aqueous
  layer (around 9 mL) was transferred to a fresh 40 mL tube containing 9
  mL of solution II (2 M guanidinium thiocyanate, 0.5 M sodium citrate,
  1.5 M ammonium acetate, 1 % N-lauroylsarcosine) buffer, pH 5.2, mixed by gentle inversion, and allowed to incubate for 10 min at room
  temperature.
After incubation, a 4.5 mL phenol:chloroform:isoamyl
  alcohol (25:24:1), pH 6.7 was added, mixed thoroughly for 5 min,
  centrifuged for 10 min at 13,000g, and the aqueous layer (around 16
  mL) was transferred to a new 40 mL tube.
To the transferred solution,
  9 mL 1.2 M NaCl and 9 mL isopropanol were added, mixed, placed on ice
  for at least 1 h, and centrifuged for 15 min at 13,000g. The liquid
  was discarded and the resulting pellet was washed with 2 mL cold 70 %
  ethanol, dried, and resuspended in 4 mL RNase-free water.
4 mL 4 M
  LiCl was added, mixed, placed on ice in the refrigerator for at least
  1 h, and centrifuged for 15 min at 4°C at 13,000g. The supernatant
  (around 8 mL) was transferred to a new 40 mL tube for DNA isolation
  and the pellet was retained for RNA isolation. For RNA isolation, the
  pellet was washed with 2 mL ice-cold 70 % ethanol, dried, and
  resuspended in 750 lL RNase-free water.
For DNA isolation, 8 mL
  isopropanol was added to the transferred supernatant tube, mixed well,
  centrifuged for 5 min, discarded the liquid, washed pellet with 2 mL
  ice-cold 70 % ethanol, dried, and resulting pellet was resuspended in
  500 lL 10 mMTris, pH7.5. The amount of DNA or RNA was determined using
  Nanodrop 2000c spectrophotometer (Thermo Scientific, Wilmington, DE).


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Phage base Biosensor
What kind of biosensor is made by Phages?
I need a list of published paper that used Phages for make LCR(inductance (L), capacitance (C), and resistance (R) of a component) biosensor for detection. for example detection of E.coli

If you are looking for the bacterial receptor that is used by phages then the following review may contain helpful info with respect to E.coli and the lambda phage. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3509688/

Hmm, No I am looking for application of these communication for making Biosensor for example immobilization a phage in a surface and use for detection a specific bacteria by attaching bacterial receptor to phage.

What is LCR? Ligase chain reaction? What is that? I suggest to elaborate your question, or at the very least explain (or better omit) acronyms.

@ChrisStronks An LCR meter is a piece of electronic test equipment used to measure the inductance (L), capacitance (C), and resistance (R) of a component.

So you want to immobilize phages on a surface, then use those to capture bacteria, then look for changes in electrical properties? Whole phages might not be necessary, antibodies against specific bacterial proteins might be easier to use.

This reminded me of something a friend of mine was working on, trying to attach antibodies to specific portions of a CD, then trying to detect protein binding with a standard CD drive. He hoped the proteins would change the reflection enough for the laser to be detect them, but I don't think he ever got it working. If it had worked he would have had a cheap way to detect lots of different proteins at once.

@user137 similar works about it has been worked and I want to use it to determine recombinant phage attachment quality to bacterial cell for treatment in most antibiotic resistant infections. and one more thing, I think your friend will made that.

@M007 That's his name, but I don't like giving out potentially identifying information on the internet. I'd ask you to say for me, but he wouldn't recognize my username.


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PCR limits of detection calculate method
Is any standard method for use to gain PCR sensivity or limit of detection? my mean is not for RT-PCR or Real-Time or any other kind and just simple PCR. After making PCR product free of dNTP and Primers I have a microtube that contain 40ng/micro Liter dsDNA. My product size is 200bp. If I  should diluted it or any other standard acceptable method expain to me please.


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Does sour food cause sweating?
While eating sour food or candy, I start to sweat if it's sour enough. My body feels much hotter although my actual temperature is the same, my forehead starts sweating a lot and I feel like it just got twice as hot wherever I am.
Is this a biological phenomena or is my DNA just stupid? Is it somehow related to the digestive system, that sour food is harder to digest?

In general, sweating is caused by too much heat, even if you're not aware of the heat. This can happen if the bowel moves and so raises the core temperature. Such movement is often accompanied with sweating, and since you only feel the normal temperature on the skin, it is cold sweat. But at the same time your core is hot so you think it's cold, but it will later mix to normal.
Anyway, it points to unusual bowel movement. This can be due to food allergy or, in a milder form, in food intolerances which are quite common. When it comes to sour ingredients, they are often in fruits, so I'll make a shot in the blue and say that you have a food intolerance against some fruits. You can check this hypothesis by trying chemically pure acetic acid to sour your food. If that doesn't result in sweat/hotness then it's probably the fruits.
http://en.wikipedia.org/wiki/Food_intolerance
The Wikipedia points even directly to salicylate in fruits but I think you cannot exclude allergies against essential oils like limonene and such. Plants are really chemistry factories and not all is well that you can get with them.

I do happen to have some fruit allergies, I had no idea it could be connected. I'll try to get my hands on some acetic acid and test what happens like you said. Thank you!

Note that usual vinegar may trigger a grape intolerance/allergy and even seemingly "chemical" acetic essence may be in part extracted.


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What is the advantage of the inverted image on the retina?
Recently, I learned that the image of the world which we see actually reaches the retina inverted.
This is due to the fact that the retina lies behind the focus of our eyes.
I have two questions:

When the retina lies behind the focus and the lens in our eyes has a spherical shape, shouldn't left and right also be interchanged?
What is the advantage of this? Why does the retina lie behind the focus and not in front of it?
Or doesn’t it matter since our brain is not a real screen and it’s only a question of the correct interpretation of the electic signals?

The reason lies in the physics of lenses. There is no advantage for us.

As is said, i totally understand the reason (i.e. the physics going on). But i only read that up and down interchange and not that left and right do the same which makes for me no sense.

If the focus is exactly on the retina, then how should the brain know where the light originally came from. I mean if the light is not separated in space, all information is gone and you left with a bright point.

Right and left also get inverted. A spherical retina ensures that every point of the retina is at equal distance to the pupil to ensure no distortion. In healthy eyes, the focus point should be on the retina. If any of this is unclear to you, then you really should have consider your question on Physics.SE but not on Biology.SE. Our brain inverses the image received in the retina. Assuming it takes a tiny bit of energy to do so, then this inversion really does not come at an advantage. It is just a basic fact of physics, any living creature with an eye has to deal with.

I'm voting to close this question as off-topic because the question is about basic physical optics and not biology.

@b.nota According to my opinion, convex lenses do not automatically invert pictures. The law of nature says 'If the lens is biconvex or plano-convex, a collimated beam of light passing through the lens converges to a spot (a focus) behind the lens'. So all light beams intersect in the focal point and split again (now interchanged) behind the focal point. So therefore i wanted to know if it is an advantage that you have the retina behind the focal point for maybe a better focusing.

@Remi.b I asked the question here in Biology.SE because i am no expert considering the human eye and what advantages it might have to have the retina behind the focal point. The phiscis are far too simple to see any advantage if condsider only a lense and its focus point. I thought something more goes on here that only biologists might know.

@Remi.b I came to that opinion simply by thinking. And it can not work if the focal point lies exactly on the retina. How do you split the information apart if every lightbeam meets in one single point?

@MaxW That isn't what in focus means. Focus is about taking all the light originating from the same point and putting it in the same place on the surface of the retina. Not putting all of the light from everywhere in the same place. The only way to do this is with inversion.  "according to your opinion" doesn't change physics.

Don't confuse the focal point of a lens with the pinhole effect of the eye. The latter inverts the image. I have seen diagrams that also confuse these concepts.

"not that left and right do the same which makes for me no sense." Double check your physics.

There may be no advantage of the inverted image on the retina. But there is an advantage with the lens that refractes the image inverted.
Our eye lens is of convex in nature. Now lets see what is the advantage of convex lens being our eye lens.

Source : http://www.ivyroses.com/HumanBody/Eye/concave-and-convex-lenses.php
The light from the object, when reaches the convex lens it gets refracted and gets "converged" and is a "real image" and also "diminished" but the problem is it makes the light inverted.
Now let us see what happens if our eye lens is a concave lens.

Source : http://www.ivyroses.com/HumanBody/Eye/concave-and-convex-lenses.php
In this case, when the light from the object from a distance reaches the lens, the lens "diverges" the light, also it "enlarges" the image, but it produces an "erect" image but the major problem is that the image is "virtual".
We know how evolution works, it selects more advantageous option generally.
Case - 1: If the lens is convex, the only problem the eye has to handle is that the image is inverted.
Case - 2: But if the lens is concave, it should converge the diverged light, it should diminish it and it should also make it real.
If we take both cases into consideration, case - 1 seems to be easily handled, that's why we have inverted image falling in the retina. There maybe no other specific advantage associated with it.

I totally understand that the lens should be convex, this is not my question. You could simply place the retina a bit in front of the focal point and the picture would not be flipped. So, does this little extra space of moving the retina away from the lens give any optical advantage?

Say me the exact point where the retina should be placed so that convex lens gives an erect image, at f or between between f and 2f or where exactly? I have been taught that you get  an inverted image where ever you place the screen. Refer - http://physics.tutorvista.com/light/convex-lens.html . Only when the object is at 0cm to 25cm, you will get an erect image but that will damage the lens.

@MaxW That's not at all how it works. Whether in front or behind the focal plane, the image will not be in focus; it will be blurry. The pictures in the answer here are showing light from one origin, one object, not light from different objects. It is flipped as soon as it goes through the lens.


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Are the changes required to produce genetically manipulated organisms (GMOS) considered to be mutations
By definition, are mutations required to be natural, or are synthetic lab-induced genetic changes considered mutations too? Furthermore, are genetically manipulated organisms (GMOs) considered forced mutants?

What is a mutation?
A mutation is any change to the DNA sequence. From wikipedia

In biology, a mutation is the permanent alteration of the nucleotide sequence of the genome of an organism, virus, or extrachromosomal DNA or other genetic elements.

Whether a given alteration to the DNA sequence occurred in nature or in a lab changes nothing to the fact that we call this alteration a mutation.
How common are mutations?
Just so that you realize how common mutations are: In humans, a couple having a baby typically transmit about 40 new mutations to this baby. This mutation rate is not quite the same between women and men (see Kong et al.(2012)).
What is a GMO?
I have never seen the term "forced mutants" before but it sounds like you might have a misrepresentation of what GMOs are and esp. in your misrepresentation, you might think that there is such natural category which are GMOs and other that are non GMOs but the boundaries between the two is more than vague.
Consider for example that the vast majority of our food has been manipulated by humans through artificial selection. Check out the ancestor of modern-day corn (from Genetic Society of America; original source: teosinte.wisc.edu; thanks @John)

This evolutionary change occurred via artificial selection mainly and without using modern genetic tools.

What's the source of that image?

It is some google image I found. I forgot the link. I put another one where I could verify the source a bit better. Why the question? Is it just for legal reasons or was there something wrong about the image?

Well I think attribution should be given for other's work, but I was more interested in reading about it. Thanks for the edit.

Orriginal source for the image is here, https://teosinte.wisc.edu/images.html, I use it in my classes. The small ancestral plant is called Teosinte.

I've downsized the image as I assume you didn't know how to do that. 1000px high was hardly necessary.

You quote the Wikipedia article for a definition of ‘mutation’ and then go on to imply — although not to state explicitly — that this means GMOs are produced by mutations. That, after all, was the question. However the extensive Wikipedia article on mutation does not feature a single mention of ‘GMO’ (or genetically manipulated organism). I suggest that this is because, as I have stated in my own answer, the manipulations used to produce GMOs are not generally referred to as mutations. Do you agree or not?

From NIH :

A gene mutation is a permanent alteration in the DNA sequence that makes up a gene, such that the sequence differs from what is found in most people. Mutations range in size; they can affect anywhere from a single DNA building block (base pair) to a large segment of a chromosome that includes multiple genes.

So both naturally occurring, and lab-induced modifications could be considered mutations.
I've never come across the term "forced mutants", but for perspective, a GMO can be created by purposefully exposing the organism to radiation in a controlled manner. In the wild, it is possible that organisms are thusly exposed as well, but in an uncontrolled manner.
For further reading, see this article.

This really is semantics.
There is no clear-cut definition of mutation, whatever you find in a dictionary or in an anonymous article in Wikipedia. However most molecular biologist have a certain picture in their minds when they see or hear the word ‘mutation’, and a certain picture in their minds when they see or hear the phrase ‘genetic manipulation of an organism’.
The two pictures in my mind are very different, but tend to be related to the extent and complexity of the changes rather than whether they occur in the environment or are produced in the laboratory.
Mutation
In plain English mutation just means change, but in molecular genetics one thinks of small-scale changes: base changes, additions or deletions of a base or a short stretch of bases. Those that occur in the environment are random in the general sense, and originally this was also true of those induce in the laboratory through agents such as mutagenic chemicals or ionizing radiation. With advances in recombinant DNA technology the changes could be directed: introduced at particular points in order to produce the desired mutation — site-directed mutagenesis. However the picture is one of small changes, even if they can have major consequences. Certainly the fact that the mutation is directed to produce the desired outcome (presumably what the poster means by ‘forced’ — although this term is not in common use.)
Genetic Manipulation
Genetic manipulated organisms (whether bacteria or mammals) often have a completely new gene inserted into them so that they can produce an entirely different protein — something non-functional like a fluorescent protein, or practical utility like insulin or a protein that provides a plant with resistance to pesticides. The organism is certainly changed, but ‘engineered’ would seem more descriptive of the extent of the change and the technology involved than ‘mutated’. (And although one of the other answers suggests there is no difference in principle between directed plant breeding and and such manipulations, this seems a little ingenuous to me. There is no way you could breed corn so that it expressed the green fluorescent protein from jellyfish.)
My apparently subjective remarks on genetic manipulated organisms and the non-use (or less frequent use) of the term ‘mutation’ is supported by the abstracts you find on googling for GMOs. I cite the first four below:

A genetically modified organism, or GMO, is an organism that has had its DNA altered or modified in some way through genetic engineering.
A genetically modified organism (GMO) is any organism whose genetic material has been altered using genetic engineering techniques (i.e., a genetically engineered organism).
Agricultural plants are one of the most frequently cited examples of genetically modified organisms (GMOs). Some benefits of genetic engineering in agriculture  ...
Genetically modified organisms (GMOs) are living organisms whose genetic material has been artificially manipulated in a laboratory through genetic engineering.


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Reproduction in horses and donkeys
How are horses and donkeys able to interbreed and produce a mule. Don't their genetypic variation or chromosomal difference prevent them from doing so? If not, then why not?

In closely related species chromosome has only some genetic variations. Therefore there is chance of their chromosomes joins. But if interbreed occurs the species will not be fertile. The ova of female species can take the most compatible from the closest male type .
It's not like that different species can't breed, in many cases they can. For example Donkey and horse , tiger and lion, etc, but the fact is that when different species breed they do not Produce fertile offsprings. Hinney, mules, liger and other animals that are produced by breeding between different species are infertile.


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How closely related will your descendants be to you?
I wonder how similar my DNA will be to that of my great-grand-children. If a new person enters my family tree every new generation, he/she will bring in half of his/her DNA, therefore decreasing the amount of DNA that each new generation shares with me. I assume, then, that after several generations, my descendants are going to be no more closely related (genetically) to me than to random people on the streets?
I also once heard that even though the share of my genes will be descreasing, the mutations unique to me will stay. Is that true, and, if so, how is that possible?
And what about all-males descendants? For example, if I have a son and he has XY, then if there always will be a son down the line then will the Y chromosome stay the same through each generation? More specifically, will it still be the Y chromosome from me?

This hasn't been researched or even thought about at all before posting. I'm voting to close for hwk reasons. Clue: Children have ~50% of either parent. Keep halving the amount every generation.

This depends on what you mean by genetic similarity. If you mean the fraction DNA that are still direct copies of your DNA in the n'th generation, then the answer is (1/2)^n.  But if you mean sequence similarity, then the answer is quite different, and depends on the structure of genetic variation in the population.  If some piece of your DNA gets swapped for another piece of DNA, but this DNA has the exact same sequence, do you consider your genetic material to be lost?  See https://en.wikipedia.org/wiki/Identity_by_descent

For how genetically related to you your  my grand-grand-children will be....
Well on the surface the answer is simple. Your grand grand children will 12.5% of your DNA.
Dig a little deeper... the question becomes a bit more difficult to answer.
(1) Humans do cheat a small but significantly amount of time. On average about 0.7-3% of all children are unknowingly raised by men who are not their biological father http://theconversation.com/what-are-the-chances-that-your-dad-isnt-your-father-24802. This is less than the 9-30% which has been reported. The reason appears to be that the data was derived from paternity clinics where  there was already suspicion on paternity of the child. Not the best data set to represent the population, even if the data set was large and mostly free to researchers.
So which that factored in... it depend on what gender you are, and how said grand grand child is related to you. Are you a woman? Is that grand grand child, the child of your daughter's daughter. A pure maternal descended would guarantee a 12.5% genetic relatedness.
But if you are a man, and the grand grand child, is the child of your son's, son... on average genetic relatedness falls to 11-12% (on average). But since a person is related to your or not, there is a 3%-10% that your grand grand child is not related to you if that child is your son's son's child.
(2)Rural (old world) populations tend to share more genetic material since they have had less outside influence into the genepool. This is a reflection of history, where mobility was limited and families tend to stay for generations. In these places, a random stranger isn't that random after all. In which case genetic relatedness calculations become more complicated. Terms to look up are founder effect, population structure. Large cities, with massive influx of people moving in and out tend to be more mixed. Also note isolation, can also because by social stratification. The nobility is a great example where two random nobles are not as random as you think.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1685612/pdf/ajhg00202-0030.pdf
http://link.springer.com/article/10.1007/BF02442864
http://www.nytimes.com/2004/07/31/us/by-accident-utah-is-proving-an-ideal-genetic-laboratory.html rare american example.
https://en.wikipedia.org/wiki/Stoccareddo
http://gizmodo.com/5882644/iceland-is-so-inbred-it-needs-a-website-to-avoid-incest

And I also once heard that even though the share of my genes will be
  descreasing, the mutations unique to me will stay. Is that so and how
  is that possible?

Not quite. A mutation unique to you has only 50% chance of passing on to a child. (Or a 50% chance of not passing to a child.) So if you have 2 children, that mutation will have a (0.5*0.5=0.25) 25% chance of failing to pass to the next generation. In fact unless that mutation has some sort of selective advantage (awesome X-men powers), or your family has really big families for several generation or you and your families becomes a founder of a new colony/town (founder effect), your unique mutation will likely fallout after a few generations.

And what about all-males descendants? Like, if I have a son and he has
  XY, then if there always will be a son down the line then Y chromosome
  is going to stay the same, being the one from me?

yeah they will inherit your Y chromosome.. which will change very little over the generations. It will accumulate a few mutations but that is over thousands of years.

I am sorry you find that offensive. Most old villagers and towns are inbred. (Some more so then others.) It is very useful for population genetics especially when paired up with the marriages information from the local parish. Also depending on how you look at a population, everyone is inbreed. Go back 1000 years ago, and all europeans are related to each other. This is why population genetics has been such a minefield to work with.  I guess I am also not looking at people... but how they are related to each other over centuries. The effective founder population size.The genetic variability

I think we are imagining different countries and rural communities. Stay specific when possible. Which rural study are you referring to?

Thank you for your answer. Yes, I heard about that - how populations in countries that are isolated - like, islands, or just small communities tend to be really related to each other. But why does relatedness for all-male descendants fall to 11-12%? If the same Y chromosomes gets passed on. And it looks like for women the relatedness should be smaller - X chromosome can be piged both from mother and father and therefore already grand-daughter of a woman may not have her X chromosome, only that of her grandfather and her father...

Since at least 99% of all DNA is identical between all humans, it's a little strange to say that only 12.5% will be shared.

@swbarnes2 You're mixing up inheritance and shared DNA. So whereas 99.9% of the DNA is identical to every other human, 12.5% of your genome is from each of your great-grandparents.


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Why is the BRCA-1 mutation dominant?
BRCA-1 is a tumor suppressor gene and on mutation can undergo a loss of function to become cancer-inducing.
Loss of function mutations are usually recessive and require the mutation of both alleles.
However in this case only one allele needs to be mutated to cause loss of function. Why is this so?

The answer depends on when and where you are identifying the phenotype. www.cancer.gov has much useful info, including a fact sheet:
https://www.cancer.gov/about-cancer/causes-prevention/genetics/brca-fact-sheet
From that:

Even if someone has inherited a harmful variant in BRCA1 or BRCA2 from
one parent, they would have inherited a normal copy of that gene from
the other parent ... But the normal copy can be lost or change in some
cells in the body during that person’s lifetime. Such a change is
called a somatic alteration. Cells that don’t have any functioning
BRCA1 or BRCA2 proteins can grow out of control and become cancer.

The pre-existing loss of one functional allele from conception makes any later somatic inactivation of the other allele a homozygous loss of function rather than just a heterozygous LOF.


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Besides fats, proteins, and carbs, what compounds can the body use for energy?
What kinds of chemical species that do not belong to the category of fats, carbohydrates or proteins can the body metabolise?
Clarifications: By metabolise, I mean extract energy from (e.g. as ATP). The chemicals would be ingested as “food” regardless of whether they occur in natural dietary nutrients.
I already know of one, ethanol.
At a wild guess, I suspect the body can extract energy from acetate and citrate too.

@classy_BLINK I'd be very impressed if you could find me somebody who could ingest enough of those to obtain food energy from them without instantly ODing.

I suspect this question needs a little more detail to be answerable. Are you specifically after things that a reasonable user might think of as 'normal food'? We metabolise pyruvate to release energy, and you can buy it as a supplement. If pyruvate is in, then we can start with a list of most of the intermediate metabolites in the Krebs cycle.

Also: human bodies only?

@bshane Yes human bodies, and no it doesn't necessarily have to be 'normal food'. Sounds like the intermediates of the krebs cycle would count. I'm interested in anything a human can extract a non-negligible amount of food energy from without dying in the process. By 'non negligible' I mean at the very least something that would stave off death for a starving person in the short term.

I see two ways to approach this. First, molecules used as part of respiration to store energy as mentioned by bshane. Alternatively, it may be worth considering environmental context (e.g. what other energy sources would humans naturally intake; think chemosynthesis in the deep ocean). Sure, supplementing a human body with pyruvate and/or friends may fit the bill, but (as hinted by classy_BLINK, it would seem likely that having that as a sole (or majority) form of energy intake would probably cause significant dysregulation of metabolism.

The phrase “food energy” means nothing to a biochemist. “Energy” would suffice or ATP if you wish to specify the common chemical intermediate. It appears from the comments(Krebs Cycle intermediates) that you mean food to indicate the form in which the “chemical species are supplied. In which case I suggest “ingested” as a better way of putting it. I will try to edit it, but as there is a bounty on it I may not be able.

@David I stipulated 'food energy' because the energy listed on Nutritional Information boxes is usually derived from calorimetry -i.e. burning the food in the lab and measuring the heat coming off. I wanted to head off any 'look at the back of the packet' comments.

There are two significant energy sources for humans besides fats, carbohydrates, and protein listed in this USDA report that I found:

Organic acids: these are compounds like citric acid and malic acid that make up a small but significant portion of the energy content of many fruits and some vegetables. The energy content is in the range of 2-4 Calories per gram, so slightly less than from protein or carbohydrates.
Alcohol provides about 7 Calories per gram.


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The genetic code and the effect of point mutations on proteins
I was asked a question, "Considering degenerate and non ambiguous nature of genetic code, Why is that certain mutations don't disturb the protein synthesis leading to synthesis of functional proteins where as certain mutations cause synthesis of non functional proteins or diseased proteins?"
My argument was that according to Wobble hypothesis, the tRNA carries anticodons that have A,U,G,C,I where I is inosine (sugar phosphate with hypoxanthine) that can bind with A,C,U of the codon and also G binding with U and vice versa is possible. Then, I gave the example of serine -AGU- whose anticodon is -UCI- for instance and after mutation say, -AGU- becomes -AGC-, it still codes for serine and -UCI- stills agrees to bind with -AGC- giving us serine as before and hence no disturbance is brought up leading to synthesis of functional protein. But suppose -AGU- got mutated to -CGU- , then the anticodon -UCI- no longer can bind with the codon and hence another tRNA molecule with anticodon of that of arginine gets attached and hence leading to interruption in the amino acid sequence which ultimately leads to non functional protein.
But my professor disagrees with my argument and says I am not clear with the concept. Can anyone please help with where I am going wrong ?

Nonambiguity refers to the fact that codon X will always code for the same amino acid.
Degeneracy refers to the fact that an amino acid can be coded for by many codons.
I rephrase the question to get to the gist of things:

Why do certain mutations cause no difference for protein synthesis, while others make a big difference?

Certain mutations can change the codon but still code for the same amino acid, so the resulting peptide sequence is unaltered (synthesis of a functionally identical protein). This is due to degeneracy, explained above. Certain other mutations change the codon in a way that produces a completely different amino acid, and these result in the synthesis of a different, distinct peptide that may be dysfunctional. This due to nonambiguity of the code. Simple!
It's best to refer to our translation guide, the codon table. If you know your codon table, you might have noticed that within a codon frame, changing the 3rd nucleotide often has no effect on the translated amino acid (see outer ring, below). Changing the 1st and 2nd nucleotide produces a more drastic effect in the translation of the codon.
That means that the position of a nucleotide mutation within the reading frame is key to the effect of the mutation on protein synthesis.

Where I am going wrong?

You are complicating the picture needlessly. You fail to explain that the resulting amino acid depends on its codon, and that the effect of changing the codon in different places (position 1, 2 or 3) has different outcomes. You also have to think about different kinds of mutations; we are discussing substitutions, but you must also consider what deletions and insertions of nucleotides do to the translation of the peptide! You may also get bonus points for discussing the start and stop codons... they are special cases.

OK, I completely agree that I haven't been specific to the point considering the degeneracy and non-ambiguity, but I need some clarification. Does the point about wobble hypothesis explain the concept of synthesis of functional and non-functional proteins ?

@SurajS — The wobble hypothesis is irrelevant to the question you have been asked. That answers how the degenerate genetic code operates. If the answer were through 61 different tRNAs it was make no difference to the effect of the degeneracy on the likelihood of a mutation having a detrimental effect. The genetic code diagram in this answer may look pretty, but I think you would do better looking at the standard tabular presentation found in text books and Wikipedia. This makes it easier to see how mutations would affect both the amino acid encoded, and the “type” of amino acid encoded.

@David Oh, now I get it. Thanks a lot


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What is the difference between a viral strain and a viral isolate?
Both are characterized, their genes are usually described and published, they are kept safe, they could be used as inoculum or to produce vaccine... Would it be correct to say a strain would be somehow a successful isolate ?

An isolate is a sample. It's this particular virus in this fridge, that was isolated from this, e.g., sputum sample, and cultured. A strain is more abstract -- it is a distinguishable, stable genetic variant of a species. An isolate may be identified as a particular strain of a particular species. That's how I and my colleagues use these terms, in any case, and how they're generally used in the literature. You can read more about this here and here
From the first reference (since it's behind a paywall)
Isolate

An isolate may be defined as “a sample of biological material, especially a microorganism, that has been cultured for study” which is clear, perfectly acceptable and useable by virologists.

Strain

Although there is no official definition of a strain, the strain concept is widely used and a de facto definition states “strains are viruses that belong to the same species and differ in having stable and heritable biological, serological, and/or molecular characters”.


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Peptides neither produced by the ribosome or the non-ribosomal peptide synthase complexes
I read in Wikipedia:

While there exist a wide range of peptides that are not synthesized by
  ribosomes, the term nonribosomal peptide typically refers to a very
  specific set of these as discussed in this article.

I was wondering what peptides are being referred to. I can only think of synthetically produced peptides. I can not find any source for other peptides not produced either by the ribosome or by the non-ribosomal peptide synthases described.

One peptide that comes to mind is the metabolically important reducing tripeptide glutathione — γ-L-Glutamyl-L-cysteinylglycine:

This is synthesized from cysteine, glutamate and glycine by reactions catalysed by glutamate cysteine ligase and glutathione synthase:

Synthesis of glutathione (GSH) — two subunits of glutamate cysteine ligase (GCL) are shown
Other examples may involve amino acids not specified by the genetic code which have particular roles in metabolism. For example, taurine, which has a sulphonic — rather than a carboxylic — acid group, can be metabolized to the dipeptide γ-Glutamyltaurine which may have a role in the brain.
These two examples relate to L-amino acids, albeit with a peptide bond between the side-chain glutamyl carboxyl group rather than the α-carboxyl group. However a D-amino acid dipeptide, D-alanyl-D-alanine, synthesized in the reaction catalysed by D-alanine-D-alanine ligase, is a precursor of bacterial peptidoglycan synthesis.
All the examples given have in common the fact that the peptides are very short (di- or tri-peptides) and can be synthesized in reactions requiring one or two specialized enzymes. Bacterial antibiotics synthesized by the non-ribosomal peptide complex tend to be appreciably larger, requiring repeated formation of peptide bonds.


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Why is the GenBank entry for the genomes of RNA viruses like coronavirus written as DNA?
The reference genome in GenBank of the sars coronavirus from Wuhan is written in the following format:
attaaaggtttataccttcc

(The first 20 nucleotides)
Considering that coronaviruses are RNA viruses, the bases of which are adenine, cytosine, guanine and uracil, I was surprised to see the t symbol in the sequence, which stands for thymine, found in DNA, not in RNA. Additionally, no u symbols are present in the sequence.
So, what's going on here? Where did Thymine come from, why no Uracil?

RNA is sequenced by reverse transcribing it to cDNA, and this is the sequence that is submitted. In fact, I don't think I've ever seen a sequence in NCBI specifying uracil instead of thymine (not that I've looked).

Thanks! Some further questions persist. Is this cDNA ever present in nature or is it an artifact of the secuencing procedure? Are there any other differences between ARN and the transcripted cDNA?

Retroviruses naturally have cDNA as part of their life cycle. The mechanism of retrotransposon transposition also involves cDNA.  In this case, it’s just due to the sequencing method.

It would appear that the current policy at GenBank is to represent all genomic sequences as DNA, even though this is not made explicit in any of the easily retrievable documentation on their website or in their publications. The way in which one determines the nature of the genome is from the first (LOCUS) line in the report, which, in the case of SARS-CoV-2 is:
LOCUS       NC_045512              29903 bp ss-RNA     linear   VRL 30-MAR-2020

The ss-RNA indicates a single-stranded RNA genome.
The only indication I could find that this might be GenBank policy was a reference to the fact that a separate RNA division of GenBank used to exist, but was discontinued in 1999:

The RNA division of GenBank was removed in release 113.0 (August 1999). Sequences that were previously in the RNA division have been moved to the appropriate organismal division.

The genomes of certain RNA phages were originally sequenced as RNA (as were bacterial rRNAs and 18S rRNA) — that of phage MS2 was the first in 1976. The GenBank entries for these are currently in DNA format. Thus V00642.1 contains references to the 1976 MS2 paper by Fiers et al., but is in DNA format. As GenBank was not established until 1982 it is not clear whether the original entry in GenBank was in RNA or DNA format.

UPDATE 15.04.2020
I wrote to GenBank to ask them whether there was a specific policy and if so when it had been introduced. I had a reply from someone on their help desk to the effect that GenBank policy was that of International Nucleotide Sequence Database Collaboration, the shared rules of which includes table "7.4.1 Nucleotide base codes (IUPAC)". This states that "t" can represent thymine in DNA and  uracil in RNA. However my respondent could not find out whether this representation was used in GenBank for RNA viruses from the beginning or introduced later. As originally GenBank releases were on CD-ROM this is difficult to check.

It's not GenBank's policy, it is a long standing tradition in molecular biology to express sequences in DNA form.

@TumbiSapichu — unsubstantiated assertions are valueless on SE Biology. If you read my post you will see that RNA sequences were determined before DNA sequence methodology emerged, and that originally they were stored in databases as RNA. I was there and remember it. So much for "traditions in molecular biology"! For ribosomal RNA and tRNA it is still necessary to have databases with the actual bases because many are modified.